A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19.
A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM.
An alpha-globulin of about 453 amino acids, depending on the species. It is produced by the liver and secreted into blood circulation. Angiotensinogen is the inactive precursor of natural angiotensins. Upon successive enzyme cleavages, angiotensinogen yields angiotensin I, II, and III with amino acids numbered at 10, 8, and 7, respectively.
A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Compounds based on fumaric acid.
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
A decapeptide that is cleaved from precursor angiotensinogen by RENIN. Angiotensin I has limited biological activity. It is converted to angiotensin II, a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME.
Oligopeptides which are important in the regulation of blood pressure (VASOCONSTRICTION) and fluid homeostasis via the RENIN-ANGIOTENSIN SYSTEM. These include angiotensins derived naturally from precursor ANGIOTENSINOGEN, and those synthesized.
A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
Physiologically inactive substances that can be converted to active enzymes.
A diet which contains very little sodium chloride. It is prescribed by some for hypertension and for edematous states. (Dorland, 27th ed)
A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.
Organic compounds containing the -CO-NH2 radical. Amides are derived from acids by replacement of -OH by -NH2 or from ammonia by the replacement of H by an acyl group. (From Grant & Hackh's Chemical Dictionary, 5th ed)
Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.
Hypertension due to RENAL ARTERY OBSTRUCTION or compression.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.
A peptidyl-dipeptidase that catalyzes the release of a C-terminal dipeptide, -Xaa-*-Xbb-Xcc, when neither Xaa nor Xbb is Pro. It is a Cl(-)-dependent, zinc glycoprotein that is generally membrane-bound and active at neutral pH. It may also have endopeptidase activity on some substrates. (From Enzyme Nomenclature, 1992) EC 3.4.15.1.
One of two salivary glands in the neck, located in the space bound by the two bellies of the digastric muscle and the angle of the mandible. It discharges through the submandibular duct. The secretory units are predominantly serous although a few mucous alveoli, some with serous demilunes, occur. (Stedman, 25th ed)
Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.
Excision of kidney.
The circulation of the BLOOD through the vessels of the KIDNEY.
A condition of markedly elevated BLOOD PRESSURE with DIASTOLIC PRESSURE usually greater than 120 mm Hg. Malignant hypertension is characterized by widespread vascular damage, PAPILLEDEMA, retinopathy, HYPERTENSIVE ENCEPHALOPATHY, and renal dysfunction.
The amount of a substance secreted by cells or by a specific organ or organism over a given period of time; usually applies to those substances which are formed by glandular tissues and are released by them into biological fluids, e.g., secretory rate of corticosteroids by the adrenal cortex, secretory rate of gastric acid by the gastric mucosa.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
An adrenal disease characterized by the progressive destruction of the ADRENAL CORTEX, resulting in insufficient production of ALDOSTERONE and HYDROCORTISONE. Clinical symptoms include ANOREXIA; NAUSEA; WEIGHT LOSS; MUSCLE WEAKNESS; and HYPERPIGMENTATION of the SKIN due to increase in circulating levels of ACTH precursor hormone which stimulates MELANOCYTES.
A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. Defects in STEROID 21-HYDROXYLASE; STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES); TESTOSTERONE 5-ALPHA-REDUCTASE; or steroidogenic acute regulatory protein; among others, underlie these disorders.
Pathological processes of the ADRENAL GLANDS.
A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.
Conditions in which the production of adrenal CORTICOSTEROIDS falls below the requirement of the body. Adrenal insufficiency can be caused by defects in the ADRENAL GLANDS, the PITUITARY GLAND, or the HYPOTHALAMUS.
A condition caused by prolonged exposure to excess levels of cortisol (HYDROCORTISONE) or other GLUCOCORTICOIDS from endogenous or exogenous sources. It is characterized by upper body OBESITY; OSTEOPOROSIS; HYPERTENSION; DIABETES MELLITUS; HIRSUTISM; AMENORRHEA; and excess body fluid. Endogenous Cushing syndrome or spontaneous hypercortisolism is divided into two groups, those due to an excess of ADRENOCORTICOTROPIN and those that are ACTH-independent.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.

Effects of long-term administration of clonidine on plasma renin activity. (1/3749)

Plasma renin activity (PRA) was studied before and during long-term treatment with moderate oral doses (0.2 or 0.3 mg/d) of clonidine. Nine outpatients with essential hypertension received clonidine for 12 weeks; a significant decrease in blood pressure was evident in all patients. Except for a nonsignificant increase after 12 weeks of treatment, PRA values were not notably changed by clonidine therapy. No correlation was found between individual blood pressure changes and PRA variation during the study. The absence of a net effect on PRA in this study does not exclude more complex interactions of clonidine with the renin-angiotensin system. Nonetheless, clonidine cannot generally be classified as a "renin-inhibiting" drug.  (+info)

Intrarenal site of action of calcium on renin secretion in dogs. (2/3749)

We studied the effects of intrarenal calcium infusion on renin secretion in sodium-depleted dogs in an attempt to elucidate the major site of calcium-induced inhibition of renin release. Both calcium chloride and calcium gluconate reduced renal blood flow and renin secretion while renal perfusion pressure was unchanged. These data indicate that calcium inhibition of renin secretion did not occur primarily at the renal vascular receptor; decreased renal blood flow is usually associated with increased renin secretion. Calcium chloride infusion increased urinary chloride excretion without affecting sodium excretion, and calcium gluconate failed to increase either sodium or chloride excretion. Also, the filtered loads of sodium and chloride were unchanged during the calcium infusions. These results give no indication that calcium inhibited renin secretion by increasing the sodium or chloride load at the macula densa. The effects of intrarenal calcium infusion on renin release were also assessed in dogs with a nonfiltering kidney in which renal tubular mechanisms could not influence renin secretion. The observation that calcium still suppressed renin release in these dogs provides additional evidence that the the major effect of calcium involved nontubular mechanisms. Thus, it appears likely that calcium acted directly on the juxtaglomerular cells to inhibit renin secretion.  (+info)

Stimulation of renin release from rabbit renal cortex by arachidonic acid and prostaglandin endoperoxides. (3/3749)

The mechanism by which renal prostaglandins stimulate renin secretion in vivo is unknown. In this in vitro study we measured the effects of activation of the prostaglandin (PG) system on renin release from slices of rabbit renal cortex. The PG precursor arachidonic acid (C20:4), a natural PG endoperoxide (PGG2), two stable synthetic PG endoperoxide analogues (EPA I and II), PGE2, PGF2alpha, and two different PG synthesis inhibitors [indomethacin and 5,8,11,14-eicosatetraynoic acid (ETA)] were used to evaluate the possibility of a direct action of the cortical PG system on renin secretion. Renin release increased significantly with time after addition of C20:4, PGG2, EPA I, and EPA II to the incubation medium. Stimulation of renin release was se-related for C20:4 in concentrations of 0.6 to 4.5 X 10(-6) M, for EPA I in concentrations of 0.7 to 2.8 X 10(-6) M, and for EPA II in concentrations of 1.4 to 14.0 X 10(-6) M. Indomethacin (10(-4) M) and ETA (10(-4) M) significantly decreased basal renin release as well as the renin release stimulated by C20:4 and EPA I. PGE2(10(-12) to 10(-6) M) had no effect on renin release, whereas PGF2alpha (10(-12) to 10(-6) M) decreased renin release in a dose-dependent manner. These data raise the possibility of a direct action of the renal cortical PG system on renin secretion. The results further indicate that stimulation of renin release by C20:4 may depend more specifically on the action of PG endoperoxides than on the primary prostaglandins.  (+info)

An alternative transcript of the rat renin gene can result in a truncated prorenin that is transported into adrenal mitochondria. (4/3749)

Characterization of the local renin-angiotensin system in the rat adrenal zona glomerulosa indicated a dual targeting of renin both to the secretory pathway and mitochondria. To investigate the transport of renin into mitochondria, we constructed a series of amino-terminal deletion variants of preprorenin. One of these variants, lacking the complete signal sequence for the endoplasmic reticulum and 10 amino acids of the profragment, was transported efficiently into isolated mitochondria. The transport was further shown to be dependent on mitochondrial membrane potential and ATP synthesis. Analysis of adrenal RNA revealed the existence of 2 renin transcripts. While one of the transcripts corresponds to the known full-length transcript, the other one lacks exon 1; instead, exon 2 is preceded by a domain of 80 nucleotides originating from intron 1. This domain, as well as the following region of intron 1 being excised, shows all essential sequence elements defining an additional, so-far-unknown exon. The second mRNA possibly derives from an additional transcription start in intron 1 and an alternative splicing process. Translation of this mRNA could result in a truncated prorenin representing a cytosolic form of renin, which is required for transport into mitochondria. This truncated prorenin corresponds exactly to the deletion variant being imported into mitochondria in vitro.  (+info)

Low calorie diet enhances renal, hemodynamic, and humoral effects of exogenous atrial natriuretic peptide in obese hypertensives. (5/3749)

The expression of the natriuretic peptide clearance receptor is abundant in human and rat adipose tissue, where it is specifically inhibited by fasting. In obese hypertensives, plasma atrial natriuretic peptide (ANP) levels were found to be lower than in obese normotensives. Therefore, the increased adipose mass might influence ANP levels and/or its biological activity. The aim of the present study was to evaluate whether the humoral, hemodynamic, and renal effects of exogenous ANP in obese hypertensives might be enhanced by a very low calorie diet. Eight obese hypertensives received a bolus injection of ANP (0.6 mg/kg) after 2 weeks of a normal calorie/normal sodium diet, and blood pressure (BP), heart rate, ANP, cGMP, plasma renin activity, and aldosterone were evaluated for 2 hours before and after the injection. Diuresis and natriuresis were measured every 30 minutes. The patients then started a low calorie/normal sodium diet (510 kcal/150 mmol/d) for 4 days, and then the ANP injection protocol was repeated. The low calorie diet induced a slight weight loss (from 90.6+/-1.1 to 87. 7+/-1.2 kg; P<0.01), which was accompanied by increase of cGMP excretion (from 146.0+/-10.1 to 154.5+/-9.5 nmol/24 h; P<0.05) together with a reduction of BP (P<0.01 versus basal levels). ANP injection after diet was followed by an increase of ANP levels similar to that observed before diet, but plasma cGMP, diuresis, and natriuresis increased significantly only after diet. Similarly, the decrease of BP after ANP administration was significantly higher after diet (change in mean arterial pressure, -6.4+/-0.7 versus -4. 0+/-0.6 mm Hg; P<0.05) as well as that of aldosterone (P<0.01). These data show that a low calorie diet enhances the humoral, renal, and hemodynamic effects of ANP in obese hypertensives and confirm the importance of caloric intake in modulating the biological activity of ANP, suggesting that the natriuretic peptide system can play a role in the acute changes of natriuresis and diuresis associated with caloric restriction.  (+info)

Recovery following relief of unilateral ureteral obstruction in the neonatal rat. (6/3749)

BACKGROUND: Obstructive nephropathy is a primary cause of renal insufficiency in infants and children. This study was designed to distinguish the reversible and irreversible cellular consequences of temporary unilateral ureteral obstruction (UUO) on the developing kidney. METHODS: Rats were subjected to UUO or sham operation in the first 48 hours of life, and the obstruction was removed five days later (or was left in place). Kidneys were removed for study 14 or 28 days later. In additional groups, kidneys were removed at the end of five days of obstruction. Immunoreactive distribution of renin was determined in arterioles, and the distribution of epidermal growth factor, transforming growth factor-beta1, clusterin, vimentin, and alpha-smooth muscle actin was determined in tubules and/or interstitium. The number of glomeruli, glomerular maturation, tubular atrophy, and interstitial collagen deposition was determined by morphometry. Renal cellular proliferation and apoptosis were measured by proliferating cell nuclear antigen and the TdT uridine-nick-end-label technique, respectively. The glomerular filtration rate was measured by inulin clearance. RESULTS: Renal microvascular renin maintained a fetal distribution with persistent UUO; this was partially reversed by the relief of obstruction. Although glomerular maturation was also delayed and glomerular volume was reduced by UUO, the relief of obstruction prevented the reduction in glomerular volume. Although relief of obstruction did not reverse a 40% reduction in the number of nephrons, the glomerular filtration rate of the postobstructed kidney was normal. The relief of obstruction did not improve tubular cell proliferation and only partially reduced apoptosis induced by UUO. This was associated with a persistent reduction in the tubular epidermal growth factor. In addition, the relief of obstruction reduced but did not normalize tubular expression of transforming growth factor-beta1, clusterin, and vimentin, all of which are evidence of persistent tubular injury. The relief of obstruction significantly reduced interstitial fibrosis and expression of alpha-smooth muscle actin by interstitial fibroblasts, but not to normal levels. CONCLUSIONS: The relief of obstruction in the neonatal rat attenuates, but does not reverse, renal vascular, glomerular, tubular, and interstitial injury resulting from five days of UUO. Hyperfiltration by remaining nephrons and residual tubulointerstitial injury in the postobstructed kidney are likely to lead to deterioration of renal function later in life.  (+info)

Long-term effects of growth hormone (GH) on body fluid distribution in GH deficient adults: a four months double blind placebo controlled trial. (7/3749)

OBJECTIVE: Short-term growth hormone (GH) treatment normalises body fluid distribution in adult GH deficient patients, but the impact of long-term treatment on body fluid homeostasis has hitherto not been thoroughly examined in placebo controlled trials. To investigate if the water retaining effect of GH persists for a longer time we examined the impact of 4 months GH treatment on extracellular volume (ECV) and plasma volume (PV) in GH deficient adults. DESIGN: Twenty-four (18 male, 6 female) adult GH deficient patients aged 25-64 years were included and received either GH (n=11) or placebo (n=13) in a double blind parallel design. METHODS: Before and at the end of each 4 month period ECV and PV were assessed directly using 82Br- and 125I-albumin respectively, and blood samples were obtained. RESULTS: During GH treatment ECV increased significantly (before: 20.48+/-0.99 l, 4 months: 23.77+/-1.38 l (P<0.01)), but remained unchanged during placebo administration (before: 16.92+/-1.01 l, 4 months: 17.60+/-1.24 l (P=0.37)). The difference between the groups was significant (P<0.05). GH treatment also increased PV (before: 3.39+/-0.27 l. 4 months: 3.71+/-0.261 (P=0.01)), although an insignificant increase in the placebo treated patients (before: 2.81+/-0.18 l, 4 months: 2.89+/-0.20 l (P=0.37)) resulted in an insignificant treatment effect (P=0.07). Serum insulin-like growth factor-I increased significantly during GH treatment and was not affected by placebo treatment. Plasma renin (mIU/l) increased during GH administration (before: 14.73+/-2.16, 4 months: 26.00+/-6.22 (P=0.03)) and remained unchanged following placebo (before: 20.77+/-5.13, 4 months: 20.69+/-6.67 (P=0.99)) leaving no significant treatment effect (P=0.08). CONCLUSION: The long-term impact of GH treatment on body fluid distribution in adult GH deficient patients involves expansion of ECV and probably also PV. These data substantiate the role of GH as a regulator of fluid homeostasis in adult GH deficiency.  (+info)

Tranilast suppresses vascular chymase expression and neointima formation in balloon-injured dog carotid artery. (8/3749)

BACKGROUND: Activation of vascular chymase plays a major role in myointimal hypertrophy after vascular injury by augmenting the production of angiotensin (ANG) II. Because chymase is synthesized mainly in mast cells, we assumed that the chymase-dependent ANG II formation could be downregulated by tranilast, a mast cell-stabilizing antiallergic agent. We have assessed inhibitory effects of tranilast on neointima formation after balloon injury in the carotid artery of dogs, which share a similar ANG II-forming chymase with humans, and further explored the pathophysiological significance of vascular chymase. METHODS AND RESULTS: Either tranilast (50 mg/kg BID) or vehicle was orally administered to beagles for 2 weeks before and 4 weeks after balloon injury. Four weeks after the injury, remarkable neointima was formed in the carotid arteries of vehicle-treated dogs. Chymase mRNA levels and chymaselike activity of vehicle-treated injured arteries were increased 10.2- and 4.8-fold, respectively, those of uninjured arteries. Angiotensin-converting enzyme (ACE) activity was slightly increased in the injured arteries, whereas ACE mRNA levels were not. Tranilast treatment completely prevented the increase in chymaselike activity, reduced the chymase mRNA levels by 43%, and decreased the carotid intima/media ratio by 63%. In vehicle-treated injured arteries, mast cell count in the adventitia showed a great increase, which was completely prevented by the tranilast treatment. Vascular ACE activity and mRNA levels were unaffected by tranilast. CONCLUSIONS: Tranilast suppressed chymase gene expression, which was specifically activated in the injured arteries, and prevented neointima formation. Suppression of the chymase-dependent ANG II-forming pathway may contribute to the beneficial effects of tranilast.  (+info)

Renin is a medically recognized term and it is defined as:

"A protein (enzyme) that is produced and released by specialized cells (juxtaglomerular cells) in the kidney. Renin is a key component of the renin-angiotensin-aldosterone system (RAAS), which helps regulate blood pressure and fluid balance in the body.

When the kidney detects a decrease in blood pressure or a reduction in sodium levels, it releases renin into the bloodstream. Renin then acts on a protein called angiotensinogen, converting it to angiotensin I. Angiotensin-converting enzyme (ACE) subsequently converts angiotensin I to angiotensin II, which is a potent vasoconstrictor that narrows blood vessels and increases blood pressure.

Additionally, angiotensin II stimulates the adrenal glands to release aldosterone, a hormone that promotes sodium reabsorption in the kidneys and increases water retention, further raising blood pressure.

Therefore, renin plays a critical role in maintaining proper blood pressure and electrolyte balance in the body."

The Renin-Angiotensin System (RAS) is a complex hormonal system that regulates blood pressure, fluid and electrolyte balance, and vascular resistance. It plays a crucial role in the pathophysiology of hypertension, heart failure, and kidney diseases.

Here's a brief overview of how it works:

1. Renin is an enzyme that is released by the juxtaglomerular cells in the kidneys in response to decreased blood pressure or reduced salt delivery to the distal tubules.
2. Renin acts on a protein called angiotensinogen, which is produced by the liver, converting it into angiotensin I.
3. Angiotensin-converting enzyme (ACE), found in the lungs and other tissues, then converts angiotensin I into angiotensin II, a potent vasoconstrictor that narrows blood vessels and increases blood pressure.
4. Angiotensin II also stimulates the release of aldosterone from the adrenal glands, which promotes sodium and water reabsorption in the kidneys, further increasing blood volume and blood pressure.
5. Additionally, angiotensin II has direct effects on the heart, promoting hypertrophy and remodeling, which can contribute to heart failure.
6. The RAS can be modulated by various medications, such as ACE inhibitors, angiotensin receptor blockers (ARBs), and aldosterone antagonists, which are commonly used to treat hypertension, heart failure, and kidney diseases.

Angiotensinogen is a protein that is produced mainly by the liver. It is the precursor to angiotensin I, which is a molecule that begins the process of constriction (narrowing) of blood vessels, leading to an increase in blood pressure. When angiotensinogen comes into contact with an enzyme called renin, it is cleaved into angiotensin I. Angiotensin-converting enzyme (ACE) then converts angiotensin I into angiotensin II, which is a potent vasoconstrictor and a key player in the body's regulation of blood pressure and fluid balance.

Angiotensinogen is an important component of the renin-angiotensin-aldosterone system (RAAS), which helps to regulate blood pressure and fluid balance by controlling the volume and flow of fluids in the body. Disorders of the RAAS can lead to high blood pressure, kidney disease, and other health problems.

Aldosterone is a hormone produced by the adrenal gland. It plays a key role in regulating sodium and potassium balance and maintaining blood pressure through its effects on the kidneys. Aldosterone promotes the reabsorption of sodium ions and the excretion of potassium ions in the distal tubules and collecting ducts of the nephrons in the kidneys. This increases the osmotic pressure in the blood, which in turn leads to water retention and an increase in blood volume and blood pressure.

Aldosterone is released from the adrenal gland in response to a variety of stimuli, including angiotensin II (a peptide hormone produced as part of the renin-angiotensin-aldosterone system), potassium ions, and adrenocorticotropic hormone (ACTH) from the pituitary gland. The production of aldosterone is regulated by a negative feedback mechanism involving sodium levels in the blood. High sodium levels inhibit the release of aldosterone, while low sodium levels stimulate its release.

In addition to its role in maintaining fluid and electrolyte balance and blood pressure, aldosterone has been implicated in various pathological conditions, including hypertension, heart failure, and primary hyperaldosteronism (a condition characterized by excessive production of aldosterone).

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

Fumarates are the salts or esters of fumaric acid, a naturally occurring organic compound with the formula HO2C-CH=CH-CO2H. In the context of medical therapy, fumarates are used as medications for the treatment of psoriasis and multiple sclerosis.

One such medication is dimethyl fumarate (DMF), which is a stable salt of fumaric acid. DMF has anti-inflammatory and immunomodulatory properties, and it's used to treat relapsing forms of multiple sclerosis (MS) and moderate-to-severe plaque psoriasis.

The exact mechanism of action of fumarates in these conditions is not fully understood, but they are thought to modulate the immune system and have antioxidant effects. Common side effects of fumarate therapy include gastrointestinal symptoms such as diarrhea, nausea, and abdominal pain, as well as flushing and skin reactions.

Angiotensin II is a potent vasoactive peptide hormone that plays a critical role in the renin-angiotensin-aldosterone system (RAAS), which is a crucial regulator of blood pressure and fluid balance in the body. It is formed from angiotensin I through the action of an enzyme called angiotensin-converting enzyme (ACE).

Angiotensin II has several physiological effects on various organs, including:

1. Vasoconstriction: Angiotensin II causes contraction of vascular smooth muscle, leading to an increase in peripheral vascular resistance and blood pressure.
2. Aldosterone release: Angiotensin II stimulates the adrenal glands to release aldosterone, a hormone that promotes sodium reabsorption and potassium excretion in the kidneys, thereby increasing water retention and blood volume.
3. Sympathetic nervous system activation: Angiotensin II activates the sympathetic nervous system, leading to increased heart rate and contractility, further contributing to an increase in blood pressure.
4. Thirst regulation: Angiotensin II stimulates the hypothalamus to increase thirst, promoting water intake and helping to maintain intravascular volume.
5. Cell growth and fibrosis: Angiotensin II has been implicated in various pathological processes, such as cell growth, proliferation, and fibrosis, which can contribute to the development of cardiovascular and renal diseases.

Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are two classes of medications commonly used in clinical practice to target the RAAS by blocking the formation or action of angiotensin II, respectively. These drugs have been shown to be effective in managing hypertension, heart failure, and chronic kidney disease.

Blood pressure is the force exerted by circulating blood on the walls of the blood vessels. It is measured in millimeters of mercury (mmHg) and is given as two figures:

1. Systolic pressure: This is the pressure when the heart pushes blood out into the arteries.
2. Diastolic pressure: This is the pressure when the heart rests between beats, allowing it to fill with blood.

Normal blood pressure for adults is typically around 120/80 mmHg, although this can vary slightly depending on age, sex, and other factors. High blood pressure (hypertension) is generally considered to be a reading of 130/80 mmHg or higher, while low blood pressure (hypotension) is usually defined as a reading below 90/60 mmHg. It's important to note that blood pressure can fluctuate throughout the day and may be affected by factors such as stress, physical activity, and medication use.

Angiotensin I is a decapeptide (a peptide consisting of ten amino acids) that is generated by the action of an enzyme called renin on a protein called angiotensinogen. Renin cleaves angiotensinogen to produce angiotensin I, which is then converted to angiotensin II by the action of an enzyme called angiotensin-converting enzyme (ACE).

Angiotensin II is a potent vasoconstrictor, meaning it causes blood vessels to narrow and blood pressure to increase. It also stimulates the release of aldosterone from the adrenal glands, which leads to increased sodium and water reabsorption in the kidneys, further increasing blood volume and blood pressure.

Angiotensin I itself has little biological activity, but it is an important precursor to angiotensin II, which plays a key role in regulating blood pressure and fluid balance in the body.

Angiotensins are a group of hormones that play a crucial role in the body's cardiovascular system, particularly in regulating blood pressure and fluid balance. The most well-known angiotensins are Angiotensin I, Angiotensin II, and Angiotensin-(1-7).

Angiotensinogen is a protein produced mainly by the liver. When the body requires an increase in blood pressure, renin (an enzyme produced by the kidneys) cleaves angiotensinogen to form Angiotensin I. Then, another enzyme called angiotensin-converting enzyme (ACE), primarily found in the lungs, converts Angiotensin I into Angiotensin II.

Angiotensin II is a potent vasoconstrictor, causing blood vessels to narrow and increase blood pressure. It also stimulates the release of aldosterone from the adrenal glands, which leads to increased sodium reabsorption in the kidneys, further raising blood pressure and promoting fluid retention.

Angiotensin-(1-7) is a more recently discovered member of the angiotensin family. It has opposing effects to Angiotensin II, acting as a vasodilator and counterbalancing some of the negative consequences of Angiotensin II's actions.

Medications called ACE inhibitors and ARBs (angiotensin receptor blockers) are commonly used in clinical practice to target the renin-angiotensin system, lowering blood pressure and protecting against organ damage in various cardiovascular conditions.

Furosemide is a loop diuretic medication that is primarily used to treat edema (fluid retention) associated with various medical conditions such as heart failure, liver cirrhosis, and kidney disease. It works by inhibiting the sodium-potassium-chloride cotransporter in the ascending loop of Henle in the kidneys, thereby promoting the excretion of water, sodium, and chloride ions. This increased urine output helps reduce fluid accumulation in the body and lower blood pressure.

Furosemide is also known by its brand names Lasix and Frusid. It can be administered orally or intravenously, depending on the patient's condition and the desired rate of diuresis. Common side effects include dehydration, electrolyte imbalances, hearing loss (in high doses), and increased blood sugar levels.

It is essential to monitor kidney function, electrolyte levels, and fluid balance while using furosemide to minimize potential adverse effects and ensure appropriate treatment.

Hypertension is a medical term used to describe abnormally high blood pressure in the arteries, often defined as consistently having systolic blood pressure (the top number in a blood pressure reading) over 130 mmHg and/or diastolic blood pressure (the bottom number) over 80 mmHg. It is also commonly referred to as high blood pressure.

Hypertension can be classified into two types: primary or essential hypertension, which has no identifiable cause and accounts for about 95% of cases, and secondary hypertension, which is caused by underlying medical conditions such as kidney disease, hormonal disorders, or use of certain medications.

If left untreated, hypertension can lead to serious health complications such as heart attack, stroke, heart failure, and chronic kidney disease. Therefore, it is important for individuals with hypertension to manage their condition through lifestyle modifications (such as healthy diet, regular exercise, stress management) and medication if necessary, under the guidance of a healthcare professional.

Enzyme precursors are typically referred to as zymogens or proenzymes. These are inactive forms of enzymes that can be activated under specific conditions. When the need for the enzyme's function arises, the proenzyme is converted into its active form through a process called proteolysis, where it is cleaved by another enzyme. This mechanism helps control and regulate the activation of certain enzymes in the body, preventing unwanted or premature reactions. A well-known example of an enzyme precursor is trypsinogen, which is converted into its active form, trypsin, in the digestive system.

A sodium-restricted diet is a meal plan designed to limit the amount of sodium (salt) intake. The recommended daily sodium intake for adults is less than 2,300 milligrams (mg), but for those with certain medical conditions such as high blood pressure, heart failure, or chronic kidney disease, a lower daily sodium limit of 1,500 to 2,000 mg may be recommended.

A sodium-restricted diet typically involves avoiding processed and packaged foods, which are often high in sodium, and limiting the use of salt when cooking or at the table. Fresh fruits, vegetables, lean proteins, and whole grains are encouraged as they are naturally low in sodium. It is important to read food labels carefully, as some foods may contain hidden sources of sodium.

Adhering to a sodium-restricted diet can help manage blood pressure, reduce fluid retention, and decrease the risk of heart disease and stroke. However, it is important to consult with a healthcare provider or a registered dietitian before starting any new diet plan to ensure that it meets individual nutritional needs and medical conditions.

Captopril is a medication that belongs to a class of drugs called ACE (angiotensin-converting enzyme) inhibitors. It works by blocking the action of a chemical in the body called angiotensin II, which causes blood vessels to narrow and release hormones that can increase blood pressure. By blocking the action of angiotensin II, captopril helps relax and widen blood vessels, which lowers blood pressure and improves blood flow.

Captopril is used to treat high blood pressure (hypertension), congestive heart failure, and to improve survival after a heart attack. It may also be used to protect the kidneys from damage due to diabetes or high blood pressure. The medication comes in the form of tablets that are taken by mouth, usually two to three times per day.

Common side effects of captopril include cough, dizziness, headache, and skin rash. More serious side effects may include allergic reactions, kidney problems, and changes in blood cell counts. It is important for patients taking captopril to follow their doctor's instructions carefully and report any unusual symptoms or side effects promptly.

An amide is a functional group or a compound that contains a carbonyl group (a double-bonded carbon atom) and a nitrogen atom. The nitrogen atom is connected to the carbonyl carbon atom by a single bond, and it also has a lone pair of electrons. Amides are commonly found in proteins and peptides, where they form amide bonds (also known as peptide bonds) between individual amino acids.

The general structure of an amide is R-CO-NHR', where R and R' can be alkyl or aryl groups. Amides can be classified into several types based on the nature of R and R' substituents:

* Primary amides: R-CO-NH2
* Secondary amides: R-CO-NHR'
* Tertiary amides: R-CO-NR''R'''

Amides have several important chemical properties. They are generally stable and resistant to hydrolysis under neutral or basic conditions, but they can be hydrolyzed under acidic conditions or with strong bases. Amides also exhibit a characteristic infrared absorption band around 1650 cm-1 due to the carbonyl stretching vibration.

In addition to their prevalence in proteins and peptides, amides are also found in many natural and synthetic compounds, including pharmaceuticals, dyes, and polymers. They have a wide range of applications in chemistry, biology, and materials science.

Renal hypertension, also known as renovascular hypertension, is a type of secondary hypertension (high blood pressure) that is caused by narrowing or obstruction of the renal arteries or veins, which supply blood to the kidneys. This can lead to decreased blood flow and oxygen delivery to the kidney tissue, activating the renin-angiotensin-aldosterone system (RAAS) and resulting in increased peripheral vascular resistance, sodium retention, and extracellular fluid volume, ultimately causing hypertension.

Renal hypertension can be classified into two types:

1. Renin-dependent renal hypertension: This is caused by a decrease in blood flow to the kidneys, leading to increased renin release from the juxtaglomerular cells of the kidney. Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that causes an increase in peripheral vascular resistance and blood pressure.
2. Renin-independent renal hypertension: This is caused by increased sodium retention and extracellular fluid volume, leading to an increase in blood pressure. This can be due to various factors such as obstructive sleep apnea, primary aldosteronism, or pheochromocytoma.

Renal hypertension is often asymptomatic but can lead to serious complications such as kidney damage, heart failure, and stroke if left untreated. Diagnosis of renal hypertension involves imaging studies such as renal artery duplex ultrasound, CT angiography, or magnetic resonance angiography (MRA) to identify any narrowing or obstruction in the renal arteries or veins. Treatment options include medications such as ACE inhibitors, angiotensin receptor blockers (ARBs), calcium channel blockers, and diuretics, as well as interventions such as angioplasty and stenting to improve blood flow to the kidneys.

Renovascular hypertension is a type of secondary hypertension (high blood pressure) that is caused by renal artery stenosis or narrowing. This condition reduces blood flow to the kidneys, leading to the activation of the renin-angiotensin-aldosterone system (RAAS), which causes an increase in peripheral vascular resistance and blood volume, resulting in hypertension.

Renovascular hypertension is often seen in people with atherosclerosis or fibromuscular dysplasia, which are the most common causes of renal artery stenosis. Other conditions that can lead to renovascular hypertension include vasculitis, blood clots, and compression of the renal artery by nearby structures.

Diagnosis of renovascular hypertension typically involves imaging studies such as duplex ultrasound, CT angiography, or magnetic resonance angiography to visualize the renal arteries and assess for stenosis. Treatment may involve medications to control blood pressure, lifestyle modifications, and procedures such as angioplasty and stenting to open up the narrowed renal artery. In some cases, surgery may be necessary to restore blood flow to the kidney.

Sodium is an essential mineral and electrolyte that is necessary for human health. In a medical context, sodium is often discussed in terms of its concentration in the blood, as measured by serum sodium levels. The normal range for serum sodium is typically between 135 and 145 milliequivalents per liter (mEq/L).

Sodium plays a number of important roles in the body, including:

* Regulating fluid balance: Sodium helps to regulate the amount of water in and around your cells, which is important for maintaining normal blood pressure and preventing dehydration.
* Facilitating nerve impulse transmission: Sodium is involved in the generation and transmission of electrical signals in the nervous system, which is necessary for proper muscle function and coordination.
* Assisting with muscle contraction: Sodium helps to regulate muscle contractions by interacting with other minerals such as calcium and potassium.

Low sodium levels (hyponatremia) can cause symptoms such as confusion, seizures, and coma, while high sodium levels (hypernatremia) can lead to symptoms such as weakness, muscle cramps, and seizures. Both conditions require medical treatment to correct.

Angiotensin-Converting Enzyme (ACE) inhibitors are a class of medications that are commonly used to treat various cardiovascular conditions, such as hypertension (high blood pressure), heart failure, and diabetic nephropathy (kidney damage in people with diabetes).

ACE inhibitors work by blocking the action of angiotensin-converting enzyme, an enzyme that converts the hormone angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor, meaning it narrows blood vessels and increases blood pressure. By inhibiting the conversion of angiotensin I to angiotensin II, ACE inhibitors cause blood vessels to relax and widen, which lowers blood pressure and reduces the workload on the heart.

Some examples of ACE inhibitors include captopril, enalapril, lisinopril, ramipril, and fosinopril. These medications are generally well-tolerated, but they can cause side effects such as cough, dizziness, headache, and elevated potassium levels in the blood. It is important for patients to follow their healthcare provider's instructions carefully when taking ACE inhibitors and to report any unusual symptoms or side effects promptly.

Peptidyl-dipeptidase A is more commonly known as angiotensin-converting enzyme (ACE). It is a key enzyme in the renin-angiotensin-aldosterone system (RAAS), which regulates blood pressure and fluid balance.

ACE is a membrane-bound enzyme found primarily in the lungs, but also in other tissues such as the heart, kidneys, and blood vessels. It plays a crucial role in converting the inactive decapeptide angiotensin I into the potent vasoconstrictor octapeptide angiotensin II, which constricts blood vessels and increases blood pressure.

ACE also degrades the peptide bradykinin, which is involved in the regulation of blood flow and vascular permeability. By breaking down bradykinin, ACE helps to counteract its vasodilatory effects, thereby maintaining blood pressure homeostasis.

Inhibitors of ACE are widely used as medications for the treatment of hypertension, heart failure, and diabetic kidney disease, among other conditions. These drugs work by blocking the action of ACE, leading to decreased levels of angiotensin II and increased levels of bradykinin, which results in vasodilation, reduced blood pressure, and improved cardiovascular function.

The submandibular glands are one of the major salivary glands in the human body. They are located beneath the mandible (jawbone) and produce saliva that helps in digestion, lubrication, and protection of the oral cavity. The saliva produced by the submandibular glands contains enzymes like amylase and mucin, which aid in the digestion of carbohydrates and provide moisture to the mouth and throat. Any medical condition or disease that affects the submandibular gland may impact its function and could lead to problems such as dry mouth (xerostomia), swelling, pain, or infection.

Antihypertensive agents are a class of medications used to treat high blood pressure (hypertension). They work by reducing the force and rate of heart contractions, dilating blood vessels, or altering neurohormonal activation to lower blood pressure. Examples include diuretics, beta blockers, ACE inhibitors, ARBs, calcium channel blockers, and direct vasodilators. These medications may be used alone or in combination to achieve optimal blood pressure control.

Nephrectomy is a surgical procedure in which all or part of a kidney is removed. It may be performed due to various reasons such as severe kidney damage, kidney cancer, or living donor transplantation. The type of nephrectomy depends on the reason for the surgery - a simple nephrectomy involves removing only the affected portion of the kidney, while a radical nephrectomy includes removal of the whole kidney along with its surrounding tissues like the adrenal gland and lymph nodes.

Renal circulation refers to the blood flow specifically dedicated to the kidneys. The main function of the kidneys is to filter waste and excess fluids from the blood, which then get excreted as urine. To perform this function efficiently, the kidneys receive a substantial amount of the body's total blood supply - about 20-25% in a resting state.

The renal circulation process begins when deoxygenated blood from the rest of the body returns to the right side of the heart and is pumped into the lungs for oxygenation. Oxygen-rich blood then leaves the left side of the heart through the aorta, the largest artery in the body.

A portion of this oxygen-rich blood moves into the renal arteries, which branch directly from the aorta and supply each kidney with blood. Within the kidneys, these arteries divide further into smaller vessels called afferent arterioles, which feed into a network of tiny capillaries called the glomerulus within each nephron (the functional unit of the kidney).

The filtration process occurs in the glomeruli, where waste materials and excess fluids are separated from the blood. The resulting filtrate then moves through another set of capillaries, the peritubular capillaries, which surround the renal tubules (the part of the nephron that reabsorbs necessary substances back into the bloodstream).

The now-deoxygenated blood from the kidneys' capillary network coalesces into venules and then merges into the renal veins, which ultimately drain into the inferior vena cava and return the blood to the right side of the heart. This highly specialized circulation system allows the kidneys to efficiently filter waste while maintaining appropriate blood volume and composition.

Malignant hypertension is a severe form of hypertension (high blood pressure) that is characterized by extremely high blood pressure readings, typically greater than 180/120 mmHg, along with evidence of damage to one or more organ systems. This condition is considered a medical emergency and requires immediate treatment.

Malignant hypertension can cause rapid and severe damage to various organs in the body, including the brain, heart, kidneys, and eyes. Symptoms may include severe headache, visual disturbances, confusion, shortness of breath, chest pain, nausea, vomiting, seizures, and even coma.

The exact cause of malignant hypertension is not always known, but it can be associated with certain underlying medical conditions such as kidney disease, autoimmune disorders, pregnancy-related complications, or the use of certain medications. Treatment typically involves aggressive blood pressure control using intravenous medications in a hospital setting, along with management of any underlying conditions and prevention of further organ damage.

Secretory rate refers to the amount or volume of a secretion produced by a gland or an organ over a given period of time. It is a measure of the productivity or activity level of the secreting structure. The secretory rate can be quantified for various bodily fluids, such as saliva, sweat, digestive enzymes, hormones, or milk, depending on the context and the specific gland or organ being studied.

In clinical settings, measuring the secretory rate might involve collecting and analyzing samples over a certain duration to estimate the production rate of the substance in question. This information can be helpful in diagnosing conditions related to impaired secretion, monitoring treatment responses, or understanding the physiological adaptations of the body under different circumstances.

Losartan is an angiotensin II receptor blocker (ARB) medication that is primarily used to treat hypertension (high blood pressure), but can also be used to manage chronic heart failure and protect against kidney damage in patients with type 2 diabetes. It works by blocking the action of angiotensin II, a hormone that causes blood vessels to narrow and blood pressure to rise. By blocking this hormone's effects, losartan helps relax and widen blood vessels, making it easier for the heart to pump blood and reducing the workload on the cardiovascular system.

The medical definition of losartan is: "A synthetic angiotensin II receptor antagonist used in the treatment of hypertension, chronic heart failure, and diabetic nephropathy. It selectively blocks the binding of angiotensin II to the AT1 receptor, leading to vasodilation, decreased aldosterone secretion, and increased renin activity."

Addison disease, also known as primary adrenal insufficiency or hypocortisolism, is a rare endocrine disorder characterized by the dysfunction and underproduction of hormones produced by the adrenal glands, specifically cortisol and aldosterone. The adrenal glands are located on top of the kidneys and play a crucial role in regulating various bodily functions such as metabolism, blood pressure, stress response, and immune system function.

The primary cause of Addison disease is the destruction of more than 90% of the adrenal cortex, which is the outer layer of the adrenal glands responsible for hormone production. This damage can be due to an autoimmune disorder where the body's immune system mistakenly attacks and destroys the adrenal gland tissue, infections such as tuberculosis or HIV, cancer, genetic disorders, or certain medications.

The symptoms of Addison disease often develop gradually and may include fatigue, weakness, weight loss, decreased appetite, low blood pressure, darkening of the skin, and mood changes. In some cases, an acute crisis known as acute adrenal insufficiency or Addisonian crisis can occur, which is a medical emergency characterized by sudden and severe symptoms such as extreme weakness, confusion, dehydration, vomiting, diarrhea, low blood sugar, and coma.

Diagnosis of Addison disease typically involves blood tests to measure hormone levels, imaging studies such as CT scans or MRIs to assess the adrenal glands' size and structure, and stimulation tests to evaluate the adrenal glands' function. Treatment usually involves replacing the missing hormones with medications such as hydrocortisone, fludrocortisone, and sometimes mineralocorticoids. With proper treatment and management, individuals with Addison disease can lead normal and productive lives.

Congenital Adrenal Hyperplasia (CAH) is a group of inherited genetic disorders that affect the adrenal glands, which are triangular-shaped glands located on top of the kidneys. The adrenal glands are responsible for producing several essential hormones, including cortisol, aldosterone, and androgens.

CAH is caused by mutations in genes that code for enzymes involved in the synthesis of these hormones. The most common form of CAH is 21-hydroxylase deficiency, which affects approximately 90% to 95% of all cases. Other less common forms of CAH include 11-beta-hydroxylase deficiency and 3-beta-hydroxysteroid dehydrogenase deficiency.

The severity of the disorder can vary widely, depending on the degree of enzyme deficiency. In severe cases, the lack of cortisol production can lead to life-threatening salt wasting and electrolyte imbalances in newborns. The excess androgens produced due to the enzyme deficiency can also cause virilization, or masculinization, of female fetuses, leading to ambiguous genitalia at birth.

In milder forms of CAH, symptoms may not appear until later in childhood or even adulthood. These may include early puberty, rapid growth followed by premature fusion of the growth plates and short stature, acne, excessive hair growth, irregular menstrual periods, and infertility.

Treatment for CAH typically involves replacing the missing hormones with medications such as hydrocortisone, fludrocortisone, and/or sex hormones. Regular monitoring of hormone levels and careful management of medication doses is essential to prevent complications such as adrenal crisis, growth suppression, and osteoporosis.

In severe cases of CAH, early diagnosis and treatment can help prevent or minimize the risk of serious health problems and improve quality of life. Genetic counseling may also be recommended for affected individuals and their families to discuss the risks of passing on the disorder to future generations.

Adrenal gland diseases refer to a group of medical conditions that affect the function or structure of the adrenal glands. The adrenal glands are small, triangular-shaped glands located on top of each kidney. They are responsible for producing several essential hormones, including cortisol, aldosterone, and adrenaline (epinephrine).

There are various types of adrenal gland diseases, some of which include:

1. Adrenal Insufficiency: A condition where the adrenal glands do not produce enough hormones, particularly cortisol and aldosterone. This can lead to symptoms such as fatigue, weight loss, low blood pressure, and skin hyperpigmentation.
2. Cushing's Syndrome: A condition characterized by an excess of cortisol in the body. It can be caused by a tumor in the pituitary gland or adrenal glands, or it can result from long-term use of steroid medications.
3. Adrenal Cancer: A rare type of cancer that affects the adrenal glands. Symptoms may include abdominal pain, weight loss, and high blood pressure.
4. Pheochromocytoma: A tumor that develops in the adrenal glands and causes an overproduction of adrenaline (epinephrine) and noradrenaline (norepinephrine). Symptoms may include high blood pressure, headaches, sweating, and anxiety.
5. Adrenal Hemorrhage: A condition where bleeding occurs in the adrenal glands, often as a result of severe trauma or infection. This can lead to adrenal insufficiency and other complications.
6. Congenital Adrenal Hyperplasia: An inherited disorder that affects the production of cortisol and other hormones in the adrenal glands. Symptoms may include ambiguous genitalia, precocious puberty, and short stature.

Treatment for adrenal gland diseases varies depending on the specific condition and its severity. Treatment options may include medication, surgery, or radiation therapy.

The adrenal glands are a pair of endocrine glands that are located on top of the kidneys. Each gland has two parts: the outer cortex and the inner medulla. The adrenal cortex produces hormones such as cortisol, aldosterone, and androgens, which regulate metabolism, blood pressure, and other vital functions. The adrenal medulla produces catecholamines, including epinephrine (adrenaline) and norepinephrine (noradrenaline), which help the body respond to stress by increasing heart rate, blood pressure, and alertness.

Adrenal insufficiency is a condition in which the adrenal glands do not produce adequate amounts of certain hormones, primarily cortisol and aldosterone. Cortisol helps regulate metabolism, respond to stress, and suppress inflammation, while aldosterone helps regulate sodium and potassium levels in the body to maintain blood pressure.

Primary adrenal insufficiency, also known as Addison's disease, occurs when there is damage to the adrenal glands themselves, often due to autoimmune disorders, infections, or certain medications. Secondary adrenal insufficiency occurs when the pituitary gland fails to produce enough adrenocorticotropic hormone (ACTH), which stimulates the adrenal glands to produce cortisol.

Symptoms of adrenal insufficiency may include fatigue, weakness, weight loss, decreased appetite, nausea, vomiting, diarrhea, abdominal pain, low blood pressure, dizziness, and darkening of the skin. Treatment typically involves replacing the missing hormones with medications taken orally or by injection.

Cushing syndrome is a hormonal disorder that occurs when your body is exposed to high levels of the hormone cortisol for a long time. This can happen due to various reasons such as taking high doses of corticosteroid medications or tumors that produce cortisol or adrenocorticotropic hormone (ACTH).

The symptoms of Cushing syndrome may include:

* Obesity, particularly around the trunk and upper body
* Thinning of the skin, easy bruising, and purple or red stretch marks on the abdomen, thighs, breasts, and arms
* Weakened bones, leading to fractures
* High blood pressure
* High blood sugar
* Mental changes such as depression, anxiety, and irritability
* Increased fatigue and weakness
* Menstrual irregularities in women
* Decreased fertility in men

Cushing syndrome can be diagnosed through various tests, including urine and blood tests to measure cortisol levels, saliva tests, and imaging tests to locate any tumors. Treatment depends on the cause of the condition but may include surgery, radiation therapy, chemotherapy, or adjusting medication dosages.

Pregnancy is a physiological state or condition where a fertilized egg (zygote) successfully implants and grows in the uterus of a woman, leading to the development of an embryo and finally a fetus. This process typically spans approximately 40 weeks, divided into three trimesters, and culminates in childbirth. Throughout this period, numerous hormonal and physical changes occur to support the growing offspring, including uterine enlargement, breast development, and various maternal adaptations to ensure the fetus's optimal growth and well-being.

... is not commonly referred to as a hormone, albeit it having a receptor, the (pro)renin receptor, also known as the renin ... The normal concentration of renin in adult human plasma is 1.98-24.6 ng/L in the upright position. Renin activates the renin- ... Angiotensin-converting enzyme Plasma renin activity Renin inhibitor Renin stability regulatory element (REN-SRE) GRCh38: ... all of which may produce renin. Renin is usually measured as the plasma renin activity (PRA). PRA is measured specially in case ...
"Purification and properties of renin and gamma-renin from the mouse submaxillary gland". The Journal of Biological Chemistry. ... Gamma-renin (EC 3.4.21.54) is an enzyme. This enzyme catalyses the following chemical reaction Cleavage of the Leu-Leu bond in ... Gamma-renin at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Portal: Biology (EC 3.4.21). ... Drinkwater CC, Evans BA, Richards RI (June 1988). "Sequence and expression of mouse gamma-renin". The Journal of Biological ...
... s bind to the active site of renin and inhibit the binding of renin to angiotensinogen, which is the rate- ... Brown, M. J. (2006). "Direct renin inhibition - a new way of targeting the renin system". Journal of the Renin-Angiotensin- ... Consequently, renin inhibitors prevent the formation of Ang I and Ang II. Renin inhibitors may also prevent Ang-(1-7), Ang-(1-9 ... Renin is a circulating enzyme that acts on a circulating peptide, angiotensinogen. Renin cleaves the peptide at the Leu10-Val11 ...
The renin receptor binds renin and prorenin. Binding of renin to this receptor induces the conversion of angiotensinogen to ... "Pivotal role of the renin/prorenin receptor in angiotensin II production and cellular responses to renin". J. Clin. Invest. 109 ... The renin receptor also known as ATPase H(+)-transporting lysosomal accessory protein 2, or the prorenin receptor, is a protein ... 2006). "Renin increases mesangial cell transforming growth factor-beta1 and matrix proteins through receptor-mediated, ...
Renin (Persian: رنين) may refer to: Renin-e Bozorg Renin-e Kuchek This disambiguation page lists articles about distinct ...
Direct renin inhibitors can also be used for hypertension. The drugs that inhibit renin are aliskiren and the investigational ... The renin-angiotensin system (RAS), or renin-angiotensin-aldosterone system (RAAS), is a hormone system that regulates blood ... PMID 9570034.[permanent dead link] Nguyen G (March 2011). "Renin, (pro)renin and receptor: an update". Clinical Science. 120 (5 ... into renin and secrete it directly into the circulation. Plasma renin then carries out the conversion of angiotensinogen, ...
... (Persian: رنين بزرگ, also Romanized as Renīn-e Bozorg; also known as Renīn-e Shams od Dīn) is a village in ... Renin-e Bozorg can be found at GEOnet Names Server, at this link, by opening the Advanced Search box, entering "10406724" in ...
... can be found at GEOnet Names Server, at this link, by opening the Advanced Search box, entering "10406724" in ... Renin-e Kuchek (Persian: رنين كوچك, also Romanized as Renīn-e Kūcheḵ) is a village in Gowharan Rural District, Gowharan ...
... (PRA), also known as the renin (active) assay or random plasma renin, is a measure of the activity of the ... Renin Direct. New Assays for Aldosterone, Renin and Parathyroid Hormone Archived 2011-10-27 at the Wayback Machine University ... Cloning and sequence analysis of cDNA for human renin precursor. PubMed. Pivotal role of the renin/prorenin receptor in ... Different secretory pathways of renin from mouse cells transfected with the human renin gene. 1988 Mar 5; PubMed Free text. ...
... (ARR) is the mass concentration of aldosterone divided by the plasma renin activity or by serum ... The aldosterone/renin ratio is recommended as screening tool for primary hyperaldosteronism. There is more than one way to ... 1] Aldosterone-Renin Ratio in Primary Hyperaldosteronism by Allan S. Brett. Posted: 03/15/2005; Journal Watch. 2005;4(2) (All ... If the inverse ratio (i.e. renin-to-aldosterone) ratio is used, a value lower than the cutoff indicates primary ...
... of the renin (REN) gene. It acts to regulate the levels of renin protein produced in the cell. Renin is secreted by renal ... untranslated region of human renin mRNA and differentially modulate renin expression". J. Biol. Chem. 278 (45): 44894-44903. ... Page for Renin stability regulatory element (REN-SRE) at Rfam v t e (Cis-regulatory RNA elements, All stub articles, Molecular ... The Renin stability regulatory element (REN-SRE) is a cis-acting element identified in the 3'untranslated region (3'UTR) ...
... is a peer-reviewed academic journal that publishes papers in the field of ... Journal of the Renin-Angiotensin-Aldosterone System is abstracted and indexed in, among other databases: SCOPUS, and the Social ... Journal of the Renin-Angiotensin-Aldosterone System is a resource for biomedical professionals, including basic scientists and ... Journal of the Renin-Angiotensin-Aldosterone System also publishes research on other peptides, such as vasopressin, the ...
Renin-e Bozorg , Renin-e Kuchek , Reza Alichi , Rezayi , Rezvan , Rig Deraz , Rig Kag , Rig Muled , Rig , Rig , Rigu , Riku , ...
Wilben Albert, Renin. "IPL 2021: [Watch] KKR players have a ball while enjoying a game of 'Maram Pitti'". www.sportskeeda.com. ...
... is an antagonist to renin. Renin, the first enzyme in the renin-angiotensin-aldosterone system, plays a role in blood ... Aliskiren (brand names Tekturna and Rasilez) is the first in a class of drugs called direct renin inhibitors. It is used for ... Therefore, pharmacologists have been looking for a drug to inhibit renin directly. Aliskiren is the first drug to do so. "First ... PharmaXChange: Direct Renin Inhibitors as Antihypertensive Drugs Archived 2010-12-07 at the Wayback Machine "Aliskiren". Drug ...
Blood pressure and fluid and electrolyte homeostasis is regulated by the renin-angiotensin-aldosterone system.Renin, an enzyme ... Renin and Angiotensin; Jackson E.K., 789-821) Editors; Brunton L.L., Lazo J.S., Parker K.L. New York McGraw Hill 2006. ISBN 0- ... In 1939, renin was found not to cause the rise in blood pressure, but was an enzyme which catalyzed the formation of the ... Their results suggested the kidneys produced a protein, which they named renin, that caused a rise in blood pressure. In the ...
Rather, both renin and aldosterone are measured, and a resultant aldosterone-to-renin ratio (ARR) is used for case detection. A ... Tiu SC, Choi CH, Shek CC, Ng YW, Chan FK, Ng CM, Kong AP (January 2005). "The use of aldosterone-renin ratio as a diagnostic ... "Renin/Aldosterone Protocol". United Bristol Healthcare NHS Trust. Archived from the original on 2007-08-13. Funder JW, Carey RM ... The increased blood pressure will lead to increased glomerular filtration rate and cause a decrease in renin released from the ...
Therefore, the granular (JG) cells seem to be the only source of active renin. "Renin , Definition of Renin by Lexico". Lexico ... Prorenin (/prəˈriːnɪn/) is a protein that constitutes a precursor for renin, the hormone that activates the renin-angiotensin ... Jan Danser, A. H.; Batenburg, W. W.; van Esch, J. H. M. (8 March 2007). "Prorenin and the (pro)renin receptor--an update". ... Morganti, Alberto (2019). "Renin and Prorenin". Encyclopedia of Endocrine Diseases. pp. 478-482. doi:10.1016/B978-0-12-801238- ...
Renin activates a circulating liver derived prohormone angiotensinogen by proteolytic cleavage of all but its first ten amino ... The renin-angiotensin-aldosterone system is a major blood pressure regulating mechanism. Markers of electrolyte and water ... Renin and Angiotensin". In Brunton, Laurence L.; Lazo, John S.; Parker, Keith (eds.). Goodman & Gilman's The Pharmacological ... Luno J, Praga M, de Vinuesa SG (2005). "The reno-protective effect of the dual blockade of the renin angiotensin system (RAS ...
Renin and Angiotensin". In Brunton LL, Chabner B, Knollmann BC (eds.). Goodman & Gilman's The Pharmacological Basis of ... The packaging for valsartan includes a warning stating the drug should not be used with the renin inhibitor aliskiren in people ... Makani H, Bangalore S, Desouza KA, Shah A, Messerli FH (January 2013). "Efficacy and safety of dual blockade of the renin- ... The U.S. prescribing information lists the following drug interactions for valsartan: Other inhibitors of the renin-angiotensin ...
The production of aldosterone is regulated via the renin-angiotensin II-aldosterone system, a system composed of baroreceptors ... Secondary hyperaldosteronism may occur from a renin-producing tumor, or other edematous disorders that affect the baroreceptors ... Fountain JH, Kaur J, Lappin SL (2023). "Physiology, Renin Angiotensin System". StatPearls. Treasure Island (FL): StatPearls ...
At the same time, the juxtaglomerular cells sense the decrease in blood pressure and release renin. Renin converts ... Renin-angiotensin system (RAS): This system is generally known for its long-term adjustment of arterial pressure. This system ... Aldosterone release: This steroid hormone is released from the adrenal cortex in response to activation of the renin- ... Fountain J, Lappin SL (January 2022). "Physiology, Renin Angiotensin System.". StatPearls. Treasure Island, FL: StatPearls ...
The elevated blood pressure seen in Page kidney is thought to be caused by the activation of the renin-angiotensin-aldosterone ... This decrease in blood flow is recognized by the juxtaglomerular (JG) cells and promotes the cleavage of prorenin into renin. ... The compression is believed to cause activation of the renin-angiotensin-aldosterone system (RAAS) via microvascular ischemia.[ ... Fountain, JH; Lappin, SL (July 27, 2020). Physiology, Renin Angiotensin System. Treasure Island, FL: StatPearls Publishing. ...
The renin-angiotensin system and its blockers. Igić R, Škrbić R. Srp Arh Celok Lek. 2014 Nov-Dec;142(11-12):756-63. doi: ... Activity of renin and angiotensin converting enzyme in retina and ciliary body. (In Serbo-croatian). Liječ Vjes 1977;99:482-4. ... Farmakologija renin-angiotenzin sistema. Banja Luka, Medicinski fakultet, 2014. Igić R, Erdos EG, Yeh HS, Sorells K, Nakajima T ... Igić R, Škrbić R. The renin-angiotensin system and its blockers. Srp Arh Celok Lek 2014;142:756-63. Sokolova-Djokic L, Zizic- ...
Inhibitors of the renin-angiotensin system (RAS) are recommended in heart failure. The angiotensin receptor-neprilysin ... Over time, these increases in workload, which are mediated by long-term activation of neurohormonal systems such as the renin- ... Vasopressin levels are usually increased, along with renin, angiotensin II, and catecholamines to compensate for reduced ... renin-angiotensin system inhibitors; and beta-blockers. In 2011, nonhypertensive heart failure was one of the 10 most expensive ...
"Renin-positive granulated Goormaghtigh cells. Immunohistochemical and electron-microscopic studies on biopsies from patients ... although it has been associated with the secretion of erythropoietin and secretion of renin. They are distinguished from ... and play a role in renal autoregulation of blood flow to the kidney and regulation of systemic blood pressure through the renin ...
Paul, Renin (7 March 2006). "GM reduces Suzuki alliance by 17.4 percent to raise $2bn". Earthtimes.com. Webster, Mark (2002), ...
Succinate serves as a modulator of blood pressure by stimulating renin release in macula densa and juxtaglomerular apparatus ... Peti-Peterdi, János; Gevorgyan, Haykanush; Lam, Lisa; Riquier-Brison, Anne (2012-06-23). "Metabolic control of renin secretion ...
Ruilope LM, Tamargo J (April 2017). "Renin-angiotensin system blockade: Finerenone". Nephrologie & Therapeutique. 13 Suppl 1: ...
Sumners C, Horiuchi M, Widdop RE, McCarthy C, Unger T, Steckelings UM (2013). "Protective arms of the renin-angiotensin-system ... Angiotensin II is an octapeptide hormone central to the renin-angiotensin system. It regulates blood pressure control, water ... Receptor agonists and antagonist of angiotensin II receptors that target various parts of the complicated renin-angiotensin ... Alterman M. (2010). "Development of selective non-peptide angiotensin II type 2 receptor agonists". J Renin Angiotensin ...
Renin is not commonly referred to as a hormone, albeit it having a receptor, the (pro)renin receptor, also known as the renin ... The normal concentration of renin in adult human plasma is 1.98-24.6 ng/L in the upright position. Renin activates the renin- ... Angiotensin-converting enzyme Plasma renin activity Renin inhibitor Renin stability regulatory element (REN-SRE) GRCh38: ... all of which may produce renin. Renin is usually measured as the plasma renin activity (PRA). PRA is measured specially in case ...
Renin is a hormone that controls the production of aldosterone, a hormone made in the adrenal glands. The two hormones are ... A renin test measures renin levels in the blood. ... What is a renin test?. This test measures the level of renin in ... Other names: renin blood test, plasma renin activity (PRA) aldosterone-renin ratio (ARR) ... A renin test (or renin and aldosterone test) is used to find out if the adrenal glands are making too much or too little ...
Antlanger, M. et al. Molecular remodeling of the renin-angiotensin system after kidney transplantation. J. Renin. Angiotensin ... Gleeson, P. J. et al. Renin as a marker of tissue-perfusion and prognosis in critically Ill patients. Crit. Care Med. 47(2), ... Chen, L. et al. Stimulation of renin secretion by angiotensin II blockade is Gsalpha-dependent. J. Am. Soc. Nephrol. 21(6), 986 ... Vaduganathan, M. et al. Renin-angiotensin-aldosterone system inhibitors in patients with Covid-19. N. Engl. J. Med. 382(17), ...
Renin-angiotensin system edit Main article: Renin-angiotensin system. The renin-angiotensin system, showing role of renin at ... Renin is not commonly referred to as a hormone, albeit it having a receptor, the (pro)renin receptor, also known as the renin ... Further information: Plasma renin activity. Renin is usually measured as the plasma renin activity (PRA). PRA is measured ... Renin Direct. *^ Phillips MI, Schmidt-Ott KM (Dec 1999). "The Discovery of Renin 100 Years Ago". News in Physiological Sciences ...
The renin-angiotensin system (RAS), or renin-angiotensin-aldosterone system (RAAS), is a hormone system that regulates blood ... Fetal renin-angiotensin system edit In the fetus, the renin-angiotensin system is predominantly a sodium-losing system,[ ... Local renin-angiotensin systems edit Locally expressed renin-angiotensin systems have been found in a number of tissues, ... Direct renin inhibitors can also be used for hypertension.[19] The drugs that inhibit renin are aliskiren[20] and the ...
"Renin continues to be a much sought-after target, and our team has been one of the few that has been able to generate highly ... The renin inhibitor program, which was in the lead optimization phase when GSK signed on as a partner, now has a lead compound ... Home News Vitae Regains Rights to Preclinical Renin Inhibitor Program from GSK ... The companies inked a deal in June 2005 vaued at $175 million to develop and commercialize novel renin inhibitor drug compounds ...
Alkyl Amine Renin Inhibitors: Filling S1 from S3 ... Renin. A, B. 340. Homo sapiens. Mutation(s): 0 Gene Names: REN ... Biphenyl/diphenyl ether renin inhibitors: Filling the S1 pocket of renin via the S3 pocket.. Yuan, J., Simpson, R.D., Zhao, W. ... Structure-based design led to the discovery of a novel class of renin inhibitors in which an unprecedented phenyl ring filling ... Alkyl Amine Renin Inhibitors: Filling S1 from S3. *PDB DOI: https://doi.org/10.2210/pdb3Q3T/pdb ...
... renin-angiotensin system) is the part of the endocrine system that plays a prime role in the control of essential hypertension ... Renin and cathepsins have a similar structure, which in the absence of renin leads to the generation of Ang II. Tonin is a ... Converting Enzymes of the Brain RAS: Renin/Prorenin. The active form of renin in the brain is prorenin. It is present in a low ... In the brain, it is present within neurons and astrocytes in two forms: intracellular renin and secreted renin (prorenin) [30, ...
... "It is not the answers that enlighten, but the questions." - Ionesco ... Discuss the recent data of the blood pressure-lowering effects achieved through renin inhibition. ... Discuss the role of the renin-angiotensin-Aldosterone system (RAS) in development of hypertension ... The renin-angiotensin system (RAS) is a major hormonal autocrine/paracrine system that under normal conditions contributes to ...
Renin-Angiotensin-Aldosterone System in Pregnancy. Normal pregnancy is associated with many changes in the renin-angiotensin- ... Plasma renin levels should be decreased in patients with primary hyperaldosteronism. In a healthy pregnancy, plasma renin ... In pregnant patients, prolonged upright posture results in a modest increase in plasma renin activity. If the renin activity ... Blood pressure, the renin-aldosterone system and sex steroids throughout normal pregnancy. Am J Med. 1980 Jan. 68(1):97-104. [ ...
Inhibitors of the renin-angiotensin-aldosterone system and CoViD-19-affected patients: A two-faced Janus?. ... Inhibitors of the renin-angiotensin-aldosterone system and CoViD-19-affected patients: A two-faced Janus? ... Inhibitors of the renin-angiotensin-aldosterone system and CoViD-19-affected patients: A two-faced Janus? ... The antagonists of the renin-angiotensin-aldosterone system (RAAS) have been shown to interfere with angiotensin converting ...
New Approaches Targeting the Renin-Angiotensin System: Inhibition of Brain Aminopeptidase A, ACE2 Ubiquitination, and ... as well as the substrate of renin- angiotensinogen-in the liver. It raises the possibility that centrally acting amino ... with regard to interference with the renin-angiotensin system, focusing on the enzymes aminopeptidase A and angiotensin- ...
... and the renin and pro-renin concentrations [39], suggesting that gene regulation of RAAS is affected by the gonadal steroids [ ... J Renin Angiotensin Aldosterone Syst. 2011; [PMID: 21421656] * Rigat B, Hubert C, Alhenc-Gelas F, Cambien F, Corvol P, Soubrier ... J Renin Angiotensin Aldosterone Syst. 2007; 8:42-4. [PMID: 17487825] * Li Y, Zagato L, Kuznetsova T, Tripodi G, Zerbini G, ... J Renin Angiotensin Aldosterone Syst. 2006; 7:92-7. [PMID: 17083063] * Gallagher PE, Li P, Lenhart JR, Chappell MC, Brosnihan ...
... of renin-angiotensin system (RAS) genes are associated with hypertension (HT) but most of them are focusing on single locus ... The renin-angiotensin system (RAS) represents a critical endocrine regulator for maintaining blood pressure and blood fluid ... C.-T. Tsai, J.-J. Hwang, M. D. Ritchie et al., "Renin-angiotensin system gene polymorphisms and coronary artery disease in a ... S.-J. Wu, L.-Y. Chuang, Y.-D. Lin et al., "Particle swarm optimization algorithm for analyzing SNP-SNP interaction of renin- ...
Renin-angiotensin-aldosterone system-Operative pathway regulating vascular volume, salt and water retention. ... Renin is the first enzyme in the renin-angiotensin-aldosterone system.. Renin cleaves angiotensinogen to angiotensin I, which ... When decreased blood flow due to the low volume is recognized by kidney cells they secrete the enzyme renin. ... Angiotensinogen is encoded by the gene AGT, and is a glycoprotein secreted by hepatocytes that is cleaved by renin to yield ...
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Centers RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.. ...
0.2 pg renin/micrograms total RNA), adrenal gland (1.15 +/- 0.15 pg renin/micrograms total RNA), placenta (0.7 +/- 0.1 pg renin ... we established a competitive PCR assay for quantification of renin, using a 155-basepair deletion mutant of the human renin ... Activation of tissue-specific gene expression of the components of the renin-angiotensin system (RAS) in humans may play an ... Gene expression of the renin-angiotensin system in human tissues. Quantitative analysis by the polymerase chain reaction.. ...
Immunoblotting confirmed diminished expression of renin within cultured skin fibroblasts. To our knowledge, this is the first ... Autosomal recessively inherited pathogenic variants in genes associated with the renin-angiotensin-aldosterone system (RAAS) ... A novel homozygous variant in REN in a family presenting with classic features of disorders involving the renin-angiotensin ... Immunoblotting confirmed diminished expression of renin within cultured skin fibroblasts. To our knowledge, this is the first ...
3. Progressive suppression of plasma renin activity and concentration without change in renin substrate occurred in animals ... Suppression of Plasma Renin by Atherogenic Levels of Serum Cholesterol in Rabbits D. J. Campbell; D. J. Campbell ... D. J. Campbell, S. L. Skinner, A. J. Day; Suppression of Plasma Renin by Atherogenic Levels of Serum Cholesterol in Rabbits. ... 5. Commonly recognized influences seemed not to account for the findings and the possibility is raised of a dependence of renin ...
... interactions between the cationic renin-inhibitor, [5(4-amino-piperidyl-1-carbonyl-L-2,6[3H]phenyl-alanyl-beta-alanyl(4S- amino ... Interactions between hydrophilic linear renin-inhibiting peptides and transport systems for endogenous substrates in liver ... interactions between the cationic renin-inhibitor, [5(4-amino-piperidyl-1-carbonyl-L-2,6[3H]phenyl-alanyl-beta-alanyl(4S- amino ... competitively inhibited the uptake of the renin inhibitor. Several substrates of other endogenous transport systems (e.g. ...
... and high-renin categories revealed significant decreases of renin in all six patients with high renin- and in four out of 12 ... Effects of Prazosin on Blood Pressure and Plasma Renin Activity in Man J. Rosenthal; J. Rosenthal ... J. Rosenthal, H. Jaeger, I. Arlart; Effects of Prazosin on Blood Pressure and Plasma Renin Activity in Man. Clin Sci Mol Med 1 ... 1. The effects of oral administration of 4·5 mg of prazosin/day on blood pressure and on plasma renin activity were assessed in ...
Renin Activity. Clinical Use. 1 Diagnosis of, and differentiation between, primary and secondary causes of hyper- or ... Plasma renin activity should be compatible with age. Changes in PRA may take 6 weeks to develop in response to changes in the ... 3 Renin secreting tumour.. In the absence of chronic renal disease or renal artery stenosis, a greatly elevated PRA in renal ... 3 Renin secreting tumour.. Hypertensive patients with very high levels of PRA in the peripheral circulation, and in whom ...
The plasma renin test reveals the contribution of body sodium-volume content (V) and renin-angiotensin (R) vasoconstriction to ... The screening test suggested by the ES guidelines is the aldosterone to renin (or plasma renin activity) ratio (ARR).5 In fact ... The evaluation of the activity of the renin-angiotensin-aldosterone system (RAAS) by measurement of renin and aldosterone ... Patients are divided into two groups: low renin hypertensives (LRH) and normal high renin hypertensives (NHRH). According to ...
Phenylbutyrate rescues the transport defect of the Sec61α mutations V67G and T185A for renin. Publication Type : Journal ... Similarly, dominant mutations in the signal peptide of renin also cause ADTKD and point to impaired transport of this renal ... HomePublicationsPhenylbutyrate rescues the transport defect of the Sec61α mutations V67G and T185A for renin ... Treatment with the molecular chaperone phenylbutyrate reversed the defective protein transport of renin and the imbalanced ...
10 Endogenous and exogenous loading of extracellular vesicles for therapeutic delivery of renin-angiotensin system peptides in ... 10 Endogenous and exogenous loading of extracellular vesicles for therapeutic delivery of renin-angiotensin system peptides in ...
Measurements of active renin and inactive renin precursor in human plasma during stimulation of renin release evidence for a ... Kaufmann, W. 1984: Direct relationship between inverse changes of active and inactive renin evidence for renin activation in ... Similarity between active and trypsin-activated inactive renin in dog plasma by means of renin inhibition: the dog as an animal ... In vivo angiotensin-II treatment down-regulates in vitro fetal renal renin secretion and reduces inactive to active renin ratio ...
Decongestion strategies and renin-angiotensin-aldosterone system activation in acute heart failure. ... OBJECTIVES: The purpose of this study was to assess the relationship between biomarkers of renin-angiotensin-aldosterone system ... We assessed the relationship between 2 markers of RAAS activation (plasma renin activity [PRA] and aldosterone) from baseline ... Decongestion strategies and renin-angiotensin-aldosterone system activation in acute heart failure. JACC Heart Fail, 3(2). pp. ...
Sumners, C., Horiuchi, M., Widdop, R. E., McCarthy, C. A., Unger, T., & Steckelings, U. M. (2013). Protective arms of the renin ... Sumners, C, Horiuchi, M, Widdop, RE, McCarthy, CA, Unger, T & Steckelings, UM 2013, Protective arms of the renin-angiotensin- ... Protective arms of the renin-angiotensin-system in neurological disease. Colin Sumners, Masatsugu Horiuchi, Robert Edward ... title = "Protective arms of the renin-angiotensin-system in neurological disease",. abstract = "In recent years it has been ...
Selected Chapters from the Renin-Angiot... Edited by Aleksandar Kibel. Selected Chapters from the Renin-Angiotensin System. ... The blockade of the renin-angiotensin-aldosterone system, regardless of the level in which it is performed, by itself, is a ... Chapter 5 The Intratubular and Intracrine Renin-Angiotensin ... By Xiao C. Li, Ana Paula de Oliveira Leite, Xu Chen, ... ... Because they act primarily in one of the most important systems for the development of SAH, the renin-angiotensin-aldosterone ...
Co-trimoxazole and sudden death in patients receiving inhibitors of renin-angiotensin system: population based study. BMJ 2014; ... Cotrimoxazole is associated with sudden death in older patients receiving inhibitors of renin-angiotensin system ... Cotrimoxazole is associated with sudden death in older patients receiving inhibitors of renin-angiotensin system ...
  • Renin (etymology and pronunciation), also known as an angiotensinogenase, is an aspartic protease protein and enzyme secreted by the kidneys that participates in the body's renin-angiotensin-aldosterone system (RAAS)-also known as the renin-angiotensin-aldosterone axis-that increases the volume of extracellular fluid (blood plasma, lymph and interstitial fluid) and causes arterial vasoconstriction. (wikipedia.org)
  • The renin-angiotensin system ( RAS ), or renin-angiotensin-aldosterone system ( RAAS ), is a hormone system that regulates blood pressure , fluid and electrolyte balance, and systemic vascular resistance . (wikipedia.org)
  • We compared the effects of two renin-angiotensin-aldosterone system (RAAS) inhibitors (quinapril and aliskiren) and 2 beta-blockers (atenolol and nebivolol) on arterial stiffness variables. (nih.gov)
  • The antagonists of the renin-angiotensin-aldosterone system (RAAS) have been shown to interfere with angiotensin converting enzyme (ACE)-2 receptor expression in heart and kidney tissues. (bmj.com)
  • Forty-seven patients with NAION and 76 controls, age- and gender-matched, were recruited and genotyped for renin-angiotensin-aldosterone system (RAAS) genes. (molvis.org)
  • Autosomal recessively inherited pathogenic variants in genes associated with the renin-angiotensin-aldosterone system (RAAS) result in early onset oligohydramnios and clinical features of the Potter sequence, typically in association with proximal renal tubules dysgenesis. (bepress.com)
  • The renin-angiotensin-aldosterone system (RAAS) regulates blood pressure. (degruyter.com)
  • Plasma renin activities (PRA) and plasma aldosterone concentrations (PAC) are biomarkers related to RAAS. (degruyter.com)
  • The evaluation of the activity of the renin-angiotensin-aldosterone system (RAAS) by measurement of renin and aldosterone levels is a fundamental step in the assessment of hypertensive patients. (hospitalhealthcare.com)
  • OBJECTIVES: The purpose of this study was to assess the relationship between biomarkers of renin-angiotensin-aldosterone system (RAAS) activation and decongestion strategies, worsening renal function, and clinical outcomes. (duke.edu)
  • We assessed the relationship between 2 markers of RAAS activation (plasma renin activity [PRA] and aldosterone) from baseline to 72 h and 96 h and decongestion strategy: high- versus low-dose and continuous infusion versus bolus furosemide for DOSE-AHF and UF versus stepped pharmacologic care for CARRESS-HF. (duke.edu)
  • One important mechanism that regulates blood pressure is the Renin-Angiotensin-Aldosterone System - or RAAS for short - which is a cascade of events that ends up increasing blood pressure . (osmosis.org)
  • In type 1 diabetes (T1D), adjuvant treatment with inhibitors of the renin-angiotensin-aldosterone system (RAAS), which dilate the efferent arteriole, is associated with prevention of progressive albuminuria and renal dysfunction. (jci.org)
  • The Renin-Angiotensin-Aldosterone System (RAAS) is a hormone system within the body that is essential for the regulation of blood pressure and fluid balance. (teachmephysiology.com)
  • The first stage of the RAAS is the release of the enzyme renin . (teachmephysiology.com)
  • Some people have RAAS (renin-angiotensin-aldosterone system)-driven hypertension. (medscape.com)
  • There are several types of drugs which includes ACE inhibitors , angiotensin II receptor blockers (ARBs), and renin inhibitors that interrupt different steps in this system to improve blood pressure. (wikipedia.org)
  • Renin continues to be a much sought-after target, and our team has been one of the few that has been able to generate highly potent and bioavailable inhibitors that we believe will lead to important drug candidates in this large market. (genengnews.com)
  • Structure-based design led to the discovery of a novel class of renin inhibitors in which an unprecedented phenyl ring filling the S1 site is attached to the phenyl ring filling the S3 pocket. (rcsb.org)
  • Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) increase plasma renin activity (enhancing the production of angiotensin II via non-ACE-related pathways) whereas aliskiren does not, potentially affecting central hemodynamics differently. (nih.gov)
  • Inhibitors of the renin-angiotensin-aldosterone system and CoViD-19-affected patients: A two-faced Janus? (bmj.com)
  • Both ACE inhibitors and ARBs retard the decline in GFR associated with proteinuria which suggests that the renin-angiotensin system plays a significant role in the pathogenesis of chronic renal disease. (standardofcare.com)
  • Prolonged treatment with ACE inhibitors can lead to a partial escape of the renin-angiotensin system (RAS) via the ACE independent generation of angiotensin II by chymase, an enzyme secreted by the heart (Urata H). (standardofcare.com)
  • Since ACE inhibitors do not completely suppress angiotensin II production and its effects, a rationale has been set forth to use ACE inhibitors and ARB in combination for more complete blockade of the renin-angiotensin system. (standardofcare.com)
  • 4. Kinetic studies excluded the mediation of enzyme inhibitors in this response and made probable a true suppression of renin secretion. (portlandpress.com)
  • We predicted that blockade with the direct oral renin inhibitor aliskiren would produce renal vascular responses exceeding those induced by angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. (eur.nl)
  • Conclusions - Renal vasodilation in healthy people with the potent renin inhibitor aliskiren exceeded responses seen previously with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. (eur.nl)
  • ACE inhibitors , ARBs and direct renin inhibitors are all medications used to treat high blood pressure . (osmosis.org)
  • Direct renin inhibitors work by inhibiting renin, the enzyme that converts angiotensinogen to angiotensin I, which also reduces blood pressure. (osmosis.org)
  • Does Heterogeneity Exist in Treatment Associations with Renin-Angiotensin-System Inhibitors or Beta-blockers According to Phenotype Clusters in Heart Failure with Preserved Ejection Fraction? (physiciansweekly.com)
  • To explore the association between use of renin-angiotensin-system inhibitors (RASi) and beta-blockers, with mortality/morbidity in 5 previously identified clusters of patients with heart failure and preserved ejection fraction (HFpEF). (physiciansweekly.com)
  • The companies inked a deal in June 2005 vaued at $175 million to develop and commercialize novel renin inhibitor drug compounds for the treatment of hypertension and related cardiovascular disorders. (genengnews.com)
  • The RAS (renin-angiotensin system) is the part of the endocrine system that plays a prime role in the control of essential hypertension. (hindawi.com)
  • Several single nucleotide polymorphisms (SNPs) of renin-angiotensin system (RAS) genes are associated with hypertension (HT) but most of them are focusing on single locus effects. (hindawi.com)
  • Renin and hypertension in childhood. (bmj.com)
  • 1. The effects of oral administration of 4·5 mg of prazosin/day on blood pressure and on plasma renin activity were assessed in patients with essential hypertension and in healthy normotensive volunteer subjects. (portlandpress.com)
  • 3. Sub-classification of the hypertensive patients into low-, normal- and high-renin categories revealed significant decreases of renin in all six patients with high renin- and in four out of 12 patients with normal renin- but not in the two patients with low renin-essential hypertension. (portlandpress.com)
  • 4. The results indicate that prazosin exerts its hypotensive action and suppresses plasma renin activity particularly in patients with high renin-essential hypertension. (portlandpress.com)
  • This investigation has examined a possible role for the renin-angiotensin system as well as body mass and insulin values in mediating these cardiovascular and renal aspects of the hypertension syndrome. (scienceopen.com)
  • In the case of 11-hydroxylase and 17-hydroxylase deficiency, the cortisol precursor is DOC, which can act as a mineralocorticoid leading to low-renin hypertension and hypokalemia (see image below). (medscape.com)
  • Vitae Pharmaceuticals has reacquired full rights to its renin inhibitor program from GlaxoSmithKline. (genengnews.com)
  • The renin inhibitor program, which was in the lead optimization phase when GSK signed on as a partner, now has a lead compound, which will undergo GLP tox studies in the first quarter of 2009. (genengnews.com)
  • In contrast, the uncharged compound ouabain (Ki = 200 microM) and the bivalent organic cation d-tubocurarine (Ki = 370 microM) competitively inhibited the uptake of the renin inhibitor. (nih.gov)
  • These results indicate that aliskiren may provide more complete and thus more effective blockade of the renin-angiotensin system. (eur.nl)
  • This project presents SimBiology model implementation of the systemic Renin-Angiotensin-System that was first developed by Lo et al. (mathworks.com)
  • Renin is not commonly referred to as a hormone, albeit it having a receptor, the (pro)renin receptor, also known as the renin receptor and prorenin receptor (see also below), as well as enzymatic activity with which it hydrolyzes angiotensinogen to angiotensin I. The primary structure of renin precursor consists of 406 amino acids with a pre- and a pro-segment carrying 20 and 46 amino acids, respectively. (wikipedia.org)
  • The (pro)renin receptor to which renin and prorenin bind is encoded by the gene ATP6ap2, ATPase H(+)-transporting lysosomal accessory protein 2, which results in a fourfold increase in the conversion of angiotensinogen to angiotensin I over that shown by soluble renin as well as non-hydrolytic activation of prorenin via a conformational change in prorenin which exposes the catalytic site to angiotensinogen substrate. (wikipedia.org)
  • Renin is not commonly referred to as a hormone , albeit it having a receptor, the (pro)renin receptor, also known as the renin receptor and prorenin receptor (see also below), [4] as well as enzymatic activity with which it hydrolyzes angiotensinogen to angiotensin I . (wikipedia.org)
  • Renin then enters the blood where it catalyzes a protein called angiotensinogen to angiotensin I. (standardofcare.com)
  • Renin catalyzes inactive angiotensinogen to angiotensin I. (standardofcare.com)
  • Renin cleaves angiotensinogen to angiotensin I, which is in turn converted by angiotensin-converting enzyme (ACE) to angiotensin II. (standardofcare.com)
  • The renal juxtaglomerular apparatus generates renin, an enzyme that converts angiotensinogen to angiotensin I. Angiotensinogen, derived from the liver, is an alpha-2-globulin. (loinc.org)
  • This is the most direct causal link between blood pressure and renin secretion (the other two methods operate via longer pathways). (wikipedia.org)
  • Human renin is secreted by at least 2 cellular pathways: a constitutive pathway for the secretion of the precursor prorenin and a regulated pathway for the secretion of mature renin. (wikipedia.org)
  • Renin secretion is also stimulated by sympathetic nervous stimulation, mainly through β1 adrenoreceptor activation. (wikipedia.org)
  • 5. Commonly recognized influences seemed not to account for the findings and the possibility is raised of a dependence of renin secretion upon serum cholesterol. (portlandpress.com)
  • In order to study changes of gene expression in small tissue samples (e.g., renal biopsies) obtained from patients, we established a competitive PCR assay for quantification of renin, using a 155-basepair deletion mutant of the human renin cDNA as an internal standard. (jci.org)
  • The enzyme renin is secreted by pericytes in the vicinity of the afferent arterioles and similar microvessels of the kidney from specialized cells of the juxtaglomerular apparatus-the juxtaglomerular cells, in response to three stimuli: A decrease in arterial blood pressure (that could be related to a decrease in blood volume) as detected by baroreceptors (pressure-sensitive cells). (wikipedia.org)
  • If the perfusion of the juxtaglomerular apparatus in the kidney's macula densa decreases, then the juxtaglomerular cells (granular cells, modified pericytes in the glomerular capillary) release the enzyme renin . (wikipedia.org)
  • When decreased blood flow due to the low volume is recognized by kidney cells they secrete the enzyme renin. (standardofcare.com)
  • The juxtaglomerular cells are also stimulated to release renin by signaling from the macula densa. (wikipedia.org)
  • It can also be activated by a decrease in the filtrate sodium chloride (NaCl) concentration or a decreased filtrate flow rate that will stimulate the macula densa to signal the juxtaglomerular cells to release renin. (wikipedia.org)
  • Renin activates the renin-angiotensin system by using its endopeptidase activity to cleave the peptide bonds between leucine and valine residues in angiotensinogen, produced by the liver, to yield angiotensin I, which is further converted into angiotensin II by ACE, the angiotensin-converting enzyme primarily within the capillaries of the lungs. (wikipedia.org)
  • SARS-CoV-2 gains cell entry via angiotensin-converting enzyme (ACE) 2, a membrane-bound enzyme of the "alternative" (alt) renin-angiotensin system (RAS). (nature.com)
  • The renin-angiotensin system (RAS) is a complex network that regulates blood pressure and blood volume through the hormone angiotensin II via its type 1 (AT 1 ) receptor ('classical' RAS) 1 . (nature.com)
  • The renin-angiotensin system (RAS) is of paramount importance, having a role in the regulatory pathway involved in the maintenance of blood pressure (BP), body fluid volume, and sodium homeostasis. (hindawi.com)
  • The results indicated that the components of the renin/angiotensin system are available at the level of the brain cell itself. (hindawi.com)
  • Ionesco The renin-angiotensin system (RAS) is a major hormonal autocrine/paracrine system that under normal conditions contributes to the regulation of. (cyberounds.com)
  • The renin-angiotensin system genes exhibit three common polymorphisms: the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme ( ACE ) gene, the M235T polymorphism of the angiotensinogen gene ( AGT ), and the A1166C polymorphism of the angiotensin II type 1 receptor gene ( AT1-receptor ). (molvis.org)
  • The renin-angiotensin system (RAS) represents a critical endocrine regulator for maintaining blood pressure and blood fluid volume in the circulatory system. (hindawi.com)
  • Usage information: Gene expression of the renin-angiotensin system in human tissues. (jci.org)
  • Gene expression of the renin-angiotensin system in human tissues. (jci.org)
  • Activation of tissue-specific gene expression of the components of the renin-angiotensin system (RAS) in humans may play an important role in cardiovascular regulation and pathophysiology. (jci.org)
  • Background - Pharmacological interruption of the renin-angiotensin system focuses on optimization of blockade. (eur.nl)
  • These findings suggest that in overweight patients cardiovascular and renal values depend chiefly on body weight and insulin, but that in normal weight hypertensives the renin-angiotensin system may play the major role. (scienceopen.com)
  • Using a Systems Biology Approach to Explore Hypotheses Underlying Clinical Diversity of the Renin Angiotensin System and the Response to Antihypertensive Therapies. (mathworks.com)
  • Discuss the recent data of the blood pressure-lowering effects achieved through renin inhibition. (cyberounds.com)
  • Blockade of the renin-angiotensin-aldosterone system (RASS) with angiotensin-converting enzyme inhibition or angiotensin receptor blockade are central therapies for both renal and cardiovascular protection in patients with chronic kidney disease. (standardofcare.com)
  • Renin is a hormone made by the kidneys. (medlineplus.gov)
  • When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the precursor prorenin (already present in the blood) into renin and secrete it directly into the circulation . (wikipedia.org)
  • Certain antihypertensives act upon the renin-angiotensin-aldosterone system to decrease blood pressure by inhibiting vasoconstriction and water reabsorption in the kidneys. (osmosis.org)
  • The kidneys respond by secreting renin into the bloodstream. (osmosis.org)
  • In addition, renin and prorenin binding results in phosphorylation of serine and tyrosine residues of ATP6AP2. (wikipedia.org)
  • Activity assays and immunoassays for plasma renin and prorenin: information provided and precautions necessary for accurate measurement. (degruyter.com)
  • The macula densa senses changes in sodium delivery to the distal tubule, and responds to a drop in tubular sodium load by stimulating renin release in the juxtaglomerular cells. (wikipedia.org)
  • Renin is an asparyl protease that cleaves angiotensinogen into angiotension I in the plasma. (glpbio.cn)
  • Renin is a protein ( enzyme ) released by special kidney cells when you have a decreased salt (sodium) level or low blood volume. (adam.com)
  • Renin activity is affected by diuretics and low sodium stimulates activity. (loinc.org)
  • Plasma samples were collected at 15-min intervals and analyzed for intact PTH, calcium, sodium, potassium, magnesium, phosphate, plasma renin activity (PRA), and aldosterone up to 6h after furosemide injection. (rero.ch)
  • Renin cleaves a decapeptide from angiotensinogen , a globular protein . (wikipedia.org)
  • Using cellular disease models for ADTKD-SEC61A1, we identified an impaired protein transport of the renal secretory protein renin and a reduced abundance of regulatory calcium transporters, including SERCA2. (amrita.edu)
  • Treatment with the molecular chaperone phenylbutyrate reversed the defective protein transport of renin and the imbalanced calcium homeostasis. (amrita.edu)
  • Renin is a proteolytic enzyme that breaks down a protein made in the liver called angiotensinogen, and this gives rise to angiotensin I. (osmosis.org)
  • Angiotensinogen is a precursor protein produced in the liver and cleaved by renin to form angiotensin I. (teachmephysiology.com)
  • Intracellular cAMP, the production of which is catalyzed by the α-subunit of the stimulatory G protein (Gsα), controls renin synthesis and release by juxtaglomerular (JG) cells of the kidney , but may also have relevance for the physiologic integrity of the kidney . (bvsalud.org)
  • Because the two hormones work together, an aldosterone test is often done at the same time as a renin test. (medlineplus.gov)
  • A renin test (or renin and aldosterone test) is used to find out if the adrenal glands are making too much or too little aldosterone. (medlineplus.gov)
  • Most often, your renin test results will be compared with aldosterone test results. (medlineplus.gov)
  • If you have high blood pressure , your doctor may order a renin and aldosterone test to help determine the cause of your elevated blood pressure. (adam.com)
  • Renin is secreted from juxtaglomerular kidney cells, which sense changes in renal perfusion pressure, via stretch receptors in the vascular walls. (wikipedia.org)
  • In heart failure decreased cardiac output and reduced renal perfusion leads to stimulation of plasma renin activity and thus to release of angiotensin II and aldosterone. (standardofcare.com)
  • Coupled Receptor Signaling in Renin-Producing Cells Leads to Renal Endothelial Damage. (bvsalud.org)
  • Check the patient's renin-aldosterone levels. (medscape.com)
  • The primary structure of renin precursor consists of 406 amino acids with a pre- and a pro-segment carrying 20 and 46 amino acids, respectively. (wikipedia.org)
  • Renin activity is elevated in renal vascular diseases and suppressed in primary hyperaldosteronism. (loinc.org)
  • 3. Progressive suppression of plasma renin activity and concentration without change in renin substrate occurred in animals receiving the high cholesterol diet. (portlandpress.com)
  • Patterns of circadian rhythms were noted for personal tempo, acoustic adaptation, rectal temperature, oral temperature, pulse rate, axillary temperature, skin resistance, plasma cortisol and renin levels, urine volume, and normal daytime activity under conditions of normal and altered sleep wake cycles. (cdc.gov)
  • The renin enzyme circulates in the bloodstream and hydrolyzes (breaks down) angiotensinogen secreted from the liver into the peptide angiotensin I. Angiotensin I is further cleaved in the lungs by endothelial-bound angiotensin-converting enzyme (ACE) into angiotensin II, the most vasoactive peptide. (wikipedia.org)
  • The renin enzyme circulates in the bloodstream and hydrolyzes (breaks down) angiotensinogen secreted from the liver into the peptide angiotensin I . (wikipedia.org)
  • The investigation of disorders of aldosterone production requires both aldosterone and plasma renin activity (PRA) measurements. (sas-centre.org)
  • Agents that inhibit the activity of RENIN and cause VASODILATION. (bvsalud.org)
  • The screening test suggested by the ES guidelines is the aldosterone to renin (or plasma renin activity) ratio (ARR).5 In fact many PA patients have aldosterone levels within the normal range but associated to suppressed renin levels: these patients would be missed if the ARR is not calculated. (hospitalhealthcare.com)
  • Most often, the renin blood test is done at the same time as an aldosterone blood test to calculate the renin to aldosterone ratio. (adam.com)
  • This test measures the level of renin in the blood. (medlineplus.gov)
  • You may need a renin test if you've been diagnosed with high blood pressure, especially if it doesn't respond well to standard blood pressure medicines . (medlineplus.gov)
  • Conventional RAS involves the conversion of inactive angiotensinogen into angiotensin I (Ang I) in the presence of renin which is released from the kidney in response to low blood volume. (hindawi.com)
  • As plasma renin is unable to cross the blood-brain barrier, it was predicted that there is the existence of brain RAS independent of the kidney. (hindawi.com)
  • The screening test should be requested by the general practitioner and performed in sitting position in the morning as for the other blood tests (recumbent and standing measurement of aldosterone and renin is not required anymore). (hospitalhealthcare.com)
  • Be aware that renin level can be affected by pregnancy, as well as the time of day and the body position when blood is drawn. (adam.com)
  • The release of renin is inhibited by atrial natriuretic peptide (ANP), which is released by stretched atria in response to increases in blood pressure. (teachmephysiology.com)
  • The role of the sympathetic nervous system, epinephrine, norepinephrine, adrenocorticotrophic hormone, and the renin angiotensin aldosterone system in the control of blood pressure was discussed. (cdc.gov)
  • The system is mainly comprised of the three hormones renin , angiotensin II, and aldosterone . (teachmephysiology.com)
  • If renin and/or aldosterone levels are not normal, it can be a sign of a serious adrenal gland disorder . (medlineplus.gov)
  • Renin-mRNA concentration was quantitated in the kidney (1.74 +/- 0.2 pg renin/micrograms total RNA), adrenal gland (1.15 +/- 0.15 pg renin/micrograms total RNA), placenta (0.7 +/- 0.1 pg renin/micrograms total RNA), and saphenous vein (0.02 +/- 0.01 pg renin/micrograms total RNA). (jci.org)
  • Angiotensinogen is encoded by the gene AGT, and is a glycoprotein secreted by hepatocytes that is cleaved by renin to yield angiotensin I which is further cleave to generate angiotensin II. (standardofcare.com)
  • Plasma renin activity (PRA-S) was calculated as the sum of RAS metabolites. (nature.com)
  • In mixed linear models, renin activity most strongly predicted angiotensin II and 1-7 levels. (nature.com)
  • in 1970 proposed that even after nephrectomy of adult mongrel dogs, the tissue's renin activity persisted even after 12 days [ 3 ]. (hindawi.com)
  • Store remaining portion frozen until the result of the renin activity is known. (sas-centre.org)
  • Plasma renin activity should be compatible with age. (sas-centre.org)
  • As a measure of intrarenal renin activity, we have examined renal plasma flow (RPF) responses in a standardized protocol. (eur.nl)
  • Plasma renin activity and angiotensin levels were reduced in a dose-related manner. (eur.nl)
  • We studied the effect of the ADRB1 Arg389Gly polymorphism on plasma renin activity (PRA) and heart rate (HR) and the genotype-dependent response to metoprolol and exercise. (ku.dk)
  • when this is not feasible, drugs that are relatively neutral on aldosterone and renin levels can be administered to the patients. (hospitalhealthcare.com)
  • Hypertensive patients with very high levels of PRA in the peripheral circulation, and in whom chronic renal disease and renal artery stenosis have been excluded, may have a renin secreting tumour. (sas-centre.org)
  • Progressive activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system contributes to chronic heart failure, including that which occurs after acute myocardial infarction. (standardofcare.com)
  • Plasma renin then carries out the conversion of angiotensinogen , released by the liver , to a decapeptide called angiotensin I . [4] Angiotensin I is subsequently converted to angiotensin II (an octapeptide) by the angiotensin-converting enzyme (ACE) found on the surface of vascular endothelial cells, predominantly those of the lungs . (wikipedia.org)