Diuresis
Sodium
Kidney
Atrial Natriuretic Factor
Natriuretic Agents
Glomerular Filtration Rate
Furosemide
Water-Electrolyte Balance
Aldosterone
Inulin
Kidney Tubules
Renin
Kidney Medulla
Sodium, Dietary
Angiotensin III
Electrolytes
Bendroflumethiazide
Kidney Tubules, Proximal
Bufanolides
Potassium
Hypertension
Vasopressins
Urine
Fenoldopam
Arginine Vasopressin
Receptor, Angiotensin, Type 2
Dogs
Sodium Chloride Symporters
Isotonic Solutions
Cyclic GMP
Renin-Angiotensin System
Osmolar Concentration
Saline Solution, Hypertonic
Solute Carrier Family 12, Member 1
Kallikrein-Kinin System
Kidney Tubules, Distal
Hemodynamics
Natriuretic Peptides
Angiotensin II
Receptors, Atrial Natriuretic Factor
Rats, Sprague-Dawley
Kidney Cortex
Kidney Function Tests
Lithium
Diet, Sodium-Restricted
Sodium Chloride Symporter Inhibitors
Parabiosis
Renal Agents
Meclofenamic Acid
Punctures
Thiorphan
Polyuria
Plasma Substitutes
Hypertension, Renal
Melanocyte-Stimulating Hormones
Sodium-Potassium-Exchanging ATPase
Anesthesia
Chlorothiazide
Neprilysin
Oxytocin
Imidazoles
Plasma Volume
Rats, Wistar
Kidney Tubules, Collecting
Pyridines
Rats, Inbred SHR
Receptors, Dopamine D1
Dihydroxyphenylalanine
Angiotensin II Type 1 Receptor Blockers
Rats, Inbred Strains
Loop of Henle
Cardenolides
Metolazone
Extracellular Space
Hematocrit
Dopamine
NG-Nitroarginine Methyl Ester
Epithelial Sodium Channels
Rats, Inbred WKY
Sodium-Potassium-Chloride Symporters
Sodium-Phosphate Cotransporter Proteins, Type II
Receptors, Vasopressin
Dose-Response Relationship, Drug
Sodium-Hydrogen Antiporter
Inappropriate ADH Syndrome
Imidazoline Receptors
Kidney Concentrating Ability
p-Aminohippuric Acid
Infusions, Intravenous
Desoxycorticosterone
Antihypertensive Agents
Deamino Arginine Vasopressin
Kinins
Pressure
Nitric Oxide
Water
Angiotensin-Converting Enzyme Inhibitors
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine
Immediate and early renal function after living donor transplantation. (1/1093)
BACKGROUND: In order to assess the immediate renal function after living donor transplantation, renal function was compared in eight renal allograft recipients and their living related kidney donors during the first 24 h after transplantation. METHODS: Substantial and comparable intraoperative volume loading with Ringer's acetate and mannitol was performed together with the administration of frusemide. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were estimated by the clearances of inulin and p-aminohippurane, respectively. Tubular reabsorptive function and injury were estimated from the clearance of lithium, the fractional excretion of sodium and the urinary excretion of N-acetyl-beta-glucosaminidase. RESULTS: One hour after completion of surgery, GFR (54 +/- 7 ml/min) and ERPF (294 +/- 35 ml/min) were only 30% lower in the grafts than in the remaining donor kidneys, increasing to similar levels within 3 h. Only minor tubular dysfunction and injury were revealed in the grafted kidneys, and these tended to normalize within 24 h. CONCLUSIONS: By the present transplantation procedure comprising short ischaemia time and substantial volume expansion combined with mannitol and frusemide administration, kidneys from living donors regain nearly normal function within a few hours after transplantation. (+info)Role of renal medullary adenosine in the control of blood flow and sodium excretion. (2/1093)
This study determined the levels of adenosine in the renal medullary interstitium using microdialysis and fluorescence HPLC techniques and examined the role of endogenous adenosine in the control of medullary blood flow and sodium excretion by infusing the specific adenosine receptor antagonists or agonists into the renal medulla of anesthetized Sprague-Dawley rats. Renal cortical and medullary blood flows were measured using laser-Doppler flowmetry. Analysis of microdialyzed samples showed that the adenosine concentration in the renal medullary interstitial dialysate averaged 212 +/- 5.2 nM, which was significantly higher than 55.6 +/- 5.3 nM in the renal cortex (n = 9). Renal medullary interstitial infusion of a selective A1 antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 300 pmol. kg-1. min-1, n = 8), did not alter renal blood flows, but increased urine flow by 37% and sodium excretion by 42%. In contrast, renal medullary infusion of the selective A2 receptor blocker 3, 7-dimethyl-1-propargylxanthine (DMPX; 150 pmol. kg-1. min-1, n = 9) decreased outer medullary blood flow (OMBF) by 28%, inner medullary blood flows (IMBF) by 21%, and sodium excretion by 35%. Renal medullary interstitial infusion of adenosine produced a dose-dependent increase in OMBF, IMBF, urine flow, and sodium excretion at doses from 3 to 300 pmol. kg-1. min-1 (n = 7). These effects of adenosine were markedly attenuated by the pretreatment of DMPX, but unaltered by DPCPX. Infusion of a selective A3 receptor agonist, N6-benzyl-5'-(N-ethylcarbonxamido)adenosine (300 pmol. kg-1. min-1, n = 6) into the renal medulla had no effect on medullary blood flows or renal function. Glomerular filtration rate and arterial pressure were not changed by medullary infusion of any drugs. Our results indicate that endogenous medullary adenosine at physiological concentrations serves to dilate medullary vessels via A2 receptors, resulting in a natriuretic response that overrides the tubular A1 receptor-mediated antinatriuretic effects. (+info)Hemodynamic and renal effects of U-46619, a TXA2/PGH2 analog, in late-pregnant rats. (3/1093)
The vasoconstrictor effects of pressor agents are attenuated during pregnancy. Thromboxane A2 (TXA2) is produced in great quantities during hypertension in pregnancy, and therefore it is important to know whether pregnancy modifies the pressor effects of TXA2. The TXA2 analog U-46619 was infused in anesthetized, acutely prepared and conscious, chronically prepared late-pregnant and nonpregnant female rats to examine its systemic hemodynamic and renal effects. Mean arterial pressure (MAP) and total peripheral resistance (TPR) were lower in anesthetized pregnant than nonpregnant rats (P < 0.01). The infusion of U-46619 into the aortic arch resulted in elevation of MAP only in pregnant rats, due to a greater elevation of TPR (60 +/- 17%) compared with nonpregnant rats (36 +/- 6%, P < 0.05). The pressor effect of intravenously infused U-46619 was also enhanced in conscious pregnant versus nonpregnant rats, and the increase in renal vascular resistance was undiminished. U-46619 increased hematocrit and plasma protein concentration more during pregnancy, which suggested greater reduction of plasma volume. The urinary excretion of sodium (-1.49 +/- 0.25 vs. -0.54 +/- 0.24 micromol/min) and water was reduced more in pregnant than nonpregnant rats during U-46619 (P < 0.01). Thus the MAP and renal effects of the TXA2 analog are exaggerated during pregnancy in the rat. (+info)The subtype 2 of angiotensin II receptors and pressure-natriuresis in adult rat kidneys. (4/1093)
The present work examined the effects of the subtype 2 of angiotensin II (AT2) receptors on the pressure-natriuresis using a new peptide agonist, and the possible involvement of cyclic guanosine 3', 5' monophosphate (cyclic GMP) in these effects. In adult anaesthetized rats (Inactin, 100 mg kg(-1), i.p.) deprived of endogenous angiotensin II by angiotensin converting enzyme inhibition (quinapril, 10 mg kg(-1), i.v.), T2-(Ang II 4-8)2 (TA), a highly specific AT2 receptor agonist (5, 10 and 30 microg kg(-1) min(-1), i.v.) or its solvent was infused in four groups. Renal functions were studied at renal perfusion pressures (RPP) of 90, 110 and 130 mmHg and urinary cyclic GMP excretion when RPP was at 130 mmHg. The effects of TA (10 microg kg(-1) min(-1)) were reassessed in animals pretreated with PD 123319 (PD, 50 microg kg(-1) min(-1), i.v.), an AT2 receptor antagonist and the action of the same dose of PD alone was also determined. Increases in RPP from 90 to 130 mmHg did not change renal blood flow (RBF) but induced 8 and 15 fold increases in urinary flow and sodium excretion respectively. The 5 microg kg(-1) min(-1) dose of TA was devoid of action. The 10 and 30 microg kg(-1) min(-1) doses did not alter total RBF and glomerular filtration rate, but blunted pressure-diuresis and natriuresis relationships. These effects were abolished by PD. TA decreased urinary cyclic GMP excretion. After pretreatment with PD, this decrease was reversed to an increase which was also observed in animals receiving PD alone. In conclusion, renal AT2 receptors oppose the sodium and water excretion induced by acute increases in blood pressure and this action cannot be directly explained by changes in cyclic GMP. (+info)Endothelin mediates renal vascular memory of a transient rise in perfusion pressure due to NOS inhibition. (5/1093)
We investigated the renal responses to NO synthase (NOS) inhibition with N-monomethyl-L-arginine (L-NMA; 30 mg/kg) in anesthetized rats in which renal perfusion pressure (RPP) to the left kidney was mechanically adjusted. Acute L-NMA increased blood pressure (BP, approximately 20%) and renal vascular resistance (RVR) rose ( approximately 50%) in the right kidneys that were always exposed to high RPP. In group 1, the left kidney was exposed to a transient increase (5 min) in RPP which was then normalized, and the rise in RVR was similar to the right kidney. In group 2 the left kidney was never exposed to high RPP, and the rise in RVR was attenuated relative to the right kidney. In group 3, rats were pretreated with the endothelin (ET) receptor antagonist Bosentan, immediately before exposure of the left kidney to a transient increase in RPP, and the rise in RVR was also attenuated relative to the right kidney. NOS inhibition resulted in a natriuresis and diuresis in the right kidneys, and approximately 50% of the natriuresis persisted in the left kidney of group 2, in the absence of any rise in RPP. ET antagonism completely prevented the natriuresis and diuresis in response to acute L-NMA in both left and right kidneys. These data suggest that transient exposure to high RPP by NOS inhibition prevents an appropriate vasodilatory response when RPP is lowered, due to the intrarenal action of ET. (+info)Enhanced natriuretic response to neutral endopeptidase inhibition in heart-transplant recipients. (6/1093)
Heart-transplant recipients (Htx) generally present with body fluid and sodium handling abnormalities and hypertension. To investigate whether neutral endopeptidase inhibition (NEP-I) increases endogenous atrial natriuretic peptide (ANP) and enhances natriuresis and diuresis after heart transplantation, ecadotril was given orally to 8 control subjects and 8 matched Htx, and levels of volume-regulating hormones and renal water, electrolyte, and cyclic guanosine monophosphate (cGMP) excretions were monitored for 210 minutes. Baseline plasma ANP, brain natriuretic peptide (BNP), and cGMP were elevated in Htx, but renin and aldosterone, like urinary parameters, did not differ between groups. NEP-I increased plasma ANP (Htx, 20.6+/-2.3 to 33.2+/-5.9 pmol/L, P<0.01; controls, 7.7+/-1. 2 to 10.6+/-2.6 pmol/L) and cGMP, but not BNP. Renin decreased similarly in both groups, whereas aldosterone decreased significantly only in Htx. Enhanced urinary sodium (1650+/-370% versus 450+/-150%, P=0.01), cGMP, and water excretions were observed in Htx and urinary cGMP positively correlated with natriuresis in 6 of the Htx subjects. Consistent with a normal circadian rhythm of blood pressure, without excluding a possible effect of NEP-I, mean systemic blood pressure increased similarly in both groups at the end of the study (6.9+/-2.0% versus 7.4+/-2.8% in controls and Htx). Thus, systemic hypertension, mild renal impairment, and raised plasma ANP levels are possible contributory factors in the enhanced natriuresis and diuresis with NEP-I in Htx. These results support a physiological role for the cardiac hormone after heart transplantation and suggest that long-term studies may be useful to determine the potential of NEP-I in the treatment of sodium retention and water retention after heart transplantation. (+info)Impact of the endothelin system on water and sodium excretion in patients with liver cirrhosis. (7/1093)
BACKGROUND: Impaired renal function in patients with liver cirrhosis is a serious complication and is characterized by sodium and water retention in the absence of identifiable specific causes of renal dysfunction. The endothelin system has been shown to be activated in liver cirrhosis and might contribute to impaired renal function. However, the mechanisms leading to an activation of the endothelin system in these patients and the effects of an activated endothelin system on renal function in these patients are as yet unknown. METHODS: To determine the correlation between the activity of the endothelin system and the ability to excrete water and sodium in patients with liver cirrhosis, we measured plasma endothelin-1 concentrations by reversed phase-HPLC followed by an endothelin RIA and performed an oral water load tests in 10 healthy control subjects and 43 patients with liver cirrhosis. In addition, we analysed possible mechanisms/factors like plasma endotoxin that might contribute to the activation of the endothelin system in liver cirrhosis. RESULTS: This study showed that the endothelin system is activated in patients with liver cirrhosis in a disease-stage-dependent manner. Patients with Child C liver cirrhosis have a 5.45-fold increased plasma ET-1 concentration compared to healthy controls, whereas plasma ET-1 is only increased 2.74-fold in Child A patients. An oral water load test revealed a highly significant (P < 0.0001) inverse correlation between the plasma endothelin-1 concentrations and the ability to excrete a given water load. Plasma endotoxin, a well-known stimulus of ET-1, is significantly (P < 0.03) correlated with plasma ET-1 in cirrhotic patients. The ET-1 concentrations in the ascites of patients with liver cirrhosis were lower and not related to plasma ET-1. CONCLUSION: The activity of the endothelin system in patients with liver cirrhosis depends on the severity of liver impairment. Plasma endotoxin might be an important stimulus of the endothelin system in liver cirrhosis. We observed a highly significant inverse correlation between the plasma endothelin-1 concentrations and the ability to excrete a given water and sodium load, suggesting that the endothelin system plays a role in the regulation of water excretion in patients with liver cirrhosis. (+info)Altered pressure-natriuresis in obese Zucker rats. (8/1093)
It has not been examined whether the pressure-natriuresis response is altered in the insulin-resistant condition. Furthermore, despite an important role of nitric oxide (NO) in modulating pressure-natriuresis, no investigations have been conducted assessing the renal interstitial NO production in insulin resistance. The present study examined whether pressure-natriuresis was altered in insulin-resistant obese Zucker rats (OZ) and assessed the cortical and medullary nitrate/nitrite (NOx) levels with the use of the renal microdialysis technique. In OZ, serum insulin/glucose ratio (23.0+/-4.0x10(-8), n=9) and blood pressure (119+/-3 mm Hg) were greater than those in lean Zucker rats (LZ; 7.0+/-1.9x10(-8) and 103+/-4 mm Hg, n=9). The pressure-natriuresis curve in OZ was shifted to higher renal perfusion pressure (RPP), and the slope was blunted compared with that in LZ (0.073+/-0.015 vs 0.217+/-0.047 microEq/min kidney weight/mm Hg, P<0.05). The basal renal NOx level was reduced in OZ (cortex, 4.032+/-0.331 micromol/L; medulla, 4. 329+/-0.515 micromol/L) compared with that in LZ (cortex, 7.315+/-1. 102 micromol/L; medulla: 7.698+/-0.964 micromol/L). Furthermore, elevating RPP increased the medullary NOx in LZ, but this pressure-induced response was lost in OZ. Four-week treatment with troglitazone, an insulin-sensitizing agent, improved hyperinsulinemia, systemic hypertension, and basal renal NOx levels (cortex, 5.639+/-0.286 micromol/L; medulla, 5.978+/-0.284 micromol/L), and partially ameliorated the pressure-natriuresis curves; the slope of pressure-natriuresis curves and elevated RPP-induced NOx, however, were not corrected. In conclusion, our study suggests that insulin resistance is closely associated with abnormal pressure-natriuresis and hypertension. These deranged renal responses to insulin resistance are most likely attributed to impaired medullary NO production within the medulla. (+info)There are two types of hypertension:
1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.
Some common causes of secondary hypertension include:
* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use
There are also several risk factors for hypertension, including:
* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress
Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:
* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease
Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.
Hyponatremia can be caused by various factors, such as excessive fluid intake, certain medications, kidney or liver disease, and hormonal imbalances. Symptoms may include headache, nausea, vomiting, fatigue, muscle weakness, and in severe cases, seizures or coma.
Treatment for hyponatremia typically involves correcting the underlying cause of the condition. This may involve discontinuing certain medications, addressing any underlying medical conditions, or limiting fluid intake. In severe cases, hospitalization may be necessary to monitor and treat the condition. In some instances, sodium supplements or diuretics may be prescribed to help correct sodium levels.
It is important to note that hyponatremia can be a serious condition, and prompt medical attention should be sought if symptoms persist or worsen over time. A healthcare professional should be consulted for proper diagnosis and treatment.
There are many potential causes of dehydration, including:
* Not drinking enough fluids
* Diarrhea or vomiting
* Sweating excessively
* Diabetes (when the body cannot properly regulate blood sugar levels)
* Certain medications
* Poor nutrition
* Infections
* Poor sleep
To diagnose dehydration, a healthcare provider will typically perform a physical examination and ask questions about the patient's symptoms and medical history. They may also order blood tests or other diagnostic tests to rule out other conditions that may be causing the symptoms.
Treatment for dehydration usually involves drinking plenty of fluids, such as water or electrolyte-rich drinks like sports drinks. In severe cases, intravenous fluids may be necessary. If the underlying cause of the dehydration is a medical condition, such as diabetes or an infection, treatment will focus on managing that condition.
Preventing dehydration is important for maintaining good health. This can be done by:
* Drinking enough fluids throughout the day
* Avoiding caffeine and alcohol, which can act as diuretics and increase urine production
* Eating a balanced diet that includes plenty of fruits, vegetables, and whole grains
* Avoiding excessive sweating by dressing appropriately for the weather and taking breaks in cool, shaded areas when necessary
* Managing medical conditions like diabetes and kidney disease properly.
In severe cases of dehydration, complications can include seizures, organ failure, and even death. It is important to seek medical attention if symptoms persist or worsen over time.
In diabetes, polyuria is caused by high levels of glucose in the blood that cannot be properly absorbed by the body. The excess glucose spills into the urine, drawing water with it and increasing the volume of urine. This can lead to dehydration and electrolyte imbalances if left untreated.
In kidney disease, polyuria can be caused by damage to the kidneys that impairs their ability to concentrate urine. As a result, the body produces more urine than usual to compensate for the lack of concentrating ability.
Polyuria can also be a symptom of certain endocrine disorders such as diabetes insipidus, where the body produces too much antidiuretic hormone (ADH) or vasopressin, which leads to an excessive amount of urine production.
To diagnose polyuria, a healthcare provider may perform a physical examination, take a medical history, and conduct diagnostic tests such as urinalysis, blood glucose testing, and imaging studies. Treatment for polyuria depends on the underlying cause and may include medication, lifestyle changes, and in some cases, dialysis.
A type of hypertension that is caused by a problem with the kidneys. It can be acute or chronic and may be associated with other conditions such as glomerulonephritis, pyelonephritis, or polycystic kidney disease. Symptoms include proteinuria, hematuria, and elevated blood pressure. Treatment options include diuretics, ACE inhibitors, and angiotensin II receptor blockers.
Note: Renal hypertension is also known as renal artery hypertension.
Water-electrolyte imbalance can be caused by various factors such as excessive sweating, diarrhea, vomiting, burns, and certain medications. It can also be a complication of other medical conditions like kidney disease, heart failure, and liver disease.
Symptoms of water-electrolyte imbalance may include:
* Dehydration or overhydration
* Changes in blood pH (acidosis or alkalosis)
* Electrolyte abnormalities (such as low sodium, high potassium, or low bicarbonate)
* Muscle weakness or cramping
* Confusion or disorientation
* Heart arrhythmias
Treatment of water-electrolyte imbalance depends on the underlying cause and the severity of symptoms. Fluid replacement, electrolyte supplements, and medications to correct pH levels may be prescribed by a healthcare professional. In severe cases, hospitalization may be necessary to monitor and treat the condition.
It is important to seek medical attention if you experience any symptoms of water-electrolyte imbalance, as untreated imbalances can lead to serious complications such as seizures, coma, and even death.
Hypernatremia can cause a range of symptoms including headache, nausea, vomiting, confusion, and in severe cases, seizures and coma. Treatment for hypernatremia typically involves correcting the underlying cause and fluid and electrolyte replacement therapy to restore normal sodium levels in the blood. In severe cases, hospitalization may be required to monitor and treat the condition closely.
It is important to note that hypernatremia can have serious complications if left untreated or if treated too late, such as seizures, coma, and even death. Therefore, prompt medical attention is essential if symptoms persist or worsen over time.
A more detailed explanation of Inappropriate ADH Syndrome may be as follows:
Inappropriate ADH syndrome is a rare endocrine disorder characterized by excessive antidiuretic hormone (ADH) secretion, leading to water retention and hyponatremia. Hyponatremia occurs when the body contains too much water and not enough sodium, causing an imbalance in the electrolyte levels of the blood. This condition can be caused by various factors such as a tumor or other abnormality that increases ADH production or decreases sodium levels in the body. Symptoms of Inappropriate ADH syndrome may include headaches, nausea, vomiting, seizures, and in severe cases, coma.
If left untreated, Inappropriate ADH Syndrome can lead to more serious complications such as seizures or coma. Treatment options for this condition typically involve surgery, radiation therapy, or medication to remove the tumor or other abnormality causing the excessive ADH production and restore sodium levels in the body. It is important to seek medical attention if symptoms persist or worsen over time as early diagnosis and treatment can improve the chances of a successful outcome for this condition.
In summary, Inappropriate ADH Syndrome is an uncommon endocrine disorder caused by excessive ADH secretion leading to hyponatremia due to water retention, which can cause severe symptoms such as headache, nausea, vomiting, seizures, and coma if left untreated. Treatment options involve surgery, radiation therapy, or medication to remove the tumor or other abnormality causing excessive ADH production and restore sodium levels in the body. Early diagnosis and treatment are crucial for a successful outcome.
Natriuresis
Dopamine receptor
Management of heart failure
Sarah K. England
ACE inhibitor
Sodium-hydrogen antiporter 3
Hypertension and the brain
Baroreflex
Ascites
Anaritide
Urodilatin
Epithelial sodium channel
Nocturia
Kaliuresis
NPR1
Natriuretic peptide
Caffeine
Omapatrilat
Osmotic diuretic
Atrial volume receptors
Deoxyepinephrine
Diastole
Miso
Chlortalidone
Progesterone
Oxytocin
Nephrogenic diabetes insipidus
16α-Hydroxyprogesterone
Amiloride
Cenderitide
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MeSH Browser
Diuresis3
- Additionally, the actions of both BNP and ANP result in a decrease in cardiac output due to an overall decrease in central venous pressure and preload as a result of the reduction in blood volume that follows natriuresis and diuresis. (wikidoc.org)
- Among the numerous metabolic effects of GLP-1 are the glucose-dependent stimulation of insulin secretion, decrease of gastric emptying, inhibition of food intake, increase of natriuresis and diuresis, and modulation of rodent β-cell proliferation. (healthworldnet.com)
- This natriuresis and diuresis is accompanied by a secondary loss of potassium and bicarbonate. (alpiedelamuralla.org)
Vasodilation1
- They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility. (lookformedical.com)
Excretion1
- The kidneys also control sodium excretion through a process called pressure natriuresis. (phyxmept.com)
Sodium1
- This "natriuresis of fasting" can cause sodium deficiency and lead to unpleasant symptoms like muscle cramps, headaches, and fatigue. (drinklmnt.com)
Hormone1
- EGF is regarded as the main protector against injuries in epithelia, and ouabain is a hormone that regulates blood pressure, natriuresis, cell survival, and cell adhesion. (intechopen.com)
Decrease1
- The physiologic actions of BNP are similar to those of ANP and include decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis . (wikidoc.org)
Increase1
- You will find known if DepoProvera natriuresis and may have undesirable effects a small increase to avoid possible. (grey-panthers.it)
Levels1
- Natriuresis levels did not differ by sex. (bvsalud.org)