Receptors adrenergic alpha 1. Medical search

A specific category of drugs that prevent sleepiness by specifically targeting sleep-mechanisms in the brain. They are used to treat DISORDERS OF EXCESSIVE SOMNOLENCE such as NARCOLEPSY. Note that this drug category does not include broadly-acting central nervous system stimulants such as AMPHETAMINES.

A subclass of alpha-adrenergic receptors found on both presynaptic and postsynaptic membranes where they signal through Gi-Go G-PROTEINS. While postsynaptic alpha-2 receptors play a traditional role in mediating the effects of ADRENERGIC AGONISTS, the subset of alpha-2 receptors found on presynaptic membranes signal the feedback inhibition of NEUROTRANSMITTER release.

Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.

One of the two major pharmacological subdivisions of adrenergic receptors that were originally defined by the relative potencies of various adrenergic compounds. The alpha receptors were initially described as excitatory receptors that post-junctionally stimulate SMOOTH MUSCLE contraction. However, further analysis has revealed a more complex picture involving several alpha receptor subtypes and their involvement in feedback regulation.

Hypoxia-inducible factor 1, alpha subunit is a basic helix-loop-helix transcription factor that is regulated by OXYGEN availability and is targeted for degradation by VHL TUMOR SUPPRESSOR PROTEIN.

Drugs that inhibit 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE. They are commonly used to reduce the production of DIHYDROTESTOSTERONE.

Saturated derivatives of the steroid pregnane. The 5-beta series includes PROGESTERONE and related hormones; the 5-alpha series includes forms generally excreted in the urine.

Increase in constituent cells in the PROSTATE, leading to enlargement of the organ (hypertrophy) and adverse impact on the lower urinary tract function. This can be caused by increased rate of cell proliferation, reduced rate of cell death, or both.

12-Carbon saturated monocarboxylic acids.

A plant genus in the family ARECACEAE, order Arecales, subclass Arecidae. The fruit or the extract (Permixon) is used for PROSTATIC HYPERPLASIA.

An oxidoreductase that catalyzes the conversion of 3-oxo-delta4 steroids into their corresponding 5alpha form. It plays an important role in the conversion of TESTOSTERONE into DIHYDROTESTOSTERONE and PROGESTERONE into DIHYDROPROGESTERONE.

A saturated 14-carbon fatty acid occurring in most animal and vegetable fats, particularly butterfat and coconut, palm, and nutmeg oils. It is used to synthesize flavor and as an ingredient in soaps and cosmetics. (From Dorland, 28th ed)

Drugs used to cause constriction of the blood vessels.

A phenethylamine found in EPHEDRA SINICA. PSEUDOEPHEDRINE is an isomer. It is an alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. It has been used for asthma, heart failure, rhinitis, and urinary incontinence, and for its central nervous system stimulatory effects in the treatment of narcolepsy and depression. It has become less extensively used with the advent of more selective agonists.

The escape of diagnostic or therapeutic material from the vessel into which it is introduced into the surrounding tissue or body cavity.

Abnormally low BLOOD PRESSURE that can result in inadequate blood flow to the brain and other vital organs. Common symptom is DIZZINESS but greater negative impacts on the body occur when there is prolonged depravation of oxygen and nutrients.

Sepsis associated with HYPOTENSION or hypoperfusion despite adequate fluid resuscitation. Perfusion abnormalities may include, but are not limited to LACTIC ACIDOSIS; OLIGURIA; or acute alteration in mental status.

An adrenergic beta-2 agonist used to control PREMATURE LABOR.

Antidiuretic hormones released by the NEUROHYPOPHYSIS of all vertebrates (structure varies with species) to regulate water balance and OSMOLARITY. In general, vasopressin is a nonapeptide consisting of a six-amino-acid ring with a cysteine 1 to cysteine 6 disulfide bridge or an octapeptide containing a CYSTINE. All mammals have arginine vasopressin except the pig with a lysine at position 8. Vasopressin, a vasoconstrictor, acts on the KIDNEY COLLECTING DUCTS to increase water reabsorption, increase blood volume and blood pressure.

alpha1-adrenergic receptor subtypes in human peripheral blood lymphocytes. (1/1045)

We investigated the expression of alpha1-adrenergic receptor subtypes in intact human peripheral blood lymphocytes using reverse transcription-polymerase chain reaction (RT-PCR) and radioligand binding assay techniques combined with antibodies against the three subtypes of alpha1-adrenergic receptors (alpha1A, alpha1B, and alpha1D). RT-PCR amplified in peripheral blood lymphocytes a 348-bp alpha1A-adrenergic receptor fragment, a 689-bp alpha1B-adrenergic receptor fragment, and a 540-bp alpha1D-adrenergic receptor fragment. Radioligand binding assay with [3H]prazosin as radioligand revealed a high-affinity binding with a dissociation constant value of 0. 65+/-0.05 nmol/L and a maximum density of binding sites of 175. 3+/-20.5 fmol/10(6) cells. The pharmacological profile of [3H]prazosin binding to human peripheral blood lymphocytes was consistent with the labeling of alpha1-adrenergic receptors. Antibodies against alpha1A-, alpha1B-, and alpha1D-receptor subtypes decreased [3H]prazosin binding to a different extent. This indicates that human peripheral blood lymphocytes express the three alpha1-adrenergic receptor subtypes. Of the three different alpha1-adrenergic receptor subtypes, the alpha1B is the most represented and the alpha1D, the least. Future studies should clarify the functional relevance of alpha1-adrenergic receptors expressed by peripheral blood lymphocytes. The identification of these sites may represent a step for evaluating whether they represent a marker of alpha1-adrenergic receptors in cardiovascular disorders or for assessing responses to drug treatment on these receptors. (+info)

Modulation of long-term synaptic depression in visual cortex by acetylcholine and norepinephrine. (2/1045)

In a slice preparation of rat visual cortex, we discovered that paired-pulse stimulation (PPS) elicits a form of homosynaptic long-term depression (LTD) in the superficial layers when carbachol (CCh) or norepinephrine (NE) is applied concurrently. PPS by itself, or CCh and NE in the absence of synaptic stimulation, produced no lasting change. The LTD induced by PPS in the presence of NE or CCh is of comparable magnitude with that obtained with prolonged low-frequency stimulation (LFS) but requires far fewer stimulation pulses (40 vs 900). The cholinergic facilitation of LTD was blocked by atropine and pirenzepine, suggesting involvement of M1 receptors. The noradrenergic facilitation of LTD was blocked by urapidil and was mimicked by methoxamine, suggesting involvement of alpha1 receptors. beta receptor agonists and antagonists were without effect. Induction of LTD by PPS was inhibited by NMDA receptor blockers (completely in the case of NE; partially in the case of CCh), suggesting that one action of the modulators is to control the gain of NMDA receptor-dependent homosynaptic LTD in visual cortex. We propose that this is a mechanism by which cholinergic and noradrenergic inputs to the neocortex modulate naturally occurring receptive field plasticity. (+info)

Modulation of basal intracellular calcium by inverse agonists and phorbol myristate acetate in rat-1 fibroblasts stably expressing alpha1d-adrenoceptors. (3/1045)

In rat-1 fibroblasts stably expressing alpha1d-adrenoceptors BMY 7378, phentolamine, chloroethylclonidine and 5-methyl urapidil decreased basal [Ca2+]i. WB 4101 induced a very small effect on this parameter but when added before the other antagonists it blocked their effect. All these agents inhibited the action of norepinephrine. Phorbol myristate acetate also blocked the effect of norepinephrine and decreased basal [Ca2+]i. Staurosporine inhibited these effects of the phorbol ester. Our results suggest that: (1) alpha1d-adrenoceptors exhibit spontaneous ligand-independent activity, (2) BMY 7378, phentolamine, chloroethylclonidine and 5-methyl urapidil act as inverse agonists and (3) protein kinase C activation blocks spontaneous and agonist-stimulated alpha1d-adrenoceptor activity. (+info)

Effect of chronic hypoxia on alpha-1 adrenoceptor-mediated inositol 1,4,5-trisphosphate signaling in ovine uterine artery. (4/1045)

The present study examined the effect of chronic hypoxia on coupling efficiency of alpha-1 adrenoceptors to inositol 1,4,5-trisphosphate (InsP3) signaling in ovine uterine artery. Chronic hypoxia did not change the time course of InsP3 formation, but significantly decreased the potency (pD2: 6.17 +/- 0.09 --> 5.26 +/- 0.12) and the maximal response (220.7 +/- 21.7 --> 147.7 +/- 15.3 pmol/mg protein) of norepinephrine-induced InsP3 synthesis. The coupling efficiency of alpha-1 adrenoceptors to InsP3 synthesis (picomoles InsP3 per femtomoles receptor) was decreased 45% by chronic hypoxia. In addition, simultaneous measurement of norepinephrine-induced contractions and InsP3 synthesis indicated that for a given amount of InsP3 generated, the contractile force of the uterine artery was significantly less in chronically hypoxic than in control tissues (0. 27 +/- 0.01 versus 0.35 +/- 0.02 g tension/pmol InsP3). InsP3 receptors were characterized using radioligand binding techniques. Although the density of InsP3 receptors was not changed by chronic hypoxia (Bmax: 325 +/- 35 --> 378 +/- 18 fmol/mg protein), the dissociation constant (Kd) of InsP3 to its receptors was significantly increased (Kd: 5.20 +/- 0.40 --> 7.81 +/- 0.34 nM). Analysis of InsP3 receptor occupancy-tension development relationship indicated no difference in intrinsic ability of the InsP3-receptor complex in eliciting contractions between the control and hypoxic tissues. Our results suggest that chronic hypoxia attenuates coupling efficiency of alpha-1 adrenoceptors to InsP3 synthesis in the uterine artery. In addition, the tissue contractile sensitivity to InsP3 is reduced, which is mediated predominantly by a decrease in InsP3 binding affinity to InsP3 receptors. (+info)

The Ca2+ channel blockade changes the behavioral and biochemical effects of immobilization stress. (5/1045)

We investigated how the effects of chronic immobilization stress in rats are modified by Ca2+ channel blockade preceding restraint sessions. The application of nifedipine (5 mg/kg) shortly before each of seven daily 2 h restraint sessions prevented the development of sensitized response to amphetamine as well as the stress-induced elevation of the densities of L-type Ca2+ channel in the hippocampus and significantly reduced the elevation of the densities of [3H]nitrendipine binding sites in the cortex and D1 dopamine receptors in the limbic forebrain. Neither stress, nor nifedipine affected the density of alpha 1-adrenoceptors and D1 receptors in the cerebral cortex nor D2 dopamine receptors in the striatum. A single restraint session caused an elevation of blood corticosterone level that remained unaffected by nifedipine pretreatment, but the reduction of this response during the eighth session was significantly less expressed in nifedipine-treated rats. We conclude that L-type calcium channel blockade prevents development of several stress-induced adaptive responses. (+info)

Altered alpha 1-adrenoceptor subtypes mediated cardiac function after treatment of propranolol to rats. (6/1045)

AIM: To study inotropic and chronotropic effects mediated by alpha 1A- and alpha 1B-adrenoceptors after 5-d propranolol (Pro) treatment. METHODS: The positive inotropic and chronotropic effects mediated by alpha 1A and alpha 1B subtypes were determined on isolated left ventricular papillary muscles and right atrium in Pro- and NaCl-treated rats. RESULTS: The basic contractility of papillary muscles induced by phenylephrine (Phe) was 90 +/- 18 mg in Pro-treated rats and 53 +/- 17 mg in control group (P < 0.05). The increment on force of contraction was 20 +/- 12 mg in Pro-pretreated rats and 5 +/- 5 mg in NaCl-treated rats (P < 0.05). After preincubated with chloroethylclonidine, the increment on force of contraction was reduced in Pro-treated rats, but was not much changed in control group. Phe in presence of 5-methylurapidil induced positive inotropic effect with 13 +/- 5 mg in Pro-treated group, but not in NaCl-treated rats. Under the normal and the inhibited cardiac state, the maximal increment in beat rate mediated by alpha 1B showed no difference between the Pro-treated and NaCl-treated rats. CONCLUSION: After chronic treatment of Pro, alpha 1-adrenoceptor-mediated positive inotropic effect in rat heart was improved, which was mainly induced by stimulation of alpha 1B when beta-adrenoceptors were blocked. (+info)

Characterization of alpha1-adrenoceptor subtypes mediating vasoconstriction in human umbilical vein. (7/1045)

1. The present study attempted to characterize pharmacologically the subtypes of alpha-adrenoceptors mediating contractions in human umbilical vein (HUV). 2. HUV rings were mounted in isolated organ baths and cumulative concentration-response curves were constructed for the alpha-adrenoceptor agonists phenylephrine and adrenaline. Adrenaline was more potent than phenylephrine (pD2=7.29 and 6.04 respectively). 3. Isoproterenol exhibited no agonism on KCl pre-contracted HUV rings. Propranolol (1 microM) and rauwolscine (0.1 microM) did not affect the concentration-response curves to adrenaline. These results demonstrate the lack of involvement of functional beta-or alpha2-adrenoceptors in adrenaline-induced vasoconstriction. 4. The non subtype selective alpha1-adrenoceptor antagonist prazosin was evaluated on phenylephrine and adrenaline concentration-response curves. The effects of the competitive alpha1A and alpha1D-adrenoceptor antagonists, 5-methyl urapidil and BMY 7378 and the irreversible alpha1B selective compound chloroethylclonidine (CEC) were also evaluated on adrenaline concentration-response curves. 5. The potencies of prazosin against responses mediated by adrenaline (pA2= 10.87) and phenylephrine (pA2= 10.70) indicate the involvement of prazosin-sensitive functional alpha1-adrenoceptor subtype in vasoconstriction of the HUV. 6. The potencies of 5-methyl urapidil (pA2 = 6.70) and BMY 7378 (pA2= 7.34) were not consistent with the activation of an alpha1A- or alpha1D-adrenoceptor population. 7. Exposure to a relatively low CEC concentration (3 microM) abolished the maximum response to adrenaline suggesting that this response was mediated by an alpha1B-adrenoceptor subtype. 8. We conclude that HUV express a prazosin-sensitive functional alpha1-adrenoceptor resembling the alpha1B-subtype according with the low pA2 values for both 5-methyl urapidil and BMY 7378 and the high sensitivity to CEC. (+info)

A decrease in the amount and function of inhibitory GTP-binding protein in the resistance small artery from spontaneously hypertensive rats. (8/1045)

The inhibitory GTP-binding protein (Gi protein) plays an important role in regulation of vascular tone. Many studies have implicated the role of Gi protein in conduit vessels. However, the physiological role of Gi protein in the control of peripheral microvascular tone in hypertension has not been established yet. Therefore, we investigated the concentration of Gi protein in the peripheral resistance arteries and aorta in the spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (WKY) and renovascular hypertensive rats (RHR), using immunohistochemical methods semiquantitatively. Changes in the function of Gi protein in relation to alpha2-adrenoceptor were also investigated by microcannulation techniques. We have shown that the amount of alpha2 subunits of Gi protein in the cremaster small artery was significantly lower in SHR aged 4 weeks and older than in age-matched WKY and that there were no significant differences between RHR and WKY. We also demonstrated that the function of Gi protein in relation to alpha2-adrenoceptor was already lower in SHR before the onset of hypertension. The quantitative and functional decline in Gi protein in the smooth muscle cells of peripheral small arteries were observed in SHR even before the onset of hypertension, whereas rats with secondary hypertension did not exhibit this finding. (+info)

Wakefulness-promoting agents are a class of medications that are used to promote and maintain alertness and wakefulness. They work by stimulating the brain's arousal centers, increasing the release of neurotransmitters such as dopamine, norepinephrine, and histamine, which help to counteract the effects of sleep-promoting substances in the brain.

Wakefulness-promoting agents are typically used to treat excessive daytime sleepiness associated with conditions such as narcolepsy, obstructive sleep apnea, shift work sleep disorder, and other disorders that cause disrupted sleep patterns. Some examples of wakefulness-promoting agents include modafinil, armodafinil, pitolisant, and solriamfetol.

It is important to note that while these medications can help to promote alertness and reduce excessive daytime sleepiness, they are not a substitute for getting adequate amounts of quality sleep. It is also important to use them under the guidance of a healthcare provider, as they may have potential side effects and interactions with other medications.

Alpha-2 adrenergic receptors are a type of G protein-coupled receptor that binds catecholamines, such as norepinephrine and epinephrine. These receptors are widely distributed in the central and peripheral nervous system, as well as in various organs and tissues throughout the body.

Activation of alpha-2 adrenergic receptors leads to a variety of physiological responses, including inhibition of neurotransmitter release, vasoconstriction, and reduced heart rate. These receptors play important roles in regulating blood pressure, pain perception, and various cognitive and emotional processes.

There are several subtypes of alpha-2 adrenergic receptors, including alpha-2A, alpha-2B, and alpha-2C, which may have distinct physiological functions and be targeted by different drugs. For example, certain medications used to treat hypertension or opioid withdrawal target alpha-2 adrenergic receptors to produce their therapeutic effects.

Alpha 1-antitrypsin (AAT, or α1-antiproteinase, A1AP) is a protein that is primarily produced by the liver and released into the bloodstream. It belongs to a group of proteins called serine protease inhibitors, which help regulate inflammation and protect tissues from damage caused by enzymes involved in the immune response.

Alpha 1-antitrypsin is particularly important for protecting the lungs from damage caused by neutrophil elastase, an enzyme released by white blood cells called neutrophils during inflammation. In the lungs, AAT binds to and inhibits neutrophil elastase, preventing it from degrading the extracellular matrix and damaging lung tissue.

Deficiency in alpha 1-antitrypsin can lead to chronic obstructive pulmonary disease (COPD) and liver disease. The most common cause of AAT deficiency is a genetic mutation that results in abnormal folding and accumulation of the protein within liver cells, leading to reduced levels of functional AAT in the bloodstream. This condition is called alpha 1-antitrypsin deficiency (AATD) and can be inherited in an autosomal codominant manner. Individuals with severe AATD may require augmentation therapy with intravenous infusions of purified human AAT to help prevent lung damage.

Adrenergic receptors are a type of G protein-coupled receptor that bind and respond to catecholamines, such as epinephrine (adrenaline) and norepinephrine (noradrenaline). Alpha adrenergic receptors (α-ARs) are a subtype of adrenergic receptors that are classified into two main categories: α1-ARs and α2-ARs.

The activation of α1-ARs leads to the activation of phospholipase C, which results in an increase in intracellular calcium levels and the activation of various signaling pathways that mediate diverse physiological responses such as vasoconstriction, smooth muscle contraction, and cell proliferation.

On the other hand, α2-ARs are primarily located on presynaptic nerve terminals where they function to inhibit the release of neurotransmitters, including norepinephrine. The activation of α2-ARs also leads to the inhibition of adenylyl cyclase and a decrease in intracellular cAMP levels, which can mediate various physiological responses such as sedation, analgesia, and hypotension.

Overall, α-ARs play important roles in regulating various physiological functions, including cardiovascular function, mood, and cognition, and are also involved in the pathophysiology of several diseases, such as hypertension, heart failure, and neurodegenerative disorders.

Hypoxia-Inducible Factor 1 (HIF-1) is a transcription factor that plays a crucial role in the body's response to low oxygen levels, also known as hypoxia. HIF-1 is a heterodimeric protein composed of two subunits: an alpha subunit (HIF-1α) and a beta subunit (HIF-1β).

The alpha subunit, HIF-1α, is the regulatory subunit that is subject to oxygen-dependent degradation. Under normal oxygen conditions (normoxia), HIF-1α is constantly produced in the cell but is rapidly degraded by proteasomes due to hydroxylation of specific proline residues by prolyl hydroxylase domain-containing proteins (PHDs). This hydroxylation reaction requires oxygen as a substrate, and under hypoxic conditions, the activity of PHDs is inhibited, leading to the stabilization and accumulation of HIF-1α.

Once stabilized, HIF-1α translocates to the nucleus, where it heterodimerizes with HIF-1β and binds to hypoxia-responsive elements (HREs) in the promoter regions of target genes. This binding results in the activation of gene transcription programs that promote cellular adaptation to low oxygen levels. These adaptive responses include increased erythropoiesis, angiogenesis, glucose metabolism, and pH regulation, among others.

Therefore, HIF-1α is a critical regulator of the body's response to hypoxia, and its dysregulation has been implicated in various pathological conditions, including cancer, cardiovascular disease, and neurodegenerative disorders.

5-alpha Reductase Inhibitors are a class of drugs that block the action of the enzyme 5-alpha reductase, which is responsible for converting testosterone to dihydrotestosterone (DHT). DHT is a more potent form of testosterone that plays a key role in the development and maintenance of male sexual characteristics and is involved in the pathogenesis of benign prostatic hyperplasia (BPH) and androgenetic alopecia (male pattern baldness).

By inhibiting the action of 5-alpha reductase, these drugs reduce the levels of DHT in the body, which can help to shrink the prostate gland and improve symptoms of BPH such as difficulty urinating, frequent urination, and weak urine stream. They are also used off-label to treat hair loss in men.

Examples of 5-alpha reductase inhibitors include finasteride (Proscar, Propecia) and dutasteride (Avodart). Common side effects of these drugs may include decreased libido, erectile dysfunction, and breast tenderness or enlargement.

Pregnanes are a class of steroid hormones and steroids that contain a pregnane nucleus, which is a steroid core with a carbon skeleton consisting of 21 carbons. This structure includes four fused rings, labeled A through D, and is derived from cholesterol.

Pregnanes are important precursors for the synthesis of various steroid hormones in the body, including progesterone, which plays a crucial role in maintaining pregnancy and regulating the menstrual cycle. Other examples of pregnanes include cortisol, a stress hormone produced by the adrenal gland, and aldosterone, a hormone that helps regulate electrolyte balance and blood pressure.

It's worth noting that pregnanes can also refer to synthetic compounds that contain this steroid nucleus and are used in various medical and research contexts.

Prostatic hyperplasia, also known as benign prostatic hyperplasia (BPH), is a noncancerous enlargement of the prostate gland. The prostate gland surrounds the urethra, the tube that carries urine and semen out of the body. When the prostate gland enlarges, it can squeeze or partially block the urethra, causing problems with urination, such as a weak stream, difficulty starting or stopping the flow, and more frequent urination, especially at night. Prostatic hyperplasia is a common condition as men age and does not necessarily lead to cancer. However, it can cause significant discomfort and decreased quality of life if left untreated. Treatment options include medications, minimally invasive procedures, and surgery.

Lauric acid is a type of saturated fatty acid, meaning it contains only single bonds between its carbon atoms. It is named after the laurel tree, from which it was originally isolated, and has the chemical formula CH3(CH2)10COOH.

In a medical context, lauric acid is often discussed in relation to its presence in certain foods and its potential effects on health. For example, lauric acid is the primary fatty acid found in coconut oil, making up about 50% of its total fat content. It is also found in smaller amounts in other foods such as palm kernel oil, dairy products, and human breast milk.

Some studies have suggested that lauric acid may have beneficial effects on health, such as raising levels of "good" HDL cholesterol and having antimicrobial properties. However, it is also high in calories and can contribute to weight gain if consumed in excess. Additionally, like other saturated fats, it can raise levels of "bad" LDL cholesterol when consumed in large amounts, which may increase the risk of heart disease over time.

Overall, while lauric acid may have some potential health benefits, it is important to consume it in moderation as part of a balanced diet.

"Serenoa" is the medical term for a type of palm tree, also known as Saw Palmetto. The fruit of this plant, Serenoa repens, is commonly used in herbal medicine, particularly for treating symptoms associated with an enlarged prostate gland, such as reducing difficulty in urinating. It contains compounds that are thought to have anti-inflammatory and hormonal effects. However, it's important to note that the effectiveness of Serenoa repbs for treating medical conditions is still a subject of ongoing research and debate.

Cholestenone 5 alpha-reductase is an enzyme that plays a role in the conversion of cholesterol and other steroid hormones in the body. Specifically, it catalyzes the reduction of 5,7-dihydroxycholest-4-en-3-one (also known as cholestenone) to 5α-androstan-3α,17β-diol, which is a precursor to the male sex hormone testosterone.

This enzyme is found in various tissues throughout the body, including the prostate gland, skin, and liver. In the prostate gland, 5 alpha-reductase helps regulate the growth and function of the gland by converting testosterone to dihydrotestosterone (DHT), a more potent form of the hormone.

Inhibitors of 5 alpha-reductase are sometimes used as medications to treat conditions such as benign prostatic hyperplasia (BPH) and male pattern baldness, as reducing DHT levels can help alleviate symptoms associated with these conditions.

Myristic acid is not typically considered a medical term, but it is a scientific term related to the field of medicine. It is a type of fatty acid that is found in some foods and in the human body. Medically, it may be relevant in discussions of nutrition, metabolism, or lipid disorders.

Here's a definition of myristic acid from a biological or chemical perspective:

Myristic acid is a saturated fatty acid with the chemical formula CH3(CH2)12CO2H. It is a 14-carbon atom chain with a carboxyl group at one end and a methyl group at the other. Myristic acid occurs naturally in some foods, such as coconut oil, palm kernel oil, and dairy products. It is also found in the structural lipids of living cells, where it plays a role in cell signaling and membrane dynamics.

Vasoconstrictor agents are substances that cause the narrowing of blood vessels by constricting the smooth muscle in their walls. This leads to an increase in blood pressure and a decrease in blood flow. They work by activating the sympathetic nervous system, which triggers the release of neurotransmitters such as norepinephrine and epinephrine that bind to alpha-adrenergic receptors on the smooth muscle cells of the blood vessel walls, causing them to contract.

Vasoconstrictor agents are used medically for a variety of purposes, including:

* Treating hypotension (low blood pressure)
* Controlling bleeding during surgery or childbirth
* Relieving symptoms of nasal congestion in conditions such as the common cold or allergies

Examples of vasoconstrictor agents include phenylephrine, oxymetazoline, and epinephrine. It's important to note that prolonged use or excessive doses of vasoconstrictor agents can lead to rebound congestion and other adverse effects, so they should be used with caution and under the guidance of a healthcare professional.

Ephedrine is a medication that stimulates the nervous system and is used to treat low blood pressure, asthma, and nasal congestion. It works by narrowing the blood vessels and increasing heart rate, which can help to increase blood pressure and open up the airways in the lungs. Ephedrine may also be used as a bronchodilator to treat COPD (chronic obstructive pulmonary disease).

Ephedrine is available in various forms, including tablets, capsules, and solutions for injection. It is important to follow the instructions of a healthcare provider when taking ephedrine, as it can have side effects such as rapid heart rate, anxiety, headache, and dizziness. Ephedrine should not be used by people with certain medical conditions, such as heart disease, high blood pressure, or narrow-angle glaucoma, and it should not be taken during pregnancy or breastfeeding without consulting a healthcare provider.

In addition to its medical uses, ephedrine has been used as a performance-enhancing drug and is banned by many sports organizations. It can also be found in some over-the-counter cold and allergy medications, although these products are required to carry warnings about the potential for misuse and addiction.

Extravasation of diagnostic and therapeutic materials refers to the unintended leakage or escape of these substances from the intended vasculature into the surrounding tissues. This can occur during the administration of various medical treatments, such as chemotherapy, contrast agents for imaging studies, or other injectable medications.

The extravasation can result in a range of complications, depending on the type and volume of the material that has leaked, as well as the location and sensitivity of the surrounding tissues. Possible consequences include local tissue damage, inflammation, pain, and potential long-term effects such as fibrosis or necrosis.

Prompt recognition and management of extravasation are essential to minimize these complications. Treatment may involve local cooling or heating, the use of hyaluronidase or other agents to facilitate dispersion of the extravasated material, or surgical intervention in severe cases.

Hypotension is a medical term that refers to abnormally low blood pressure, usually defined as a systolic blood pressure less than 90 millimeters of mercury (mm Hg) or a diastolic blood pressure less than 60 mm Hg. Blood pressure is the force exerted by the blood against the walls of the blood vessels as the heart pumps blood.

Hypotension can cause symptoms such as dizziness, lightheadedness, weakness, and fainting, especially when standing up suddenly. In severe cases, hypotension can lead to shock, which is a life-threatening condition characterized by multiple organ failure due to inadequate blood flow.

Hypotension can be caused by various factors, including certain medications, medical conditions such as heart disease, endocrine disorders, and dehydration. It is important to seek medical attention if you experience symptoms of hypotension, as it can indicate an underlying health issue that requires treatment.

Septic shock is a serious condition that occurs as a complication of an infection that has spread throughout the body. It's characterized by a severe drop in blood pressure and abnormalities in cellular metabolism, which can lead to organ failure and death if not promptly treated.

In septic shock, the immune system overreacts to an infection, releasing an overwhelming amount of inflammatory chemicals into the bloodstream. This leads to widespread inflammation, blood vessel dilation, and leaky blood vessels, which can cause fluid to leak out of the blood vessels and into surrounding tissues. As a result, the heart may not be able to pump enough blood to vital organs, leading to organ failure.

Septic shock is often caused by bacterial infections, but it can also be caused by fungal or viral infections. It's most commonly seen in people with weakened immune systems, such as those who have recently undergone surgery, have chronic medical conditions, or are taking medications that suppress the immune system.

Prompt diagnosis and treatment of septic shock is critical to prevent long-term complications and improve outcomes. Treatment typically involves aggressive antibiotic therapy, intravenous fluids, vasopressors to maintain blood pressure, and supportive care in an intensive care unit (ICU).

Ritodrine is a medication that was previously used to prevent or delay premature labor in women at high risk. It is a beta-2 adrenergic agonist, which works by relaxing uterine muscles and slowing down contractions. However, its use in clinical practice has been largely discontinued due to the availability of more effective and safer alternatives for tocolysis (the suppression of premature labor). It's important to note that Ritodrine is not currently a commonly used medication in obstetrics.

Vasopressin, also known as antidiuretic hormone (ADH), is a hormone that helps regulate water balance in the body. It is produced by the hypothalamus and stored in the posterior pituitary gland. When the body is dehydrated or experiencing low blood pressure, vasopressin is released into the bloodstream, where it causes the kidneys to decrease the amount of urine they produce and helps to constrict blood vessels, thereby increasing blood pressure. This helps to maintain adequate fluid volume in the body and ensure that vital organs receive an adequate supply of oxygen-rich blood. In addition to its role in water balance and blood pressure regulation, vasopressin also plays a role in social behaviors such as pair bonding and trust.

Other effects on smooth muscle are contraction in: Ureter Uterus (when pregnant): this is minor compared to the relaxing effects of the β2 receptor, agonists of which-notably albuterol/salbutamol-were formerly[citation needed] used to inhibit premature labor. (wikipedia.org)
Cooling augmented contractions evoked by the alpha 2-adrenergic agonists B-HT 920 and UK 14304 but did not affect responses to the full alpha 1-adrenergic agonist phenylephrine. (johnshopkins.edu)
Therefore, cooling reduces alpha 1-adrenergic responsiveness in canine cutaneous veins, but in the case of full alpha 1-adrenergic agonists such as norepinephrine and phenylephrine the inhibitory effect of cooling is buffered by an alpha 1-adrenoceptor reserve. (johnshopkins.edu)
p90 ribosomal S6 kinases play a significant role in early gene regulation in the cardiomyocyte response to G(q)-protein-coupled receptor stimuli, endothelin-1 and α(1)-adrenergic receptor agonists. (rndsystems.com)
Centrally-acting sympatholytic agent/agents (alpha2 adrenergic receptor agonists). (pharmacology2000.com)
If you combine any of these alpha 2 antagonists with caffeine or beta-agonists (aka synergists), the necessary dose decreases quite a bit. (anabolicminds.com)
This means caffeine, exercise, forskolin, and beta-agonists all work exceptionally well with alpha-2 antagonists. (anabolicminds.com)
beta-Adrenergic agonists used in therapy of premature labor and asthma cross the placenta and can affect development of the fetal nervous system. (duke.edu)
The regional and subtype selectivity are compatible with primary deficits in the development of noradrenergic projections to the cerebellum identified in previous studies and provide further evidence that therapeutic use of beta-adrenergic agonists may produce neurobehavioral teratology. (duke.edu)

Chronic administration of alpha 1-receptor antagonists is associated with loss of clinical efficacy, especially in congestive heart failure, although the mechanism is uncertain. (jci.org)
We previously demonstrated that alpha-1 adrenergic receptor (α1-AR) antagonists can prevent cytokine storm syndrome in mice. (stanford.edu)
The screen results confirm that the molecules working as alpha-1-ARs antagonists are those that greatly increase cell sensitivity to 13-cis-RA with reduction of cell viability and increase in differentiation. (unitn.it)
This level of risk was subsequently confirmed and was thereafter described with all currently used alpha-1 adrenergic receptor antagonists [3,4,5,6]. (urotoday.com)
The FDA considers the risk for IFIS to be a class effect for alpha-1 adrenergic receptor antagonists [8,9]. (urotoday.com)
As many of you may already know, alpha-2-antagonists are simply compounds that antagonize the alpha-2-adrenoreceptor. (anabolicminds.com)
And then we have the various yohimbe alkaloids like 11-OH yohimbine, that are alpha-2-antagonists (not to be confused with a broad-spectrum extract of alkaloids). (anabolicminds.com)
What works best with alpha-2-antagonists? (anabolicminds.com)
For those seeking to lose stubborn fat, alpha-2-antagonists are a great option. (anabolicminds.com)
Alpha-2 antagonists synergize with anything that potentiates catecholamine release. (anabolicminds.com)
Mccall RB, Schuette MR, Humphrey SJ, Lahti RA, Barsuhn C. "Evidence for a Central Sympathoexcitatory Action of Alpha-2 Adrenergic Antagonists" The Journal Of Pharmacolocy And Experimental Therapeutics . (erowid.org)
The effect of alpha-2 adrenergic receptor antagonists on sympathetic nerve discharge (SND) recorded from the external carotid and splanchnic nerves were studied in baroreceptor-denervated cats.Low i.v. doses of piperoxane end rauwolscine dramatically increased SND and produced a concomitant rise in mean arterial pressure and heart rate. (erowid.org)
Scholars@Duke publication: In vitro and in vivo evaluation of dihydropyrimidinone C-5 amides as potent and selective alpha(1A) receptor antagonists for the treatment of benign prostatic hyperplasia. (duke.edu)
alpha(1) Adrenergic receptors mediate both vascular and lower urinary tract tone, and alpha(1) receptor antagonists such as terazosin (1b) are used to treat both hypertension and benign prostatic hyperplasia (BPH). (duke.edu)
This paper explores 4-aryldihydropyrimidinones attached to an aminopropyl-4-arylpiperidine via a C-5 amide as selective alpha(1A) receptor subtype antagonists. (duke.edu)

We confirmed our observation in NB xenograft mice models in vivo, treating mice with a combination of 13-cis-RA and the FDA approved alpha-1 AR antagonist doxazosin. (unitn.it)
Saw palmetto extract (SPE), used widely for the treatment of benign prostatic hyperplasia (BPH) has been shown to bind alpha(1)-adrenergic, muscarinic and 1,4-dihydropyridine (1,4-DHP) calcium channel antagonist receptors. (nih.gov)
The results suggest that lauric acid and oleic acid bind noncompetitively to alpha(1)-adrenergic, muscarinic and 1,4-DHP calcium channel antagonist receptors. (nih.gov)
DESYREL (trazodone hydrochloride) tablets for oral administration contain trazodone hydrochloride, a selective serotonin reuptake inhibitor and 5HT2 receptor antagonist . (rxlist.com)
Alpha-receptor antagonist medications potentially interfere with iris muscle dilation, resulting in difficult lens removal and possibly increasing complications. (urotoday.com)
These 3 categories of alpha-2-antagonist each possess a unique goal-specific attribute, but before we delve into specifics, let's look at how effective these compounds are for fat loss. (anabolicminds.com)
If there's one supplement to consume orally for stubborn fat loss, it's an alpha 2 antagonist. (anabolicminds.com)
These data indicate that low doses of the alpha-2 receptor antagonist piperoxane and rauwolscine act centrally to increase SND. (erowid.org)
Phentolamine, an alpha-adrenergic antagonist (1 microM), reduced sympathetic constriction in controls, but abolished this response in TiO2 exposed rats (max % change -22.3+/-3.1 control, -9.7+/-2.9 TiO2). (cdc.gov)

The crystal structure of the α1B-adrenergic receptor subtype has been determined in complex with the inverse agonist (+)-cyclazosin. (wikipedia.org)
However, the contractions evoked by the partial alpha 1-adrenergic agonist St 587 were virtually abolished by cooling. (johnshopkins.edu)
Synthesis and in vitro characterisation of N -[5-(4,5-dihydro-1 H -imidazol-2-yl)-2-hydroxy-5,6,7,8-tetrahydronaphthalen-1-yl]methanesulfonamide and its enantiomers: a novel selective α 1A receptor agonist. (rndsystems.com)
A-61603, a potent α 1 -adrenergic receptor agonist, selective for the α 1A receptor subtype. (rndsystems.com)
An Alpha-1A Adrenergic Receptor Agonist Prevents Acute dox. (rndsystems.com)
Furthermore, 2,5-DMA derivatives exhibited agonist-like binding characteristics at 5-HT2 serotonin receptors with the R(-) isomer being the more potent isomer. (erowid.org)
Similar to the 2,5-DMA derivatives, MDMA and MDA exhibited agonist-like binding characteristics at 5-HT2 serotonin receptors. (erowid.org)
It is classified as a centrally acting alpha 2 adrenergic agonist and imidazoline receptor agonist and has been in clinical use since 1966. (uspharmacist.com)
Phenylephrine Hydrochloride Injection, USP is an alpha-1 adrenergic receptor agonist indicated for the treatment of clinically important low blood pressure resulting primarily from the dilation of blood vessels, which decreases blood pressure in the setting of anesthesia. (outsourcing-pharma.com)

α1-adrenergic receptors are subdivided into three highly homologous subtypes, i.e., α1A-, α1B-, and α1D-adrenergic receptor subtypes. (wikipedia.org)
α1-adrenergic receptor subtypes increase inhibition in the olfactory system, suggesting a synaptic mechanism for noradrenergic modulation of olfactory driven behaviors. (wikipedia.org)
This group also found that while both receptor subtypes were seen in the membranes and cytoplasm of cell bodies, the β 2 receptor subtype, but not the β 1 , was localized to the nucleus. (frontiersin.org)
There are 3 alpha-1-AR subtypes: alpha-1A, -1B and -1D, all of which signal through the Gq/11 family of G-proteins and different subtypes show different patterns of activation. (nih.gov)
Despite the absence of body or brain growth impairment, selective increases were seen postnatally in cerebellar alpha 1- and alpha 2-receptor subtypes, whereas the same receptor populations were decreased by small amounts in cerebral cortex and midbrain + brainstem. (duke.edu)
Unlike 2,5-DMA derivatives, MDMA and MDA demonstrated little selectivity for 5-HT2 versus 5-HT1 subtypes of receptors. (erowid.org)
Recently, three different subtypes of this receptor have been identified, with the alpha(1A) receptor being most prevalent in lower urinary tract tissue. (duke.edu)
1 nM while being greater than 100-fold selective versus the alpha(1b) and alpha(1d) receptor subtypes. (duke.edu)

At one time, there was a subtype known as α1C, but it was found to be identical to the previously discovered α1A receptor subtype. (wikipedia.org)
Pretreatment with chlorethylclonidine, which selectively alkylates the alpha-1B subtype, did not affect the Emax value of phenylephrine-induced contractions, but significantly shifted the curve to the right. (aspetjournals.org)
Receptor subtype involved in α 1A -adrenergic receptor-mediated Ca 2+ signaling in cardiomyocytes. (rndsystems.com)
The α-1D Is the predominant α-1-adrenergic receptor subtype in human epicardial coronary arteries. (rndsystems.com)
Knockout of the alpha 1A/C-adrenergic receptor subtype: the alpha 1A/C is expressed in resistance arteries and is required to maintain arterial blood pressure. (rndsystems.com)

To avoid confusion, naming was continued with the letter D. Catecholamines like norepinephrine (noradrenaline) and epinephrine (adrenaline) signal through the α1-adrenergic receptors in the central and peripheral nervous systems. (wikipedia.org)
The neurotransmitter norepinephrine has higher affinity for the α1 receptor than does the hormone adrenaline. (wikipedia.org)
In particular, norepinephrine decreases glutamatergic excitatory postsynaptic potentials by the activation of α1-adrenergic receptors. (wikipedia.org)
Norepinephrine also stimulates serotonin release by binding α1-adrenergic receptors located on serotonergic neurons in the raphe. (wikipedia.org)
Cooling (from 37 to 24 degrees C) augmented contractions to norepinephrine under control conditions and after alpha 1-adrenergic blockade (prazosin) but not following alpha 2-adrenergic blockade (rauwolscine). (johnshopkins.edu)
With norepinephrine, this permits the potentiating effect of cooling on the alpha 2-adrenergic component of the response to predominate. (johnshopkins.edu)
Epinephrine, Norepinephrine, and Phenylephrine select α1 receptors agonistically. (proprofs.com)
By binding to α2 receptors in the CNS, clonidine can modulate the release of norepinephrine, resulting in a decrease in sympathetic outflow and ultimately leading to a decrease in heart rate. (proprofs.com)
Nerve fibers that release norepinephrine are referred to as adrenergic fibers. (clambaronline.com)
Norepinephrine gets released by postganglionic neurons of the sympathetic nervous system, which binds to and activates adrenergic receptors. (clambaronline.com)
adrenergic nerve fibre, nerve fibre that releases the neurotransmitter norepinephrine (also known as noradrenaline) at the synapse, or junction, between a nerve and its end organ, which may be a muscle, gland, or another nerve. (clambaronline.com)

Furthermore, it's partially adrenolytic, as it is less selective than yohimbine on the adrenergic system, partially antagonizing alpha-1- adrenoreceptors. (anabolicminds.com)
Scholars@Duke publication: Fetal terbutaline exposure causes selective postnatal increases in cerebellar alpha-adrenergic receptor binding. (duke.edu)
SSRIs are selective to the 5-HT system but not specific for the different 5-HT receptors. (msdmanuals.com)

Autoantibodies (AAB) against nuclear and membrane structures as well as neurotransmitter receptors including muscarinic cholinergic receptor M3/M4-antibodies (M3-mAChR/M4-mAChR) and beta-1 and -2-adrenergic receptor (beta1-AR/beta2-AR) have been described in patients with ME/CFS ( 3 , 6 - 8 ). (frontiersin.org)
Other behavioral, cardiovascular, and toxic effects of MDMA and related derivatives may be mediated by actions at other central and/or peripheral recognition sites, including muscarinic cholinergic receptors and alpha 2-adrenergic receptors, for which these compounds exhibit relatively high affinity. (erowid.org)

The methylenedioxy amphetamine derivatives exhibited an inverse stereospecificity with respect to serotonin uptake sites versus postsynaptic 5-HT receptors with the S(+) isomer being more potent at the presynaptic recognition site, while the R(-) isomer was more potent at the postsynaptic recognition sites. (erowid.org)
By preventing reuptake of 5-HT presynaptically, SSRIs result in more 5-HT to stimulate postsynaptic 5-HT receptors. (msdmanuals.com)

To evaluate changes in venous alpha 1-adrenoceptor responsiveness during chronic alpha 1-adrenoceptor blockade, dose-response curves to phenylephrine and angiotensin II were constructed in 10 healthy subjects before, during, and after administration of terazosin 1 mg orally for 28 d. (jci.org)
Terazosin initially shifted the dose-response curve of phenylephrine to the right, with a significant increase in ED50 for phenylephrine from a control value of 102 to 759 ng/min on day 1 of terazosin (P (jci.org)
Moreover, following partial irreversible blockade of the alpha 1-adrenoceptors with phenoxybenzamine, cooling also reduced the contractions evoked by phenylephrine. (johnshopkins.edu)

The affinity of oleic acid, myristic acid and linoleic acid for each receptor was greater than the affinity of SPE. (nih.gov)
Yohimbine possess extreme affinity for the alpha-2-adrenoreceptor, but due to receptor homology with various 5-HT receptors, yohimbine HCl is highly anxiogenic and is clinically used to model panic disorder. (anabolicminds.com)
In vitro binding experiments indicated that piperoxane and rauwolscine bound selectively to the alpha-2 adrenergic receptor and had little affinity for alpha-1 receptor sites. (erowid.org)
Derivatives of 2,5-DMA exhibited preferential high affinity at 5-HT2 serotonin receptors when compared to their relative affinities at 5-HT1 serotonin receptors. (erowid.org)
A pharmacological profile of the methylenedioxy-substituted amphetamine derivatives indicates that MDMA and MDA exhibited highest affinity for serotonin uptake sites, 5-HT2 serotonin, alpha 2-adrenergic and M-1 muscarinic receptors. (erowid.org)

There were significant correlations between the in vitro affinities of 2,5-DMA derivatives at 5-HT2 serotonin receptors and their human hallucinogenic potencies as well as with their potencies in behavioral generalization studies, suggesting the importance of 5-HT2 serotonin receptors in mediating the hallucinogenic effects of the various 2,5-DMA derivatives. (erowid.org)
The relatively weak hallucinogenic effects of the methylenedioxy-substituted amphetamine derivatives (when compared to the 2,5-DMA derivatives) may be mediated through actions at 5-HT2 serotonin receptors. (erowid.org)
In addition, the neurotoxic, psychotomimetic, analgesic, temperature regulation, and mood-altering effects of MDMA and other methylenedioxy-substituted derivatives may be mediated, in part, through their actions at other serotonin recognition sites in brain, including serotonin uptake sites and 5-HT1A serotonin receptors. (erowid.org)

Because it crosses the blood-brain barrier so that the the alpha receptors it binds are ones in the CNS instead of on the effector organ. (proprofs.com)
This means that the alpha receptors it binds to are located in the central nervous system (CNS) rather than on the effector organ, which in this case is the heart. (proprofs.com)

The enhanced sensitivity to alpha-adrenergic receptor blockade following TiO2 exposure suggests an augmented responsiveness to tonic sympathetic activity. (cdc.gov)

Furthermore, because alpha-2 antagonism can increase insulin release, these compounds are best taken fasted. (anabolicminds.com)

In the current study, pregnant rats were given 10 mg/kg of terbutaline on gestational days 17, 18 and 19 and adrenergic receptor binding capabilities examined in brain regions of the offspring. (duke.edu)
At present, he and his group are investigating the distribution of adrenergic, muscarinic and endothelin receptors in the lower urinary tract of rats and rabbits. (yale.edu)

α1-receptors primarily mediate smooth muscle contraction, but have important functions elsewhere as well. (wikipedia.org)
During exercise, α1-adrenergic receptors in active muscles are attenuated in an exercise intensity-dependent manner, allowing the β2-adrenergic receptors which mediate vasodilation to dominate. (wikipedia.org)

Nanoparticle inhalation modulates arteriolar sympathetic constriction: role of nitric oxide, prostanoids, and alpha-adrenergic receptors. (cdc.gov)

To understand better the cellular mechanisms of NE and its adrenergic receptors in the LA, we used antibodies directed against dopamine beta-hydroxylase (DβH), the synthetic enzyme for NE, or against two different isoforms of the beta-adrenergic receptors (βARs), one that predominately recognizes neurons (βAR 248) and the other astrocytes (βAR 404), to characterize the microenvironments of DβH and βAR. (frontiersin.org)
Although metabotropic glutamate receptor (mGluR) modulation has been studied extensively in neurons, it has not been investigated in astrocytes. (jneurosci.org)
These data suggest that glutamate, acting at several metabotropic receptors expressed by astrocytes, could modulate glial activity evoked by neurotransmitters and thereby influence the ongoing modulation of neurons by astrocytes. (jneurosci.org)

α1-Adrenergic receptors are members of the G protein-coupled receptor superfamily. (wikipedia.org)
At the molecular level, this synergistic effect is followed by a marked increase in the expression of a member of the catecholamine receptor superfamily: the adrenergic receptor alpha-1B (ADRA1B) suggesting that this receptor might represent a key mediator of the synergistic effect of 13-cis-RA and isorhamnetin observed in vitro. (unitn.it)

Rauwolscine lacks significant activity at the 5HT receptors, but it has its own issues. (anabolicminds.com)

These antibodies belong to a network of natural antibodies against adrenergic, cholinergic and other G-protein coupled receptors (GPCR) which were shown to be dysregulated and dysfunctional in various autoimmune diseases ( 9 ). (frontiersin.org)

Citations to Pharmacological tolerance to alpha 1-adrenergic receptor antagonism mediated by terazosin in humans. (jci.org)
This study demonstrates that pharmacological tolerance to the alpha 1-adrenoceptor blocking action of terazosin occurs in man and may be responsible for loss in efficacy with chronic therapy. (jci.org)

Coop's Corner #4: Alpha-2 Antagonism? (anabolicminds.com)

Considering the druggable nature of the alpha-1-AR receptors, we indicate this class of receptors as a novel pharmacological target for the treatment of neuroblastoma. (unitn.it)
Pharmacological characterization of alpha adrenergic receptors in the young and old female rabbit urethra. (aspetjournals.org)
The pharmacological characteristics of alpha-1 and alpha-2 adrenergic receptors in young (6 month) and old (4.5-5 year) female rabbit urethra were studied using isolated muscle bath techniques. (aspetjournals.org)

In smooth muscle cells of blood vessels the principal effect of activation of these receptors is vasoconstriction. (wikipedia.org)
In contrast to α2-adrenergic receptors, α1-adrenergic-receptors in the arterial vasculature of skeletal muscle are more resistant to inhibition, and attenuation of α1-adrenergic-receptor-mediated vasoconstriction only occurs during heavy exercise. (wikipedia.org)
These drugs bind to α1 receptors and activate them, leading to vasoconstriction and increased blood pressure. (proprofs.com)

This finding redirected our attention to the class of adrenergic receptors (ARs) as novel targets in NB. (unitn.it)
Alpha-1-Adrenergic receptors as new targets in Neuroblastoma / Broso, Francesca. (unitn.it)

Obesity is associated with the development of the metabolic syndrome, and is also a major risk factor for obstructive sleep apnea (OSA) ( 1 ). (atsjournals.org)
25(1): 7-10 estimate autonomic nervous control of the in women with metabolic syndrome compared to cardiovascular system and reduced HRV significantly those without, while results in men were increases cardiovascular mortality9. (bvsalud.org)

Clonidine uniquely stimulates α 2 receptors, yet affects the heart rate which is normally affected by beta receptors. (proprofs.com)

B 2 adrenergic receptor gene polymorphism effect on childhood asthma severity and response to treatment. (cdc.gov)

Experiments were designed to determine the effects of cooling on alpha 1- and alpha 2-adrenergic responses in isolated canine cutaneous veins. (johnshopkins.edu)

Since NB is a catecholamine-rich tumor, we propose that antagonization of alpha-1-AR disrupts the established autocrine pro-survival circuit generated by catecholamines in NB and restores the ability of the cells to follow the pro-differentiative and pro-apoptotic programs endorsed by 13-cis-RA. (unitn.it)

Clonidine is able to affect the heart rate by stimulating α2 receptors instead of β receptors because it has the ability to cross the blood-brain barrier. (proprofs.com)
Clonidine HCl is soluble 1 g in about 13 mL water and 25 mL alcohol. (uspharmacist.com)

These experiments suggest that cooling augments alpha 2-adrenergic responsiveness without affecting alpha 1-adrenergic responsiveness. (johnshopkins.edu)

Functional alpha-1B adrenergic receptors on human epicardial coronary artery endothelial cells. (rndsystems.com)

In tumor necrosis factor (TNF)-alpha-stimulated human aortic endothelial cells, beta-sitosterol was found to significantly inhibit vascular adhesion molecule 1 and intracellular adhesion molecule 1 expression. (drugs.com)

While DAG stays near the membrane, IP3 diffuses into the cytosol and to find the IP3 receptor on the endoplasmic reticulum, triggering calcium release from the stores. (wikipedia.org)
Increased voltage-dependent calcium influx produced by alpha 1B-adrenergic receptor activation in rat medullary thyroid carcinoma 6-23 cells. (aspetjournals.org)
The inhibition could be mimicked by the L-type calcium channel blocker nimodipine (1 μ m ) as well as by protein kinase C (PKC) activators phorbol 12,13-dibutyrate (10 μ m ) and phorbol 12-myristate 13-acetate (500 n m ), and blocked by the PKC inactivator (±)-1-(5-isoquinolinesulfonyl)-2-methylpiperazine (200 μ m ), suggesting a mechanism involving PKC modulation of L-type calcium channels. (jneurosci.org)

This gene encodes alpha-1A-adrenergic receptor. (nih.gov)

Urethral sphincter Bronchioles (although minor to the relaxing effect of β2 receptor on bronchioles) Iris dilator muscle Seminal tract, resulting in ejaculation Activation of α1-adrenergic receptors produces anorexia and partially mediates the efficacy of appetite suppressants like phenylpropanolamine and amphetamine in the treatment of obesity. (wikipedia.org)
The "intra-operative floppy iris syndrome" cataract surgery complication has been reported in men using alpha-blockers. (urotoday.com)

Modafinil, a 1:1 racemic mixture of (R)-(-) and (S)-(-) enantiomers, and armodafinil, the isolated (R)-(-) enantiomer, have proved clinically useful in the treatment of narcolepsy and other causes of excessive daytime sleepiness, such as idiopathic hypersomnolence. (medscape.com)

From our results, we can conclude that the deletion or inhibition of alpha-1-AR sensitizes NB cells to 13-Cis-RA, both in terms of induction of apoptosis and neural differentiation. (unitn.it)

A Myocardial Slice Culture Model Reveals Alpha-1A-Adrenergic Receptor Signaling in the Human Heart. (rndsystems.com)
Dr. Beak discovered that the orphan nuclear receptor, RORα, is expressed in the mouse and human heart and mediates cardiac hypertrophy in response to angiotensin II. (unc.edu)

To investigate the role of ADRA1B in the synergism, we generated CHP134 NB cell lines knocked-out (KO) for the receptor and observed that exposure of CHP134 KO cell to 13-cis-RA leads to a reduction of cell viability and neural differentiation. (unitn.it)

They stimulate 5-HT 1 receptors, with antidepressant and anxiolytic effects, but they also stimulate 5-HT 2 receptors, commonly causing anxiety, insomnia, and sexual dysfunction, and 5-HT 3 receptors, commonly causing nausea and headache. (msdmanuals.com)

2. Allen LV Jr. Summary of quality-control testing for sterile and nonsterile compounded preparations, part 1: physical and chemical testing. (uspharmacist.com)

Wakefulness-Promoting Agents

Receptors, Adrenergic, alpha-2

alpha 1-Antitrypsin

Receptors, Adrenergic, alpha

Hypoxia-Inducible Factor 1, alpha Subunit

5-alpha Reductase Inhibitors

Pregnanes

Prostatic Hyperplasia

Lauric Acids

Serenoa

Cholestenone 5 alpha-Reductase

Myristic Acid

Vasoconstrictor Agents

Ephedrine

Extravasation of Diagnostic and Therapeutic Materials

Hypotension

Shock, Septic

Ritodrine

Vasopressins

alpha1-adrenergic receptor subtypes in human peripheral blood lymphocytes. (1/1045)

Modulation of long-term synaptic depression in visual cortex by acetylcholine and norepinephrine. (2/1045)

Modulation of basal intracellular calcium by inverse agonists and phorbol myristate acetate in rat-1 fibroblasts stably expressing alpha1d-adrenoceptors. (3/1045)

Effect of chronic hypoxia on alpha-1 adrenoceptor-mediated inositol 1,4,5-trisphosphate signaling in ovine uterine artery. (4/1045)

The Ca2+ channel blockade changes the behavioral and biochemical effects of immobilization stress. (5/1045)

Altered alpha 1-adrenoceptor subtypes mediated cardiac function after treatment of propranolol to rats. (6/1045)

Characterization of alpha1-adrenoceptor subtypes mediating vasoconstriction in human umbilical vein. (7/1045)

A decrease in the amount and function of inhibitory GTP-binding protein in the resistance small artery from spontaneously hypertensive rats. (8/1045)

Agonists9

Antagonists15

Antagonist9

Agonist9

Subtypes8

Subtype5

Norepinephrine11

Selective3

Muscarinic cholinergic2

Postsynaptic 5-HT recept2

Phenylephrine3

Affinity5

Serotonin3

Binds2

Blockade1

Compounds1

Rats2

Mediate2

Sympathetic1

Neurons3

Superfamily2

Rauwolscine1

Antibodies1

Terazosin2

Antagonism1

Pharmacological3

Vasoconstriction3

Targets2

Metabolic2

Stimulates1

Polymorphism1

Canine1

Catecholamine1

Clonidine2

Responsiveness1

Functional1

Endothelial cells1

Calcium3

Gene1

Iris2

Clinically1

Inhibition1

Human2

Exposure1

Dysfunction1

Preparations1