An alpha-1 adrenergic agonist that causes prolonged peripheral VASOCONSTRICTION.
Drugs that selectively bind to and activate alpha adrenergic receptors.
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.
Compounds that bind to and activate ADRENERGIC ALPHA-1 RECEPTORS.
A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.
An imidazoline sympatholytic agent that stimulates ALPHA-2 ADRENERGIC RECEPTORS and central IMIDAZOLINE RECEPTORS. It is commonly used in the management of HYPERTENSION.
A subclass of alpha-adrenergic receptors that mediate contraction of SMOOTH MUSCLE in a variety of tissues such as ARTERIOLES; VEINS; and the UTERUS. They are usually found on postsynaptic membranes and signal through GQ-G11 G-PROTEINS.
Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the actions of endogenous or exogenous adrenergic agonists. Adrenergic alpha-antagonists are used in the treatment of hypertension, vasospasm, peripheral vascular disease, shock, and pheochromocytoma.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
An alpha-adrenergic antagonist with long duration of action. It has been used to treat hypertension and as a peripheral vasodilator.
Arteries which arise from the abdominal aorta and distribute to most of the intestines.
Cell-surface proteins that bind epinephrine and/or norepinephrine with high affinity and trigger intracellular changes. The two major classes of adrenergic receptors, alpha and beta, were originally discriminated based on their cellular actions but now are distinguished by their relative affinity for characteristic synthetic ligands. Adrenergic receptors may also be classified according to the subtypes of G-proteins with which they bind; this scheme does not respect the alpha-beta distinction.
Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters.
Drugs used to cause constriction of the blood vessels.
Drugs that bind to and block the activation of ADRENERGIC ALPHA-1 RECEPTORS.
An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems.
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
A direct acting sympathomimetic used as a vasoconstrictor to relieve nasal congestion. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1251)
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.

Non-specific action of methoxamine on Ito, and the cloned channels hKv 1.5 and Kv 4.2. (1/291)

The alpha1-adrenoceptor agonist methoxamine acted independently of receptor activation to reduce Ito and the sustained outward current in rat ventricular myocytes, and hKv 1.5 and Kv 4.2 cloned K+ channel currents. Two hundred microM methoxamine reduced Ito by 36% in the presence of 2 microM prazosin, and by 37 and 38% after preincubation of myocytes with either N-ethylmaleimide or phenoxybenzamine (n=6). The EC50 values at +60 mV for direct reduction of Ito, hKv 1.5, and Kv 4.2 by methoxamine were 239, 276, and 363 microM, respectively, with Hill coefficients of 0.87-1.5. Methoxamine accelerated Ito and Kv 4.2 current inactivation in a concentration- and voltage-dependent manner. Apparent rate constants for methoxamine binding and unbinding gave Kd values in agreement with EC50 values measured from dose-response relations. The voltage-dependence of block supported charged methoxamine binding to a putative intracellular site that sensed approximately 20% of the transmembrane electrical field. In the presence of methoxamine, deactivating Kv 4.2 tail currents displayed a distinct rising phase, and were slowed relative to control, such that tail current crossover was observed. These observations support a dominant mechanism of open channel block, although closed channel block could not be ruled out. Single-channel data from hKv 1.5 patches revealed increased closed times with blank sweeps and decreased burst duration in the presence of drug, and a reduction of mean channel open time from 1.8 ms in control to 0.4 ms in 500 microM methoxamine. For this channel, therefore, both open and closed channel block appeared to be important mechanisms for the action of methoxamine.  (+info)

NO overproduction by eNOS precedes hyperdynamic splanchnic circulation in portal hypertensive rats. (2/291)

Chronic high blood flow and the hyperdynamic circulatory syndrome in portal hypertension are associated with endothelial constitutive nitric oxide (NO) synthase (eNOS) upregulation and increased NO release. In portal vein-ligated (PVL) rats the splanchnic circulation is not yet hyperdynamic on day 3 postoperatively. In vitro perfused superior mesenteric arteries (SMAs) of day 3 PVL and sham rats were challenged with increasing flow rates or the alpha-adrenoreceptor agonist methoxamine (30 and 100 microM) before and after incubation with the NO inhibitor, Nomega-nitro-L-arginine (L-NNA, 10(-4) M). Perfusate NO metabolite (NOx) concentrations were measured by chemiluminescence. PVL rats expressed a significant hyporesponsiveness to increases in flow rate or methoxamine that was overcome by incubation with L-NNA. The PVL vasculature showed significantly higher slopes of NOx production vs. flow-induced shear stress, higher increases in perfusate NOx concentration in response to methoxamine, and higher eNOS protein levels (Western blot) compared with sham rats. In conclusion, eNOS-upregulation and increased NO release by the SMA endothelium occur before the development of the hyperdynamic splanchnic circulation, suggesting a primary role of NO in the pathogenesis of arterial vasodilatation.  (+info)

Recovery of locomotion after ventral and ventrolateral spinal lesions in the cat. II. Effects of noradrenergic and serotoninergic drugs. (3/291)

The effects of serotoninergic and noradrenergic drugs (applied intrathecally) on treadmill locomotion were evaluated in two adult cats subjected to a ventral and ventrolateral spinal lesion (T13). Despite the extensive spinal lesion, severely damaging important descending pathways such as the reticulo- and vestibulospinal tracts, both cats recovered quadrupedal voluntary locomotion. As detailed in a previous paper, the locomotor recovery occurred in three stages defined as early period, when the animal could not walk with its hindlimbs, recovery period, when progressive improvement occurred, and plateau period, when a more stable locomotor performance was observed. At this latter stage, the cats suffered from postural and locomotor deficits, such as poor lateral stability, irregular stepping of the hindlimbs, and inconsistent homolateral fore- and hindlimb coupling. The present study aimed at evaluating the potential of serotoninergic and/or noradrenergic drugs to improve the locomotor abilities in the early and late stages. Both cats were implanted chronically with an intrathecal cannula and electromyographic (EMG) electrodes, which allowed determination, under similar recording conditions, of the locomotor performance pre- and postlesion and comparisons of the effects of different drugs. EMG and kinematic analyses showed that norepinephrine (NE) injected in early and plateau periods improved the regularity of the hindlimb stepping and stabilized the interlimb coupling, permitting to maintain constant locomotion for longer periods of time. Methoxamine, the alpha1-agonist (tested only at the plateau period), had similar effects. In contrast, the alpha2-agonist, clonidine, deteriorated walking. Serotoninergic drugs, such as the neurotransmitter itself, serotonin (5HT), the precursor 5-hydroxytryptophan (5HTP), and the agonist quipazine improved the locomotion by increasing regularity of the hindlimb stepping and by increasing the step cycle duration. In contrast, the 5HT1A agonist 8-hydroxy-dipropylaminotetralin (DPAT) caused foot drag in one of the cats, resulting in frequent stumbling. Injection of combination of methoxamine and quipazine resulted in maintained, regular stepping with smooth movements and good lateral stability. Our results show that the effects of drugs can be integrated to the residual voluntary locomotion and improve some of its postural aspects. However, this work shows clearly that the effects of drugs (such as clonidine) may depend on whether or not the spinal lesion is complete. In a clinical context, this may suggest that different classes of drugs could be used in patients with different types of spinal cord injuries. Possible mechanisms underlying the effect of noradrenergic and serotoninergic drugs on the locomotion after partial spinal lesions are discussed.  (+info)

Beta-adrenergic agonists regulate cell membrane fluctuations of human erythrocytes. (4/291)

1. Mechanical fluctuations of the cell membrane (CMFs) in human erythrocytes reflect the bending deformability of the membrane-skeleton complex. These fluctuations were monitored by time-dependent light scattering from a small area ( approximately 0. 25 microm2) of the cell surface by a method based on point dark field microscopy. 2. Exposure of red blood cells (RBCs) to adrenaline (epinephrine) and isoproterenol (isoprenaline) resulted in up to a 45 % increase in the maximal fluctuation amplitude and up to a 35 % increase in the half-width of the amplitude distribution. The power spectra of membrane fluctuations of control and treated cells revealed that adrenaline stimulated only the low frequency component (0.3-3 Hz). Analysis of the dose-response curves of beta-adrenergic agonists yielded an EC50 of 5 x 10-9 and 1 x 10-11 M for adrenaline and isoproterenol, respectively. Propranolol had an inhibitory effect on the stimulatory effect of isoproterenol. These findings show a potency order of propranolol > isoproterenol > adrenaline. 3. The stimulatory effect of adrenaline was a temporal one, reaching its maximal level after 20-30 min but being abolished after 60 min. However, in the presence of 3-isobutyl-1-methylxanthine, a partial stimulatory effect was maintained even after 60 min. Pentoxifylline and 8-bromo-cAMP elevated CMFs. However, exposure of ATP-depleted erythrocytes to adrenaline or 8-bromo-cAMP did not yield any elevation in CMFs. These findings suggest that the beta-agonist effect on CMFs is transduced via a cAMP-dependent pathway. 4. Deoxygenation decreased CMFs and filterability of erythrocytes by approximately 30 %. The stimulatory effect of isoproterenol on CMFs was 2.2-fold higher in deoxygenated RBCs than in oxygenated cells. 5. Exposure of RBCs to adrenaline resulted in a concentration-dependent increase in RBC filterability, demonstrating a linear relationship between CMFs and filterability, under the same exposure conditions to adrenaline. These findings suggest that beta-adrenergic agonists may improve passage of erythrocytes through microvasculature, enhancing oxygen delivery to tissues, especially under situations of reduced oxygen tension for periods longer than 20 min.  (+info)

Augmented alpha-adrenergic constriction of atherosclerotic human coronary arteries. (5/291)

BACKGROUND: Although adrenergic activation plays a major role in the initiation of experimental myocardial ischemia, the significance of alpha-adrenergic coronary constriction in humans has been questioned. The present study assessed the impact of selective alpha-adrenergic receptor activation in patients with normal or atherosclerotic coronary arteries. METHODS AND RESULTS: In 39 patients, coronary blood flow (CBF, mL/min) was determined from combined angiography and Doppler measurements. In 8 patients with normal coronary arteries (group 1) and 9 with single coronary artery stenosis (group 2), doses of 1, 2.5, 5, and 10 mg IC of the alpha1-agonist methoxamine (M) were injected. Identical doses of the alpha2-agonist BHT933 (B) were injected in 8 patients with normal coronary arteries (group 3) and 8 with single stenosis (group 4). In 6 additional patients with single stenosis (group 5), aortocoronary sinus lactate differences were measured in response to M and B. CBF remained unchanged in group 1. In contrast, CBF was decreased dose-dependently in group 2, with a maximum at 10 mg M (39.0+/-9.4 versus 15.2+/-7.0). In groups 3 and 4, CBF was also decreased dose-dependently, with a maximum at 10 mg B (63.3+/-24.8 versus 49. 1+/-27.9 and 41.5+/-19.0 versus 12.7+/-8.0, respectively). In group 5, there was more net lactate production with B than with M (-0. 34+/-0.11 versus -0.04+/-0.09 mmol/L). CONCLUSIONS: In normal coronary arteries, alpha1-adrenergic activation does not reduce CBF, whereas alpha2-adrenergic activation reduces CBF by microvascular constriction. Both alpha1- and alpha2-adrenergic epicardial and microvascular constriction are augmented by atherosclerosis and can induce myocardial ischemia.  (+info)

Enhancement of bistability in spinal motoneurons in vivo by the noradrenergic alpha1 agonist methoxamine. (6/291)

Enhancement of bistability in spinal motoneurons in vivo by the noradrenergic alpha1 agonist methoxamine. Like many types of motoneurons, spinal motoneurons in the adult mammal can exhibit bistable behavior. This means that short periods of excitatory input can initiate long periods of self-sustained firing and that equally short periods of inhibition can return the cell to the quiescent state. Usually, the presence of one of the monoamines (either serotonin or norepinephrine) is required for spinal motoneurons to express bistable behaviors. Because the decerebrate cat preparation has tonic activity in monoaminergic fibers that originate in the brain stem and project to spinal motoneurons, these cells sometimes exhibit bistable behavior. However, exogenous application of the noradrenergic alpha1 agonist methoxamine greatly enhances bistable behavior in the decerebrate. The goal of this study was to identify the mechanisms of this action of methoxamine. The total persistent inward current (IPIC) in spinal motoneurons in the decerebrate cat was measured from I-V functions generated by triangular voltage commands applied using discontinuous single electrode voltage clamp. The effect of methoxamine on IPIC was assessed by comparing its properties in a control cell sample without methoxamine to its properties in a sample of cells obtained after application of methoxamine. In most experiments, at least one cell was obtained from each sample. Our results showed that methoxamine approximately doubled the amplitude of IPIC without changing its onset voltage, its offset voltage, or its persistence. The reduced amplitude was a consistent finding within experiments and so was unlikely to be caused by interanimal variability. In addition, methoxamine depolarized motoneurons without altering their input conductances, so that a smaller amount of current was required to reach the onset voltage of IPIC. These effects of methoxamine were approximately equal in all cells. As a result of these changes, methoxamine greatly enhanced the tendency for motoneurons to become bistable. It is proposed that the methoxamine-induced increase in the amplitude of IPIC is effective in enhancing the duration of bistable firing because this increase makes IPIC more resistant to the deactivating effects of the afterhyperpolarizations between spikes.  (+info)

Hsp90 regulation of endothelial nitric oxide synthase contributes to vascular control in portal hypertension. (7/291)

The molecular chaperone, heat shock protein 90 (Hsp90), acts as an intermediate in the signaling cascades leading to activation of endothelial nitric oxide synthase (eNOS). In this study, we examine the participation of this pathway in nitric oxide (NO)-dependent vasodilation in the rat mesentery in vitro. In normal animals, immunoprecipitation of eNOS from intact mesentery coimmunoprecipitates Hsp90 and, additionally, both eNOS and Hsp90 colocalize to the endothelial lining of mesenteric vessels. In the perfused mesenteric vasculature of normal animals, geldanamycin (GA), a specific inhibitor of Hsp90 signaling, attenuates ACh-dependent vasodilation but does not affect vasodilation in response to sodium nitroprusside. Next, studies were performed in animals with experimental portal hypertension induced by portal vein ligation (PVL). In PVL animals, NOS catalytic activity is markedly enhanced in mesenteric tissue and the perfused mesentery is hyporesponsive to the vasoconstrictor methoxamine (MTX). GA significantly potentiates MTX-induced vasoconstriction after PVL, thereby partially reversing the hyporeactivity to this agent exhibited in the mesenteric vasculature after PVL. These studies suggest that Hsp90 can act as a signaling mediator of NO-dependent responses in the mesenteric circulation and indicate that the excessive NO production observed in portal hypertension is mediated in part through Hsp90 signaling.  (+info)

Comparison of the effects of venlafaxine, desipramine, and paroxetine on noradrenaline- and methoxamine-evoked constriction of the dorsal hand vein. (8/291)

AIMS: To examine whether the antidepressant venlafaxine, a novel serotonin-noradrenaline re-uptake inhibitor (SNRI), can modify alpha-adrenoceptor-mediated venoconstriction in man. The effects of venlafaxine were compared with those of desipramine, a tricyclic antidepressant with noradrenaline uptake inhibiting properties, and paroxetine, a selective serotonin re-uptake inhibitor (SSRI), on noradrenaline-and methoxamine-evoked venoconstriction using the dorsal hand vein compliance technique. METHODS: Fifteen healthy male volunteers participated in five weekly experimental sessions. Each session was associated with a clinically effective dose of an antidepressant or placebo. The following oral dosages were used: venlafaxine 75 mg, venlafaxine 150 mg, desipramine 100 mg, paroxetine 20 mg, or placebo. A double-blind, cross-over, balanced design was used. In each session, dose-response curves to both locally infused noradrenaline acid tartrate (0.1-33.33 ng min-1 ) and methoxamine hydrochloride (0.5-121.5 microg min-1 ) were constructed. Systolic and diastolic blood pressure and pulse rate were measured in the supine and erect positions. Salivation was measured by the dental roll technique. RESULTS: Venlafaxine 150 mg and desipramine 100 mg potentiated the venoconstrictor response to noradrenaline (anova of log ED50s: P<0.01; individual comparisons: venlafaxine 150 mg vs placebo: P<0.005; mean difference, 95% CI: -0. 49 (-0.81, -0.17); desipramine 100 mg vs placebo: P<0.005; mean difference, 95% CI: -0.34 (-0.60, -0.09) without affecting the response to methoxamine. Neither paroxetine nor placebo had any effects on the venoconstrictor responses. Both doses of venlafaxine increased systolic blood pressure (supine and erect) and venlafaxine 150 mg increased diastolic blood pressure (supine) (anova, P<0.05). Desipramine increased heart rate (P<0.05). Desipramine and both doses of venlafaxine reduced salivation (P<0.025). CONCLUSIONS: These results show that, similarly to desipramine 100 mg, venlafaxine 150 mg can potentiate venoconstrictor responses to noradrenaline, consistent with venlafaxine's ability to block noradrenaline uptake in man. The importance of noradrenaline uptake blockade in these observations is confirmed by the lack of effect of the antidepressants on methoxamine-evoked venoconstriction and the failure of paroxetine to modify noradrenaline-evoked venoconstriction.  (+info)

Methoxamine is a synthetic, selective α1-adrenergic receptor agonist used in scientific research and for therapeutic purposes. It has the ability to stimulate the α1 adrenergic receptors, leading to vasoconstriction (constriction of blood vessels), increased blood pressure, and reduced blood flow to the skin and extremities.

In a medical context, methoxamine is primarily used as an experimental drug or in research settings due to its specific pharmacological properties. It may be employed to investigate the role of α1-adrenergic receptors in various physiological processes or to temporarily counteract the hypotensive (low blood pressure) effects of certain medications, such as vasodilators or anesthetics.

It is important to note that methoxamine is not commonly used in routine clinical practice due to its strong vasoconstrictive properties and potential adverse effects on organ function if misused or improperly dosed.

Adrenergic alpha-agonists are a type of medication that binds to and activates adrenergic alpha receptors, which are found in the nervous system and other tissues throughout the body. These receptors are activated naturally by chemicals called catecholamines, such as norepinephrine and epinephrine (also known as adrenaline), that are released in response to stress or excitement.

When adrenergic alpha-agonists bind to these receptors, they mimic the effects of catecholamines and cause various physiological responses, such as vasoconstriction (constriction of blood vessels), increased heart rate and force of heart contractions, and relaxation of smooth muscle in the airways.

Adrenergic alpha-agonists are used to treat a variety of medical conditions, including hypertension (high blood pressure), glaucoma, nasal congestion, and attention deficit hyperactivity disorder (ADHD). Examples of adrenergic alpha-agonists include phenylephrine, clonidine, and guanfacine.

It's important to note that adrenergic alpha-agonists can have both beneficial and harmful effects, depending on the specific medication, dosage, and individual patient factors. Therefore, they should only be used under the guidance of a healthcare professional.

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.

Adrenergic alpha-1 receptor agonists are a type of medication that binds to and activates adrenergic alpha-1 receptors, which are found in various tissues throughout the body, including the smooth muscle of blood vessels, the heart, the liver, and the kidneys. When these receptors are activated, they cause a variety of physiological responses, such as vasoconstriction (constriction of blood vessels), increased heart rate and force of heart contractions, and relaxation of the detrusor muscle in the bladder.

Examples of adrenergic alpha-1 receptor agonists include phenylephrine, which is used to treat low blood pressure and nasal congestion, and midodrine, which is used to treat orthostatic hypotension (low blood pressure upon standing). These medications can have side effects such as increased heart rate, headache, and anxiety. It's important to use them under the supervision of a healthcare provider, as they may interact with other medications and medical conditions.

**Prazosin** is an antihypertensive drug, which belongs to the class of medications called alpha-blockers. It works by relaxing the muscles in the blood vessels, which helps to lower blood pressure and improve blood flow. Prazosin is primarily used to treat high blood pressure (hypertension), but it may also be used for the management of symptoms related to enlarged prostate (benign prostatic hyperplasia).

In a medical definition context:

Prazosin: A selective α1-adrenergic receptor antagonist, used in the treatment of hypertension and benign prostatic hyperplasia. It acts by blocking the action of norepinephrine on the smooth muscle of blood vessels, resulting in vasodilation and decreased peripheral vascular resistance. This leads to a reduction in blood pressure and an improvement in urinary symptoms associated with an enlarged prostate.

Clonidine is an medication that belongs to a class of drugs called centrally acting alpha-agonist hypotensives. It works by stimulating certain receptors in the brain and lowering the heart rate, which results in decreased blood pressure. Clonidine is commonly used to treat hypertension (high blood pressure), but it can also be used for other purposes such as managing withdrawal symptoms from opioids or alcohol, treating attention deficit hyperactivity disorder (ADHD), and preventing migraines. It can be taken orally in the form of tablets or transdermally through a patch applied to the skin. As with any medication, clonidine should be used under the guidance and supervision of a healthcare provider.

Alpha-1 adrenergic receptors (also known as α1-adrenoreceptors) are a type of G protein-coupled receptor that binds catecholamines, such as norepinephrine and epinephrine. These receptors are primarily found in the smooth muscle of various organs, including the vasculature, heart, liver, kidneys, gastrointestinal tract, and genitourinary system.

When an alpha-1 adrenergic receptor is activated by a catecholamine, it triggers a signaling cascade that leads to the activation of phospholipase C, which in turn activates protein kinase C and increases intracellular calcium levels. This ultimately results in smooth muscle contraction, increased heart rate and force of contraction, and vasoconstriction.

Alpha-1 adrenergic receptors are also found in the central nervous system, where they play a role in regulating wakefulness, attention, and anxiety. There are three subtypes of alpha-1 adrenergic receptors (α1A, α1B, and α1D), each with distinct physiological roles and pharmacological properties.

In summary, alpha-1 adrenergic receptors are a type of G protein-coupled receptor that binds catecholamines and mediates various physiological responses, including smooth muscle contraction, increased heart rate and force of contraction, vasoconstriction, and regulation of wakefulness and anxiety.

Adrenergic alpha-antagonists, also known as alpha-blockers, are a class of medications that block the effects of adrenaline and noradrenaline at alpha-adrenergic receptors. These receptors are found in various tissues throughout the body, including the smooth muscle of blood vessels, the heart, the genitourinary system, and the eyes.

When alpha-blockers bind to these receptors, they prevent the activation of the sympathetic nervous system, which is responsible for the "fight or flight" response. This results in a relaxation of the smooth muscle, leading to vasodilation (widening of blood vessels), decreased blood pressure, and increased blood flow.

Alpha-blockers are used to treat various medical conditions, such as hypertension (high blood pressure), benign prostatic hyperplasia (enlarged prostate), pheochromocytoma (a rare tumor of the adrenal gland), and certain types of glaucoma.

Examples of alpha-blockers include doxazosin, prazosin, terazosin, and tamsulosin. Side effects of alpha-blockers may include dizziness, lightheadedness, headache, weakness, and orthostatic hypotension (a sudden drop in blood pressure upon standing).

Norepinephrine, also known as noradrenaline, is a neurotransmitter and a hormone that is primarily produced in the adrenal glands and is released into the bloodstream in response to stress or physical activity. It plays a crucial role in the "fight-or-flight" response by preparing the body for action through increasing heart rate, blood pressure, respiratory rate, and glucose availability.

As a neurotransmitter, norepinephrine is involved in regulating various functions of the nervous system, including attention, perception, motivation, and arousal. It also plays a role in modulating pain perception and responding to stressful or emotional situations.

In medical settings, norepinephrine is used as a vasopressor medication to treat hypotension (low blood pressure) that can occur during septic shock, anesthesia, or other critical illnesses. It works by constricting blood vessels and increasing heart rate, which helps to improve blood pressure and perfusion of vital organs.

Phenylephrine is a medication that belongs to the class of drugs known as sympathomimetic amines. It primarily acts as an alpha-1 adrenergic receptor agonist, which means it stimulates these receptors, leading to vasoconstriction (constriction of blood vessels). This effect can be useful in various medical situations, such as:

1. Nasal decongestion: When applied topically in the nose, phenylephrine causes constriction of the blood vessels in the nasal passages, which helps to relieve congestion and swelling. It is often found in over-the-counter (OTC) cold and allergy products.
2. Ocular circulation: In ophthalmology, phenylephrine is used to dilate the pupils before eye examinations. The increased pressure from vasoconstriction helps to open up the pupil, allowing for a better view of the internal structures of the eye.
3. Hypotension management: In some cases, phenylephrine may be given intravenously to treat low blood pressure (hypotension) during medical procedures like spinal anesthesia or septic shock. The vasoconstriction helps to increase blood pressure and improve perfusion of vital organs.

It is essential to use phenylephrine as directed, as improper usage can lead to adverse effects such as increased heart rate, hypertension, arrhythmias, and rebound congestion (when used as a nasal decongestant). Always consult with a healthcare professional for appropriate guidance on using this medication.

Phenoxybenzamine is an antihypertensive medication that belongs to a class of drugs known as non-selective alpha blockers. It works by blocking both alpha-1 and alpha-2 receptors, which results in the relaxation of smooth muscle tissue in blood vessel walls and other organs. This leads to a decrease in peripheral vascular resistance and a reduction in blood pressure.

Phenoxybenzamine is primarily used for the preoperative management of patients with pheochromocytoma, a rare tumor that produces excessive amounts of catecholamines, such as adrenaline and noradrenaline. By blocking alpha receptors, phenoxybenzamine prevents the hypertensive crisis that can occur during surgery to remove the tumor.

It's important to note that phenoxybenzamine has a long duration of action (up to 14 days) and can cause orthostatic hypotension, tachycardia, and other side effects. Therefore, it should be used with caution and under the close supervision of a healthcare professional.

The mesenteric arteries are the arteries that supply oxygenated blood to the intestines. There are three main mesenteric arteries: the superior mesenteric artery, which supplies blood to the small intestine (duodenum to two-thirds of the transverse colon) and large intestine (cecum, ascending colon, and the first part of the transverse colon); the inferior mesenteric artery, which supplies blood to the distal third of the transverse colon, descending colon, sigmoid colon, and rectum; and the middle colic artery, which is a branch of the superior mesenteric artery that supplies blood to the transverse colon. These arteries are important in maintaining adequate blood flow to the intestines to support digestion and absorption of nutrients.

Adrenergic receptors are a type of G protein-coupled receptor that bind and respond to catecholamines, which include the neurotransmitters norepinephrine (noradrenaline) and epinephrine (adrenaline). These receptors play a crucial role in the body's "fight or flight" response and are involved in regulating various physiological functions such as heart rate, blood pressure, respiration, and metabolism.

There are nine different subtypes of adrenergic receptors, which are classified into two main groups based on their pharmacological properties: alpha (α) and beta (β) receptors. Alpha receptors are further divided into two subgroups, α1 and α2, while beta receptors are divided into three subgroups, β1, β2, and β3. Each subtype has a unique distribution in the body and mediates distinct physiological responses.

Activation of adrenergic receptors occurs when catecholamines bind to their specific binding sites on the receptor protein. This binding triggers a cascade of intracellular signaling events that ultimately lead to changes in cell function. Different subtypes of adrenergic receptors activate different G proteins and downstream signaling pathways, resulting in diverse physiological responses.

In summary, adrenergic receptors are a class of G protein-coupled receptors that bind catecholamines and mediate various physiological functions. Understanding the function and regulation of these receptors is essential for developing therapeutic strategies to treat a range of medical conditions, including hypertension, heart failure, asthma, and anxiety disorders.

Sympathomimetic drugs are substances that mimic or stimulate the actions of the sympathetic nervous system. The sympathetic nervous system is one of the two divisions of the autonomic nervous system, which regulates various automatic physiological functions in the body. The sympathetic nervous system's primary function is to prepare the body for the "fight-or-flight" response, which includes increasing heart rate, blood pressure, respiratory rate, and metabolism while decreasing digestive activity.

Sympathomimetic drugs can exert their effects through various mechanisms, including directly stimulating adrenergic receptors (alpha and beta receptors) or indirectly causing the release of norepinephrine and epinephrine from nerve endings. These drugs are used in various clinical settings to treat conditions such as asthma, nasal congestion, low blood pressure, and attention deficit hyperactivity disorder (ADHD). Examples of sympathomimetic drugs include epinephrine, norepinephrine, dopamine, dobutamine, albuterol, pseudoephedrine, and methylphenidate.

It is important to note that sympathomimetic drugs can also have adverse effects, particularly when used in high doses or in individuals with certain medical conditions. These adverse effects may include anxiety, tremors, palpitations, hypertension, arrhythmias, and seizures. Therefore, these medications should be used under the close supervision of a healthcare provider.

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.

Adrenergic alpha-1 receptor antagonists, also known as alpha-blockers, are a class of medications that block the effects of the neurotransmitter norepinephrine at alpha-1 receptors. These receptors are found in various tissues throughout the body, including the smooth muscle of blood vessels, the bladder, and the eye.

When norepinephrine binds to alpha-1 receptors, it causes smooth muscle to contract, leading to vasoconstriction (constriction of blood vessels), increased blood pressure, and other effects. By blocking these receptors, alpha-blockers can cause relaxation of smooth muscle, leading to vasodilation (expansion of blood vessels), decreased blood pressure, and other effects.

Alpha-blockers are used in the treatment of various medical conditions, including hypertension (high blood pressure), benign prostatic hyperplasia (enlarged prostate), and pheochromocytoma (a rare tumor of the adrenal gland). Examples of alpha-blockers include doxazosin, prazosin, and terazosin.

It's important to note that while alpha-blockers can be effective in treating certain medical conditions, they can also have side effects, such as dizziness, lightheadedness, and orthostatic hypotension (a sudden drop in blood pressure when standing up). As with any medication, it's important to use alpha-blockers under the guidance of a healthcare provider.

Tyramine is not a medical condition but a naturally occurring compound called a biogenic amine, which is formed from the amino acid tyrosine during the fermentation or decay of certain foods. Medically, tyramine is significant because it can interact with certain medications, particularly monoamine oxidase inhibitors (MAOIs), used to treat depression and other conditions.

The interaction between tyramine and MAOIs can lead to a hypertensive crisis, a rapid and severe increase in blood pressure, which can be life-threatening if not treated promptly. Therefore, individuals taking MAOIs are often advised to follow a low-tyramine diet, avoiding foods high in tyramine, such as aged cheeses, cured meats, fermented foods, and some types of beer and wine.

Vasoconstriction is a medical term that refers to the narrowing of blood vessels due to the contraction of the smooth muscle in their walls. This process decreases the diameter of the lumen (the inner space of the blood vessel) and reduces blood flow through the affected vessels. Vasoconstriction can occur throughout the body, but it is most noticeable in the arterioles and precapillary sphincters, which control the amount of blood that flows into the capillary network.

The autonomic nervous system, specifically the sympathetic division, plays a significant role in regulating vasoconstriction through the release of neurotransmitters like norepinephrine (noradrenaline). Various hormones and chemical mediators, such as angiotensin II, endothelin-1, and serotonin, can also induce vasoconstriction.

Vasoconstriction is a vital physiological response that helps maintain blood pressure and regulate blood flow distribution in the body. However, excessive or prolonged vasoconstriction may contribute to several pathological conditions, including hypertension, stroke, and peripheral vascular diseases.

Oxymetazoline is a direct-acting mainly α1-adrenergic receptor agonist, which is primarily used as a nasal decongestant and an ophthalmic vasoconstrictor. It constricts blood vessels, reducing swelling and fluid accumulation in the lining of the nose, thereby providing relief from nasal congestion due to allergies or colds. Oxymetazoline is available over-the-counter in various forms, such as nasal sprays, drops, and creams. It's important to follow the recommended usage guidelines, as prolonged use of oxymetazoline can lead to a rebound effect, causing further congestion.

Epinephrine, also known as adrenaline, is a hormone and a neurotransmitter that is produced in the body. It is released by the adrenal glands in response to stress or excitement, and it prepares the body for the "fight or flight" response. Epinephrine works by binding to specific receptors in the body, which causes a variety of physiological effects, including increased heart rate and blood pressure, improved muscle strength and alertness, and narrowing of the blood vessels in the skin and intestines. It is also used as a medication to treat various medical conditions, such as anaphylaxis (a severe allergic reaction), cardiac arrest, and low blood pressure.

... is an α1-adrenergic receptor agonist, somewhat similar in structure to butaxamine and 2,5-DMA. It is no longer ...
Methoxamine Positioning of the patient. In the lateral decubitus position or lying on the left side. This will make murmurs in ...
α1 selective: phenylephrine, methoxamine, midodrine, oxymetazoline. α2 selective: α-methyldopa, clonidine, brimonidine, ...
"Methoxamine (hydrochloride) Safety Data Sheet" (PDF). Caymen Chemicals. Archived (PDF) from the original on 8 April 2014. ...
Bupropion Methoxamine "Definition: butoxamine from Online Medical Dictionary". Hillman KL, Doze VA, Porter JE (August 2005). " ...
ergotamine etilefrine indanidine mephentermine metaraminol methoxamine mivazerol naphazoline norfenefrine octopamine ... Methoxamine Midodrine Metaraminol Phenylephrine Amidephrine Sdz-nvi-085 [104195-17-7]. α2 agonist: inhibits adenylyl cyclase ...
It is an intermediate in synthesis of organic compounds, including pharmaceuticals such as methoxamine and butaxamine.[citation ...
Arnerić SP, Roetker A, Long JP, Mott J, Barfknecht CF (June 1982). "Effects of semirigid methoxamine analogs on vascular smooth ...
Etilefrine Ethylnorepinephrine 5-Fluoronorepinephrine 6-Fluoronorepinephrine Indanidine Levonordefrin Metaraminol Methoxamine ...
... a natural psychedelic alkaloid Methoxamine Orciprenaline This set index page lists chemical structure articles associated with ...
Dopamine C01CA05 Norfenefrine C01CA06 Phenylephrine C01CA07 Dobutamine C01CA08 Oxedrine C01CA09 Metaraminol C01CA10 Methoxamine ...
Methoxamine (INN) Methoxsalen (INN), also known as Oxsoralen Methoxyflurane (INN) Methoxyphedrine (INN) Methoxyphenamine (INN) ...
... methoxamine MeSH D02.092.471.683.670 - p-methoxy-n-methylphenethylamine MeSH D02.092.471.683.715 - nylidrin MeSH D02.092. ... methoxamine MeSH D02.033.100.624.545 - metipranolol MeSH D02.033.100.624.550 - metoprolol MeSH D02.033.100.624.580 - nadolol ... methoxamine MeSH D02.033.755.624.545 - metipranolol MeSH D02.033.755.624.550 - metoprolol MeSH D02.033.755.624.580 - nadolol ... methoxamine MeSH D02.092.063.624.698 - phenoxypropanolamines MeSH D02.092.063.624.698.025 - acebutolol MeSH D02.092.063.624. ...
Profile of the Novel Combined Ion Channel Blocker AZD1305 and Its Proarrhythmic Potential Versus Dofetilide in the Methoxamine- ...
... to inhibit vasoconstriction of rat arteries in vitro elicited by the α1-adrenoceptors agonists phenylephrine and methoxamine, ...
Methoxamine is an α1-adrenergic receptor agonist, somewhat similar in structure to butaxamine and 2,5-DMA. It is no longer ...
... methoxamine (M) and d-amphetamine (A) in acute and chronic spinal rats Fed. Proc. 1976 35(3):270 ... "Responses of flexor reflex to LSD, tryptamine (T), 5-HTP, methoxamine (M) and d-amphetamine (A) in acute and chronic spinal ... "Responses of flexor reflex to LSD, tryptamine (T), 5-HTP, methoxamine (M) and d-amphetamine (A) in acute and chronic spinal ...
CH$NAME: Methoxamine. CH$COMPOUND_CLASS: N/A. CH$FORMULA: C11H17NO3. CH$EXACT_MASS: 211.12084. CH$SMILES: COc(c1)cc(C(O)C(C)N)c ... RECORD_TITLE: Methoxamine; LC-ESI-QQ; MS2; CE:20 V; [M+H]+. DATE: 2016.01.19 (Created 2007.07.07, modified 2011.05.10). AUTHORS ... Methoxamine; LC-ESI-QQ; MS2; CE:20 V; [M+H]+. Mass Spectrum ... Methoxamine with the InChIKey WJAJPNHVVFWKKL-UHFFFAOYSA-N. ...
methoxamine,. *phenylephrine, (NeoSynephrine, Neofrin). *phenylpropanolamine,. *ephedra (Ma Huang), and. *ephedrine may ...
We found that methoxamine notably reduced desynchronized sleep, and that this effect was both dose-dependent and site-specific ... The alpha 1-agonist methoxamine and the alpha 1-antagonist prazosin were injected into the DPT of freely moving, ...
Methoxamine: The tricyclic antidepressant, amoxapine, increases the sympathomimetic effect of methoxamine.. Moclobemide: ...
Methoxamine (Vasoxyl). * 2 Selective Adrenergic Agonists * Introduction. * Clonidine (Catapres). * Guanfacine (Tenex). * ...
Cabanes L, Costes F, Weber S, et al. Improvement in exercise performance by inhalation of methoxamine in patients with impaired ...
However, early after coronary reperfusion, methoxamine increased idioventricular rate from 33 +/- 7 to 123 +/- 21 beats/min (P ... Intracoronary methoxamine (0.1 microM) in animals depleted of myocardial catecholamines by 6-hydroxydopamine pretreatment did ...
... or methoxamine HCl) should be used to maintain blood pressure, and isoproterenol and norepinephrine should be avoided. If ...
Methoxamine Vasoxyl. *Selective Alpha 1 agonist*Treats shock and hypotension* Direct acting non-catechol ...
Serious postpartum hypertension has been described in patients who received both a vasopressor (i.e., methoxamine, ... Serious postpartum hypertension has been described in patients who received both a vasopressor (i.e., methoxamine, ...
... metaraminol bitartrate or methoxamine) should be used to maintain blood pressure, and isoproterenol and levarterenol should be ...
Phenylephrine and methoxamine are examples of drugs that selectively activate α1-adrenergic receptors (adrenomimetic). * ...
Intermittent alpha 1-adrenoceptor stimulation by methoxamine mimicked the increase in 5-nucleotidase activity and the infarct ...
Methoxamine HCl The lifecycle of HBV within a cell is definitely shown in Number ?Figure11[6]. Open in a separate window Number ... The dynamic natural history of CHB illness involves a complex interaction between Methoxamine HCl the host immune system and ... Therefore, timely analysis and CHB Methoxamine HCl treatment is vital for the reduction of mortality and morbidity[1]. There ... formation of multivesicular body and finally secretion Methoxamine HCl of subviral and virion particles. Moreover red pub lines ...
... pyrene alone or in combination with methoxamine. Arch Biochem Biophys 323:243-250. PMID:7487084 ...
When the methoxamine hydrochloride pyridine (15 mg/ml) of 80 μl was added to a glass derivative bottle, followed by 2 min of ...
Serious postpartum hypertension and stroke reported with coadministration of a vasopressor (ie, methoxamine, phenylephrine, ...
METHOXAMINE 53585 METHOXSALEN 53590 METHOXYFLURANE 53595 METHOXYPHENAMINE 53600 METHSCOPOLAMINE 53605 METHSUXIMIDE 53610 ...
Results: GF109203X (500 nM) and Go6983 (300 nM) reduced EFS-, noradrenaline-, phenylephrine-, methoxamine-, and U46619-induced ... methoxamine), thromboxane A(2) analog U46619, endothelin-1, or calcium chloride in an organ bath. ...
Inhaled methoxamine did not alter the induced rises in plasma NS, suggesting that changes in respiratory mucosal blood flow are ... Inhaled methoxamine did not alter the induced rises in plasma NS, suggesting that changes in respiratory mucosal blood flow are ...
Cirazoline is a full agonist at the α1A adrenergic receptor, a partial agonist at both the α1B and α1D adrenergic receptors,[1] and a nonselective antagonist to the α2 adrenergic receptor.[2] It is believed that this combination of properties could make cirazoline an effective vasoconstricting agent.[2] Cirazoline has also been shown to decrease food intake in rats, purportedly through activation of α1 adrenoceptors in the paraventricular nucleus in the hypothalamus of the brain.[3] Administration of cirazoline also seemed to present impairment in the spatial memory of monkeys through the activation of the same receptors that showed decreased food intake in rats.[4][5] However, in preliminary studies, through stimulation of α2 adrenoceptors, working memory is comparatively improved.[4] ...
... methoxamine, oxymetazoline or methylnorephrine; a muscarinic M3 receptor antagonist, e.g., tiotropium or ipratropium; a dual ...
Methoxamine. ... is an α1-adrenergic receptor agonist, somewhat similar in structure to butaxamine and 2,5-DMA. It is no longer ... It is an intermediate in synthesis of organic compounds, including pharmaceuticals such as methoxamine and butaxamine.[citation ... Its primary use is in experimental situations in ... Bupropion Methoxamine "Definition: butoxamine from Online Medical ...
d. Methoxamine. 10. Which of the following statements is not correct?. a. ALFA receptors increase arterial resistence, whereas ...
keywords = "Endothelin-1, Methoxamine, Penile erection, Penis, Vasodilation",. author = "Mills, {Thomas M.} and Kanchan ... If Y-27632 was given before ET-1 or methoxamine, the vasoconstrictor effect was reduced, and intracavernosal pressure and mean ... However, when given after methoxamine, Y-27632 had a reduced vasodilatory effect, and Y-27632 had no vasodilatory effect when ... If Y-27632 was given before ET-1 or methoxamine, the vasoconstrictor effect was reduced, and intracavernosal pressure and mean ...
Dive into the research topics where Laura McPherson is active. These topic labels come from the works of this person. Together they form a unique fingerprint ...
Barzilai, B., Davila-Roman, V. G., Eaton, M. H., Rosenbloom, M., Spray, T. L., Wareing, T. H., Cox, J. L. & Kouchoukos, N. T., 1992, In: Journal of Thoracic and Cardiovascular Surgery. 104, 5, p. 1410-1416 7 p.. Research output: Contribution to journal › Article › peer-review ...
Epinephrine, Norepinephrine, Phenylephrine, Methoxamine. Beta-1. Heart. Increased HR, contractility, conduction, increased ...
  • Phenylephrine and methoxamine are examples of drugs that selectively activate α 1 -adrenergic receptors (adrenomimetic). (pharmacology2000.com)
  • Contractions were induced by electric field stimulation (EFS), alpha(1)-adrenergic agonists (noradrenaline, phenylephrine, methoxamine), thromboxane A(2) analog U46619, endothelin-1, or calcium chloride in an organ bath. (uni-muenchen.de)
  • Methoxamine was a partial agonist relative to norepinephrine whereas clonidine, xylazine, B-HT 920 and B-HT 933 produced minimal contractions. (elsevierpure.com)
  • Cannabinoids also modulate the actions of vasoactive compounds including acetylcholine [nicotinic], methoxamine, angiotensin II and U46619 (thromboxane mimetic). (bryanwilliambrickner.com)
  • Melatonin impaired the efficacy of both methoxamine and clonidine by relaxing vascular smooth muscle through an undetermined mechanism in an ex-vivo experiment using thoracic aorta excised from male rats (Weekley 1991). (syrianclinic.com)
  • It is not known whether exogenous melatonin can antagonize the effects of methoxamine and clonidine in humans. (syrianclinic.com)
  • The alpha 1-agonist methoxamine and the alpha 1-antagonist prazosin were injected into the DPT of freely moving, unanaesthetized cats. (nih.gov)
  • Therefore, timely analysis and CHB Methoxamine HCl treatment is vital for the reduction of mortality and morbidity[1]. (eprf.ca)
  • Methoxamine - It is useful for treating the treatment of an acute hypotensive condition and used as a painsuppressant during mind hemorrhage, surgical difficulties, or even shock therapy. (rabbinevins.org)
  • We found that methoxamine notably reduced desynchronized sleep, and that this effect was both dose-dependent and site-specific. (nih.gov)
  • If Y-27632 was given before ET-1 or methoxamine, the vasoconstrictor effect was reduced, and intracavernosal pressure and mean arterial pressure remained elevated. (elsevierpure.com)
  • Drugs used were norepinephrine-bitartrate (51401), methoxamine- hydrochloride (61165), and D-600 (16662478), a methoxy derivative of verapamil. (cdc.gov)
  • Genotyping at the GNB3 and the eNOS gene was performed on 48 individuals receiving either the alpha(1)-adrenoceptor agonist methoxamine (5 mg i.c.) and/or the alpha(2)-adrenoceptor agonist BHT 933 (5 mg i.c. (nih.gov)
  • 5. The selective α 1 -adrenoceptor agonist methoxamine (10 μmol/l) inhibited stimulation-evoked release and this effect was blocked by the α 1 -adrenoceptor antagonist prazosin (0.1 μmol/l). (portlandpress.com)
  • Synthetic angio- tensin II or methoxamine were used to increase total peripheral vascular resistance. (nih.gov)
  • Results Increased Left Ventricular Pressure Load Angiotensin II and methoxamine increase tota] peripheral resistance without an increase in cardiac output.3 They were used to impose an acute pressure Joad on the left ventricle. (nih.gov)
  • TdP was induced by α-adrenergic stimulation by methoxamine and IKr block in 83% of YC rabbits, 18% of AC rabbits, and 21% of CH rabbits. (zcu.cz)
  • Treatment of arterial strips with D-600 before addition of methoxamine similarly decreased the magnitude of contractile response in lead treated and sodium treated rats. (cdc.gov)
  • The increase in output is due primarily to increased heart rate rather than CONTROL ME THOXAMINE ECG HEART jo SOUNDS 4S K4 CAROTID : FEMORAL Figure 2 Records showing increase in P/F and I/F ratios of the carotid pulse (see text) during elevation of arterial pressure with methoxamine. (nih.gov)
  • Gallamine, atropine, amphetamine, levarterenol and methoxamine were essentially without effect on the responses studied. (erowid.org)
  • The data indicate that the TdP susceptibility in methoxamine-sensitized rabbits is affected by the age of rabbits but probably not by hypercholesterolemia. (zcu.cz)