Vascular receptors

M.R. Bristow, Changes in myocardial and vascular receptors in heart failure, J. Am. Coll. Cardiol. 22(4 SuppI A) (1993) 61A-71A. 

Mechanism of Action A serotonin receptor agonist that binds selectively to vascular receptors, producing a vasoconstrictive effect on cranial blood vessels. Therapeutic Effect Produces relief of migraine headache. 

The renal vascular receptor functions as a stretch receptor, with decreased stretch leading to increased renin release and vice versa. The receptor is apparently located in the afferent arteriole, possibly in the juxtaglomerular cells. Stretch-induced changes in renin release are mediated by changes in Ca2+ concentration in the juxtaglomerular cells. 

The signal transduction mechanisms triggered by binding of ET-1 to its vascular receptors include stimulation of phospholipase C, formation of inositol trisphosphate, and release of calcium from the endoplasmic reticulum, which results in vasoconstriction. Conversely, stimulation of PGI2 and nitric oxide synthesis results in decreased intracellular calcium concentration and vasodilation. 

Isolated tissue Blood vessels, heart, lung, ileum (rat or guinea pig) In vitro Effects on vascular contraction and relaxation selectivity for vascular receptors effects on other smooth muscles... 

The rate at which renin is secreted by the kidney is the primary determinant of activity of the renin-angiotensin system. Renin secretion is controlled by a variety of factors, including a renal vascular receptor, the macula densa, the sympathetic nervous system, and angiotensin II. 

Cimetropium is a QTA representing an N-alkylated derivative of scopolamine (Fig. 1). It exhibits antispasmodic activity on smooth muscle cells in the GIT. Therefore, it is clinically used for oral long-term treatment of irritable bowel syndrome with minimal effects on vascular receptors [32, 61]. 

Binds selectively to vascular receptors producing a vasoconstrictive effect on cranial blood vessels... 

Terlipressin, a prodrug converted into lysine vasopressin, has been used recently in septic shock patients." This drug has a half-hfe of 6 hours and acts via vascular receptors aud reual tubular V2 receptors. In one report, terlipressin 1 mg was given intravenously to 15 patients with norepinephrine-resistant septic shock."" Terhpressin was shown to increase MAP at 30 minutes, which lasted for 24 hours. Despite a decrease in cardiac output, terlipressin increased gastric mucosal perfusion, urine output, and creatinine clearance. These preliminary findings suggest that a clinical trial should be conducted that evaluates mortality, in addition to hemodynamic effects. 

Agonist 1 increases HR, presumably through direct activation of cardiac Pj receptors because the effect is blocked by propranolol but is not influenced by the alpha blocker (prazosin), the ganglion blocker (trimethaphan), or blockade of M receptors (atropine). Only two of the listed drugs directly activate cardiac receptors epinephrine and norepinephrine. For NE, any direct cardiac stimulation is counteracted by reflex bradycardia resulting from the increase in mean BP via its activation of (Xj receptors in blood vessels (it has no effects on p2 vascular receptors). Therefore, agonist 1 is identified as epinephrine (presumably at low dose). 

Thiazide diuretics are used in the treatment of edema of cardiac and gastrointestinal origin and bring about a state of intravascular volume depletion. Because this depleted intravascular volume is replenished from the interstitial (edematous) sites, thiazide diuretics should not be administered too frequently. For example, hydrochlorothiazide is given every other day, and chlorthalidone is given once every 2 to 3 days. In small doses, thiazide diuretics are extremely effective in controlling essential hypertension. They exert their effects initially by bringing about volume depletion, then reduce the peripheral resistance and sensitivity of vascular receptor sites to catecholamine. Thiazide diuretics are also used in conjunction with antihypertensive medications. 

In small doses, thiazide diuretics are extremely effective in controlling essential hypertension. They exert their effects initially by bringing about volume depletion, then reduce the peripheral resistance and sensitivity of vascular receptor sites to catecholamine. Thiazide diuretics are also used in conjunction with antihypertensive medications. 

DA also causes the release of NE from nerve terminals, which contributes to its effects on the heart. DA usually increases systolic blood pressure and pulse pressure and either has no effect on diastolic blood pressure or increases it slightly. Total peripheral resistance usually is unchanged when low or intermediate doses of DA are given, probably because of reduced regional arterial resistance in some vascular beds (e.g., mesenteric and renal) with minor increases in others. At high concentrations, DA activates vascular receptors, leading to more... 

The physiological role of vascular receptors in the regulation of blood flow within various vascular beds is uncertain. Vacular receptors probably are preferentially stimulated by circulating catecholamines, whereas receptors are activated by NE released from sympathetic nerves. 

Epinephrine can produce severe hypertension when used with a nonselective P receptor antagonist due to the unopposed stimulation of a receptors when vascular receptors are blocked. Such paradoxical hypertensive responses to p adrenergic receptor antagonists have been observed in patients with hypoglycemia or pheochromocytoma, during withdrawal from clonidine, following administration of Epi as a therapeutic agent, or in association with the iUicit use of cocaine. 

Mais et have provided further evidence for the existence of distinct classes of receptors in platelets and blood vessels. They studied the activity of a series of 13-azapinane TXA2 antagonists in human and canine platelets and saphenous vein. The structure—activity relationship for the series of antagonists for the human platelet receptor was found to be significantly different from that for the human vascular receptor and the canine platelet... 

Martin, G.R. (1994) Vascular receptors for 5-hydroxytryptamine distribution, function and classification. Pharmacol. Then, 62, 283-324. 

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