Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin receptors are present in many tissue types, including adrenal cortex, renal glomeruli, heart, hypothalamus, liver, pancreas, pituitary, platelets, renal tubules, uterus and vascular smooth muscle. Two high-affinity receptor subtypes have been identified by radioligand binding with antagonists: losartan (DuP 753/MK954) identifies AT1 receptors; PD123177 and CGP42112A are markers for AT2 receptors. Angiotensin II may be produced locally in tissues outside the humoral system. For example, it is found in the brain, kidney and heart. Within the brain, the heptapeptide angiotensin(1-7) mimics some effects of angiotensin II, but may be formed directly from angiotensin I. Evidence for non-ACE-mediated angiotensin II production has been reported in the heart. Intravascular angiotensin II receptors are implicated in the central release of vasopressin and other hypophyseal hormones, in increasing sympathetic outflow, in the thirst response and, possibly, in cognitive function; in the inotropic and chronotropic effects of angiotensin II on the heart as well as in growth/hypertrophy; in the control of aldosterone release and in the balance between cortisol and aldosterone secretion; and in modulating sodium, chloride and bicarbonate transport within the kidney. Effects on the reproductive system, liver and pancreas have not been established. The pharmacological effects of angiotensin II antagonists will depend on their distribution characteristics as well as affinity for specific receptor subtypes. At present, however, the physiological role of AT2 receptors has not been defined.
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PMID:Role of angiotensin in the extravascular system. 823 88

We profiled the concentrations of angiotensin I (Ang I), angiotensin II (Ang II), and angiotensin(1-7) [Ang(1-7)] by the combination of radioimmunoassay and high performance liquid chromatography in the blood of 14-week-old male Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) drinking either tap water or a solution containing ceranapril (30 mg/kg) or lisinopril (20 mg/kg) for 14 days. Differences in the chemical and pharmacokinetic properties of the two converting enzyme inhibitors ruled out class-related effects. Plasma renin activity, angiotensin converting enzyme (ACE) activity, and plasma levels of Ang I and Ang II were the same in vehicle-treated WKY and SHR. In contrast, plasma levels of both Ang(1-7) and vasopressin in SHR were 3.7-fold and 2.6-fold higher, respectively (p < 0.05). Angiotensin converting enzyme inhibition reduced the blood pressure of WKY and SHR, and augmented their intake of water and output of urine. These changes were associated with increases in renin activity and plasma levels of Ang I and Ang(1-7). In both WKY and SHR, lisinopril had a greater effect in inhibiting plasma and cerebrospinal fluid ACE, reducing levels of plasma angiotensinogen, and increasing the concentrations of authentic Ang II. The principal finding of this study is that plasma Ang(1-7) is the sole component of the circulating angiotensin system that is elevated in the established phase of genetic hypertension. The finding that chronic inhibition of ACE augments circulating levels of Ang(1-7) evidenced the existence of functional pathways for the alternate processing of Ang I.
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PMID:Angiotensin(1-7) in the spontaneously hypertensive rat. 828 65

1. The effects of CGS 22652, a thromboxane (Tx) A2 synthase inhibitor and TxA2/prostaglandin (PG) H2 receptor antagonist, on blood pressure (BP) were studied in conscious freely moving spontaneously hypertensive rats (SHR). 2. Three groups of 13 male SHR were subcutaneously infused from 5 to 11 weeks of age via osmotic minipumps with CGS 22652 at doses of 5 (SHRa) or 10 (SHRb) mg/kg per 24 h or with the vehicle only (SHRc). A fourth group (SHRd, n = 13) was orally treated from 3 to 11 weeks of age with CGS 22652 (30 mg/kg) given by gavage once a day. 3. CGS 22652 dose-dependently reduced the age-related increase in systolic BP. The pressor response to noradrenaline (200 ng/kg, i.v.) but not to angiotensin I or II was slightly (P < 0.05) diminished in 11 week old SHRb and SHRd compared to SHRc. Acute ganglionic blockade by trimethaphan (10 mg/kg, i.v.), as well as angiotensin converting enzyme inhibition by perindopril (2 mg/kg, i.v.) decreased BP to a similar extent in the four groups. After combined blockade of vasopressin receptors and of the autonomic nervous system and the administration of a direct vasodilator (hydralazine, 3 mg/kg, i.v.), the residual mean BP was identical in the four groups of rats. 4. Chronic treatment with CGS 22652 dose-dependent antagonized the TxA2/PGH2 receptors but did not modify the TxA2 synthesis. The urinary sodium excretion did not differ between groups. 5. In conclusion, at the doses used, CGS 22652 given either orally or subcutaneously exhibited only TxA2/PGH2 receptor blocking properties in SHR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood pressure effects of thromboxane A2 blockade in spontaneously hypertensive rats. 830 13

Oral premedication with enalapril, 0.1 mg/kg was compared with placebo in 22 patients subjected to craniotomy and ligation of an intracranial aneurysm or extirpation of an arteriovenous malformation. Balanced hypotensive anesthesia was used with sodium nitroprusside (SNP) as the main hypotensive agent. The hypertensive response to laryngoscopy and tracheal intubation was significantly attenuated by enalapril (p = 0.020). The mean blood pressure was lower and more stable in the intensive care unit after enalapril than after placebo (p = 0.044). The median SNP dose rate tended to be lower in the enalapril-pretreated patients [0.6 (range of 0-3.5) micrograms/kg/min] compared to the placebo group [1.4 (0.4-5.8) micrograms/kg/min] (p = 0.12). Concentrations of plasma catecholamines, vasopressin, and endothelin as well as serum osmolality, arterial blood gases, and plasma electrolytes and level of consciousness were repeatedly measured. Enalapril had no significant effects on these variables. Plasma renin activity was increased and serum angiotensin converting enzyme (ACE) activity was reduced in the expected manner by enalapril. We found premedication with an ACE inhibitor favorable for hypotensive anesthesia in neurovascular patients as assessed by the circulatory responses.
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PMID:Enalapril premedication attenuates the blood pressure response to tracheal intubation and stabilizes postoperative blood pressure after controlled hypotension with sodium nitroprusside in neurovascular patients. 843 65

In this article, we have discussed the localization of components of the renal renin-angiotensin system, as well as the existing information on the regulation of this axis and the effects of Ang II on renal function. All the components of the renin-angiotensin system are present in both fetal and adult kidney. In the adult kidney, renin is principally localized to jg cells of the distal afferent arteriole, where release is stimulated by increases in intracellular cAMP and inhibited by increases in cytosolic calcium. Four distinct stimuli mediating renin release are (1) NaCl sensed at the macula densa, (2) the sympathetic nervous system, (3) humoral factors, with Ang II, vasopressin, endothelin, and adenosine inhibiting renin release, and (4) changes in intrarenal blood pressure. Alterations in renal renin gene expression have been reported in pathophysiological states, such as salt depletion, diabetes mellitus, ureteral obstruction, Bartter's syndrome, and with high protein feeding. The highest renal concentrations of mRNA for the renin substrate angiotensinogen are found in the PT, where the protein is localized to subapical granules. Both salt depletion and androgens upregulate renal angiotensinogen mRNA. Of interest, renal angiotensinogen mRNA levels are lower in SHR than in normotensive WKY rats. As with angiotensinogen, renal ACE is mainly localized to the PT, with highest concentration on the brush border. The mechanisms of regulation of both renal angiotensinogen and ACE require further study. Using recently developed specific nonpeptide Ang II receptor antagonists, it appears that adult renal Ang II receptors are principally of the AT1 class, whereas fetal kidney Ang II receptors are of the AT2 subtype. By binding to AT1 receptors, Ang II exerts constrictive effects on both afferent and efferent arterioles, with increased effect reported on efferent arterioles. Glomerular Ang II receptors are localized to mesangial cells, mediating contractile responses resulting in changes in glomerular surface area and Kf, and potentially regulating mesangial sieving and phagocytosis. These receptors are reduced with salt restriction or in experimental diabetes. The highest concentrations of tubular Ang II receptors are found in PT, on both brush border and basolateral membranes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The intrarenal renin-angiotensin system. 843 83

In both chronically sympathectomized (SNX) and sinoaortic denervated (SAD) rats, removal of vasoconstrictor influences decreases mean arterial pressure (MAP) and its variability in parallel. This study examined if this decrease in arterial pressure lability is solely a result of decreasing vascular tone. In conscious 14-week-old male sympathectomized (guanethidine at 1-13 weeks of age) and sinoaortic denervated (2 weeks before study) rats, arterial pressure was recorded beat-to-beat during 30-min consecutive periods; control; ganglionic blockade in sinoaortic denervated rats and angiotensin converting enzyme inhibition plus vasopressin antagonism in sympathectomized rats; and restoration of the initial arterial pressure with continuous infusions of phenylephrine and angiotensin II. Sympathectomized and, even more, sinoaortic denervated rats had increased pressure variability. Neural or humoral blockade markedly reduced arterial pressure and its liability in both groups of rats and subsequent restoration of the arterial pressure with vasoconstrictor infusions returned lability to levels either slightly above (sympathectomy) or below (sinoaortic denervation) control values. In basal conditions, an increased frequency of occurrence of depressor episodes was evidenced in sympathectomized rats whereas a variable ratio of pressor to depressor events was observed in sinoaortic denervated rats. During vasoconstrictor infusions, blood pressure lability was mainly due to depressor events in both groups of rats. It is concluded that the background vascular tone provided by endogenous pressor systems is necessary for the expression of the depressor component of blood pressure lability in sinoaortic denervated and in sympathectomized rats. The study also suggests that in sympathectomized rats, humoral influences act to limit rather than enhance blood pressure lability, whereas in sinoaortic denervated rats, the sympathetic nervous system may directly generate part of the lability.
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PMID:Role of vasoconstrictor tone in arterial pressure lability after chronic sympathectomy and sinoaortic denervation in rats. 843 3

The aim of this review is to comment the results described in the literature concerning the possible pharmacodynamic mechanisms involved in the improvement of quality of life of angiotensin converting enzyme inhibitors that is just a working hypothesis. These drugs, widely used in the treatment of hypertension, prevent the formation of angiotensin II and the generation of free radicals, as well as the hydrolysis of bradykinin, enkephalins and endorphins. Different mechanisms have been implicated on quality of life: 1) increase of bradykinin levels in the central nervous system that would trigger the release of nitric oxide (NO), noradrenaline, acetylcholine, excitatory amino acids and vasopressin which are involved in memory and cognition; 2) increase of brain blood supply by enhanced NO synthesis; 3) interference with cholinergic mechanisms in the central nervous system by angiotensin II inhibition of acetylcholine release; 4) decrease of endorphin metabolism; and 5) interaction with hypothalamic-pituitary-adrenal axis that releases ACTH and vasopressin.
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PMID:Effect of angiotensin converting enzyme inhibitors on quality of life in hypertensive patients. Pharmacodynamic basis. 887 Nov 40

The objective of pharmacotherapy of portal hypertension is to reduce the portal pressure and the subsequent reduction of pressure and blood flow in the oesophageal varicosities in patients with portal hypertension. Pharmacological treatment is used in acute bleeding from oesophageal varices where it is a very useful first step for arresting haemorrhage and it does not require any special training or complicated equipment. Pharmacotherapy holds its place also in primary and secondary prophylaxis of oesophageal variceal bleeding. In particular a combination of pharmacotherapy with sclerotherapy is useful to reduce the occurrence of early recurrent bleeding. Among hitherto known vasoactive drugs the following ones are used most frequently: vasopressin, terlipressin, somatostatin, beta-blockers, nitrates and ACE inhibitors. Other drugs influencing portal haemodynamics are the subject of research.
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PMID:[Pharmacologic treatment of portal hypertension]. 897 62

We investigated the relationship between exercise capacity and the level of neurohormonal activation at rest and during exercise in patients with various degrees of severity of chronic heart failure. We performed exercise testing with measurements of peak oxygen consumption (pVo2) and blood sampling at rest and at peak exercise in eight patients with moderate heart failure (pVo2 = 17 +/- 0.4 ml/kg/min) (mean +/- S.E.M.) and eight patients with severe CHF (pVo2 = 9 +/- 1 ml/kg/min). None of the patients was taking angiotensin converting enzyme inhibitors or beta-blockers. Plasma levels of atrial natriuretic peptide, cGMP, arginine-vasopressin, renin, angiotensin II, epinephrine and norepinephrine increased significantly (P < 0.01), from rest to peak exercise, in all patients. Among all the studied neurohormonal factors, only atrial natriuretic peptide levels at rest as well as at peak exercise, in patients with severe heart failure were correlated significantly to pVo2 (r = -0.77, P = 0.04; r = -0.85, P = 0.01, respectively) and to exercise duration (r = -0.72, P = 0.05; r = -0.79; P = 0.03, respectively). The relationship between plasma levels of atrial natriuretic peptide and of cGMP was shifted downward in the more severe patients suggesting the loss of biological activity of atrial natriuretic peptide.
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PMID:Plasma levels of atrial natriuretic peptide and of other vasoconstricting hormones in patients with chronic heart failure: relationship to exercise capacity. 901 65

In congestive heart failure (CHF), low cardiac output decreases the fullness of the arterial circulation. This underfilling of the arterial vascular compartment unloads the baroreceptors, resulting in a sequence of events to maintain arterial circulatory integrity. Among them, the renin-angiotensin-aldosterone axis, the sympathetic nervous system, the non-osmotic release of vasopressin and the endothelins are activated to increase vascular resistance and enhance sodium and water renal retention. Simultaneously, vasodilatory and natriuretic substances such as the natriuretic peptides are activated to counterregulate these vasoconstrictors. In the initial phase of CHF, these events contribute to the cardiorenal adaptation. However, when CHF progresses, they become maladaptive and further depress vantricular performance and increase sodium and water retention. This vicious cycle of CHF provides the rationale for the use of neurohormonal antagonists in CHF. The beneficial effects of angiotensin converting enzyme inhibitors in CHF are well described. Vasopressin V1 receptor antagonists have been associated with peripheral vasodilation and improved cardiac function in some patients with CHF. In CHF animals, the vasopressin V2 receptor antagonist has been demonstrated to reverse the defect in water excretion. Bosentan, an endothelin antagonist, is associated with an increase of cardiac index in patients with CHF. A role for exogenous natriuretic peptides is also under investigation. Modulation of the neurohumoral systems associated with CHF opens a new perspective in the treatment of cardiac edema, principally by improving cardiac performance.
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PMID:Sodium and water retention in heart failure: pathogenesis and treatment. 918 6


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