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 II (AII) is an important peptide known to regulate blood pressure and body fluid. In the present study we used a potent AII antagonist, 125I-(Sar1,Ile8)-AII (125I-SI-AII), to study AII receptor binding in Long-Evans rats 5 days after water deprivation. Specific structures evaluated include the subfornical organ (SFO) and adrenal gland. With quantitative autoradiography, we have found that there is an increase of 125I-SI-AII binding in the SFO, whereas there is a decrease in AII binding in the adrenal medulla. These observations suggest that central and peripheral AII target tissues are affected differently by dehydration. The increase in SI-AII binding in the SFO may indicate participation of this structure during dehydration, as angiotensin stimulation of SFO causes thirst and vasopressin release.
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PMID:Effects of chronic dehydration on angiotensin II receptor binding in the subfornical organ, paraventricular hypothalamic nucleus and adrenal medulla of Long-Evans rats. 301 Jan 92

We have previously shown that vasopressin exerts a marked mitogenic effect on adrenal glomerulosa cells. In the present study, we demonstrate that vasopressin (VP) stimulates the formation of inositol monophosphate (IP), inositol diphosphate (IP2) and inositol triphosphate (IP3) in primary cultures of glomerulosa as well as fasciculata cells 5- to 8-fold over the corresponding basal values. In both cell types, the relative stimulations of IP, IP2, and IP3 formation were similar. Angiotensin II (ATII) also induced glomerulosa cells to produce a dose-dependent (up to 10-fold) increase in IP, IP2, and IP3, but had only a small effect on fasciculata cells. The dose dependencies for ATII-induced IP, IP2, and IP3 formation and aldosterone production were nearly the same. We conclude that VP- and ATII-induced formation of inositol phosphates may represent an early step in the action of these peptides on adrenal cells. However, additional elements must be involved to account for the cell specificity of VP and ATII. In glomerulosa cells, VP stimulates mitotic activity and aldosterone secretion, while ATII is only steroidogenic. On fasciculata cells, VP induces a significant increase in the formation of inositol phosphates in spite of the absence of a known biological function in these cells.
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PMID:Vasopressin induces breakdown of membrane phosphoinositides in adrenal glomerulosa and fasciculata cells. 301 63

Angiotensin II (AII) and vasopressin (VP) play important roles in cardiovascular function. Using 125I-[Sar1,Ile8]-angiotensin II (125I-SI-AII), a potent AII antagonist, AII receptor binding sites were autoradiographically localized in three VP-producing areas of the hypothalamus and compared in hypertensive and normotensive rats. Within three major VP-producing areas, AII receptor binding was highest in the paraventricular hypothalamic nucleus and lowest in the supraoptic nucleus, suggesting that a differential AII regulation of separate VP systems exists in the brainstem. No statistical difference in 125I-SI-AII receptor binding was found between WKY and SHR rats in each of the three major VP-producing nuclei studied. These results are consistent with a role of AII receptors in a subtle and complicated regulation of VP in cardiovascular function.
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PMID:Different pharmacological anatomy in the paraventricular hypothalamic nucleus, supraoptic nucleus, and suprachiasmatic nucleus of rats: quantitative autoradiography on angiotensin II receptor binding sites. 301 87

Angiotensin II, a potent vasoconstrictor peptide, increases free cytoplasmic Ca2+ concentration ([Ca2+]i) in vascular smooth muscle cells (VSMC) by release of nonmitochondrial Ca2+ stores and stimulates an amiloride-sensitive Na+ influx, presumably via Na+/H+ exchange. We recently have found that the angiotensin II-mediated change in VSMC intracellular pH has two components, an early rapid acidification phase and a slower recovery phase involving Na+-dependent alkalinization. In the present study, we show that the early acidification is not mediated via Na+/H+ exchange. Instead, we propose a mechanism which involves increases in [Ca2+]i and Ca2+ efflux with a subsequent rise in intracellular H+. Agonists, in addition to angiotensin II, which increase [Ca2+]i in cultured VSMC, including platelet-derived growth factor, vasopressin, and bradykinin, induce an acidification, while agonists which fail to raise [Ca2+]i do not. The time course and magnitude of agonist-stimulated 45Ca2+ efflux correlate with the acidification response. The angiotensin II concentration-response relationship for acidification and Ca2+ mobilization are similar. Furthermore, inhibition of changes in [Ca2+]i by treatment with phorbol ester, cyclic GMP, or quin2 loading prevent agonist-mediated acidification. The effects of altering extracellular [Ca2+] and [H+] on agonist-mediated intracellular acidification and H+ efflux suggest that the acidification is due to ATP-dependent unidirectional H+ influx, perhaps via the plasma membrane Ca2+-ATPase, and not to a Ca2+/H+ antiport. This agonist-mediated acidification represents a previously undescribed ionic event in VSMC activation which may be involved in excitation-response coupling.
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PMID:Early agonist-mediated ionic events in cultured vascular smooth muscle cells. Calcium mobilization is associated with intracellular acidification. 303 Oct 38

Angiotensin II and CRF are but two of the several regulatory peptides which exert specific actions in the brain that are complementary with their peripheral effects upon end organs such as the anterior pituitary and adrenal glands. In the pituitary, the two peptides act in a coordinate manner on the corticotroph to regulate ACTH release. In the adrenal gland, angiotensin II receptors are abundant in the zona glomerulosa but are also present in the medulla, where the occurrence of CRF receptors and actions on catecholamine release reveals an additional site at which the two peptides exert related actions, in this case in the peripheral neuroendocrine system. Within the brain, the mapping of AII and CRF binding sites by topical autoradiography has provided new information about the distribution and potential functions of receptors for the two peptides. The central receptors for AII are distributed in a characteristic pattern in brain regions concerned with drinking, regulation of adrenergic function and arterial blood pressure, and control of pituitary hormone secretion. Thus, in addition to its recognized modulatory effects in the peripheral adrenergic system, angiotensin II may be involved in the central control of catecholamine release and action. A central action of AII on the release of regulatory peptides such as vasopressin and CRF, both of which are present in neurones of the paraventricular nucleus, is indicated by the high concentration of AII receptors in this region. Also, the high density of AII receptors in the median eminence suggests that AII modulates the hypothalamic secretion of neuropeptides such as CRF by actions at their site of release, as well as on the cell bodies of neurones responsible for peptide synthesis. The highly localized pattern of AII receptors at numerous specific sites in the brain differs from the more general distribution of many other CNS receptors, and reflects the selective actions of AII on discrete neural systems that subserve precisely integrated functions within the central nervous system. The widespread distribution of CRF receptors, with prominent localization in the cortical and limbic regions, is consistent with the more general neuroregulatory actions of CRF in the brain, and with the presence of immunoreactive CRF in several regions of the brain including the cortex, limbic system, and centers involved in the control of autonomic function. The cortical and limbic receptors are clearly relevant to the effects of centrally administered CRF on both behavioral and visceral responses, with prominent autonomic changes including increased catecholamine release and hypertension.
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PMID:Brain receptors for hypothalamic hormones. 303 94

The renin-angiotensin system appears to have evolved millions of years ago as a primary attempt to preserve circulatory homeostasis at a time when the principal cause of a low cardiac output was intravascular volume depletion. Angiotensin II supported systemic BP by direct systemic vasoconstriction, by facilitating the central and peripheral effects of the sympathetic nervous system, by promoting renal sodium retention by the production of aldosterone, and by increasing total body water by enhancing thirst and the synthesis of vasopressin. In addition, angiotensin II evolved as an important mechanism to preserve the glomerular filtration rate in low-flow states. These actions of angiotensin II were beneficial when the system first evolved, but its activation in patients with heart failure not only fails to reverse the low-output state but further exacerbates loading conditions in the left ventricle, thereby leading to worsening heart failure. Moreover, increased levels of angiotensin II cause heightened sympathetic nervous activity, potassium depletion, and hyponatremia, each of which can lead to further clinical deterioration. Therefore, activation of the renin-angiotensin system in heart failure might appear (at first) to be a maladaptive response. Recent evidence, however, suggests that this hormonal system continues (even in heart failure) to carry out the primary functions for which it was designed. Angiotensin II plays an important role in preserving systemic BP and in preserving the glomerular filtration rate as renal artery pressure and renal blood flow decline; in addition, by stimulating the synthesis of aldosterone, the renin-angiotensin system provides an important role for potassium disposal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adaptive and maladaptive actions of angiotensin II in patients with severe congestive heart failure. 303 91

Treatment of intact hepatocytes with glucagon, TH-glucagon [( 1-N-alpha-trinitrophenylhistidine, 12-homoarginine]glucagon), angiotensin or vasopressin led to a rapid time- and dose-dependent loss of the glucagon-stimulated response of the adenylate cyclase activity seen in membrane fractions isolated from these cells. Intracellular cyclic AMP concentrations were only elevated with glucagon. All ligands were capable of causing both desensitization/loss of glucagon-stimulated adenylate cyclase activity and stimulation of inositol phospholipid metabolism in the intact hepatocytes. Maximally effective doses of angiotensin precluded any further inhibition/desensitizing action when either glucagon or TH-glucagon was subsequently added to these intact cells, as has been shown previously for the phorbol ester TPA (12-O-tetradecanoylphorbol 13-acetate) [Heyworth, Wilson, Gawler & Houslay (1985) FEBS Lett. 187, 196-200]. Treatment of intact hepatocytes with these various ligands caused a selective loss of the glucagon-stimulated adenylate cyclase activity in a washed membrane fraction and did not alter the basal, GTP-, NaF- and forskolin-stimulated responses. Angiotensin failed to inhibit glucagon-stimulated adenylate cyclase activity when added directly to a washed membrane fraction from control cells. Glucagon GR2 receptor-stimulated adenylate cyclase is suggested to undergo desensitization/uncoupling through a cyclic AMP-independent process, which involves the stimulation of inositol phospholipid metabolism by glucagon acting through GR1 receptors. This action can be mimicked by other hormones which act on the liver to stimulate inositol phospholipid metabolism. As the phorbol ester TPA also mimics this process, it is proposed that protein kinase C activation plays a pivotal role in the molecular mechanism of desensitization of glucagon-stimulated adenylate cyclase. The site of the lesion in desensitization is shown to be at the level of coupling between the glucagon receptor and the stimulatory guanine nucleotide regulatory protein Gs, and it is suggested that one or both of these components may provide a target for phosphorylation by protein kinase C.
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PMID:The rapid desensitization of glucagon-stimulated adenylate cyclase is a cyclic AMP-independent process that can be mimicked by hormones which stimulate inositol phospholipid metabolism. 303 85

The renin-angiotensin system has a range of physiological actions concerned with the control of the circulation. Angiotensin II has both an immediate and a delayed pressor effect, it stimulates the secretion of aldosterone and antidiuretic hormone, promotes thirst, stimulates the sympathetic nervous system at various sites while inhibiting vagal tone, and has a range of direct effects on the kidney. Several aspects of this range of actions can become deranged in a number of forms of hypertension as well as in congestive cardiac failure. Hence much effort has been directed in recent years to the development of agents designed to interfere with the renin-angiotensin system and to apply these clinically in the treatment of hypertension and congestive cardiac failure. Orally active converting enzyme inhibitors are of proven benefit not only in renovascular hypertension, but also, when combined with loop diuretics, in the treatment of intractable hypertension as well as, both alone and in combination with thiazide diuretics, in the treatment of essential hypertension. In congestive cardiac failure controlled trials have shown that converting enzyme inhibitors can improve exercise tolerance while diminishing lassitude, correct potassium deficiency and limit ventricular arrhythmias. Energetic efforts are being made to develop orally active inhibitors of the enzyme renin itself, since these would be more specific in action than the presently available and very successful converting enzyme inhibitors.
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PMID:The clinical use of angiotensin converting enzyme inhibitors in hypertension and cardiac failure. 303 14

The renin-angiotensin system is activated in heart failure in proportion to the severity of the haemodynamic derangement and to diuretic dose. Angiotensin converting enzyme (ACE) inhibitors reduce circulating levels of angiotensin II and aldosterone and, in some patients, plasma noradrenaline, vasopressin and cortisol. Typically there is potassium retention and a minor increase in plasma potassium, but cumulative sodium balance may increase or decrease depending on pretreatment fluid and haemodynamic status and on policy regarding diuretic dose. Circulatory dynamics usually improve and blood flow to the brain, myocardium and kidneys is preserved. Changes in glomerular filtration rate are dictated by haemodynamic characteristics and, again, by diuretic dose and dietary sodium. There are potential hazards with ACE inhibitor therapy but most problems can be anticipated and avoided. Future trends may include the introduction of ACE inhibitors with or without concomitant diuretic therapy in early cardiac failure, and intravenous ACE inhibition immediately after acute myocardial infartion. Whether the ACE inhibitors will prove more successful than alternative antihypertensive agents in preventing cardiac complications (including heart failure) of hypertension, is an intriguing question.
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PMID:Converting enzyme inhibitors in heart failure. 304 97

Angiotensin II (AII), aldosterone (Aldo) and arginine vasopressin (AVP) in plasma were determined during basal conditions in seventeen patients with congestive heart failure and in seventeen control subjects. The same parameters were measured before and 1, 2 and 3 h after an oral water load of 20 ml (kg body weight)-1 together with urine volume (V) and free water clearance (CH2O) in seven patients with congestive heart failure and in seven control subjects. AII, Aldo and AVP were significantly higher in heart failure than in control subjects (AII:81 and 12 pmol l(-1) (medians), P less than 0.01; Aldo: 411 and 103 pmol l(-1), P less than 0.01; AVP: 5.3 and 2.0 pmol l)-1), P less than 0.01). AVP was positively correlated to Aldo in both heart failure (p = 0.593, n = 17, P less than 0.02) and control subjects (p = 0.511, n = 17, P less than 0.05), but in neither of the groups to AII. V and CH2O were significantly lower in heart failure when compared to control subjects (maximum increase in CH2O 3.55 and 5.86 ml min-1, P less than 0.02), but did not correlate directly with either A II, Aldo or AVP. Creatinine clearance was reduced in heart failure. It is concluded that the activity of both the renin-angiotensin-aldosterone system and the osmoregulatory system is enhanced in congestive heart failure, presumably as a compensatory phenomenon in order to maintain arterial blood pressure. It is suggested that the decrease in free water clearance may be attributed to both an elevated level of vasopressin and a reduced glomerular filtration rate.
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PMID:Angiotensin II, aldosterone and arginine vasopressin in plasma in congestive heart failure. 308 74


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