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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have demonstrated that angiotensin II, catecholamines, and vasopressin can stimulate the phosphorylation of hepatic cytosolic proteins via a Ca2+-linked cyclic AMP-independent mechanism. The present study used high resolution, two-dimensional gel electrophoresis to determine if the proteins phosphorylated in response to the Ca2+-linked hormones were distinct from those affected by glucagon acting via the cyclic AMP-dependent pathway. Intact hepatocytes labeled with [32P]PO4(3-) were stimulated with glucagon, angiotensin II, l-norepinephrine, and vasopressin and over 100 phosphorylated proteins resolved by two-dimensional electrophoresis and autoradiography. Six important enzymes known to be regulated through covalent modification were positively identified, including phosphorylase, phosphofructokinase, pyruvate kinase, fructose-6-phosphate, 2-kinase, phenylalanine hydroxylase, and fructose-1,6-bisphosphatase. Computer analysis of the autoradiograms from control and hormone-treated cells demonstrated that glucagon increased the phosphorylation state of 12 phosphoproteins and reduced the phosphorylation of one protein with a Mr = 21,000 and a pI = 5.9. The Ca2+-linked hormones stimulated the phosphorylation of 7 phosphoproteins and also reduced the phosphorylation state of the 21,000-dalton protein. Angiotensin II, l-norepinephrine, and vasopressin had equivalent effects on protein phosphorylation. There were six protein substrates uniquely affected by glucagon and one phosphoprotein uniquely stimulated by the Ca2+-linked hormones. Seven substrates were affected by stimulation of the cell with either glucagon or the Ca2+-linked hormones. These results demonstrate that, while there is overlap in the substrates affected by glucagon and the Ca2+-linked hormones, each pathway is able to affect the phosphorylation of unique substrates. This finding suggests that the two types of hormones may have some distinct effects on hepatic function.U
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PMID:Glucagon and the Ca2+-linked hormones angiotensin II, norepinephrine, and vasopressin stimulate the phosphorylation of distinct substrates in intact hepatocytes. 629 Apr 94

Incubation of isolated hepatocytes containing normal Ca2+ levels with angiotensin II, vasopressin or A23187 caused significant inhibition of the cAMP response to glucagon. Angiotensin II also inhibited cAMP accumulation induced by either glucagon or epinephrine in Ca2+-depleted hepatocytes. When submaximal doses of hormone were employed such that cell cAMP was elevated only 3-4-fold (approximately 2 pmol cAMP/mg wet wt cells) inhibition by angiotensin II was correlated with a decrease in phosphorylase activation. The data demonstrate that inhibition of hepatic cAMP accumulation results in reduced metabolic responses to glucagon and epinephrine and do not support the contention that the hepatic actions of glucagon are independent of cAMP.
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PMID:Angiotensin II inhibits hepatic cAMP accumulation induced by glucagon and epinephrine and their metabolic effects. 629 10

Recent studies from our laboratory indicate a primary central site of action of Angiotensin II (AII) to release ACTH. The present studies were designed to test whether AII is able to release ACTH in vivo in a similar fashion in intact, cannulated, freely moving Long-Evans (LE) or in vasopressin (AVP)-deficient, Brattleboro (DI) female rats. The in vivo response to AII was compared with that elicited by synthetic CRF. AII injected i.v. (0.4 or 2 micrograms/100 g BW) induced a significant, dose-related increase in plasma ACTH values 5 and 15 min after injection, in both LE and DI rats. CRF given to LE and DI rats at 0.4 micrograms/100 g BW elicited a larger increase in ACTH plasma values than a similar dose of AII, 5 or 15 min after the injection. Moreover, ACTH levels after CRF in DI rats were significantly greater than those obtained in LE controls. In vitro studies using dispersed anterior pituitary cells indicate that the response of cells from either LE or DI rats to AII or AVP (both at 10(-9) and 10(-8)M) was similar. Cells from DI donors were hyperresponsive to CRF (2 X 10(-11) and 10(-10)M) in terms of ACTH release when compared with the response of cells from LE rats. The present results suggest that the presence of AVP is not essential to mediate the central response to AII and that AII may act centrally to stimulate CRF release from the hypothalamus in vivo, which would then enhance ACTH output. The results in the DI rat indicate that the increased response to CRF may be an important compensatory mechanism involved in the regulation of adrenocortical function in the DI rat.
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PMID:Angiotensin II increases ACTH release in the absence of endogenous arginine-vasopressin. 632 71

Angiotensin II acts on the brain to produce a variety of effects including elevation of arterial blood pressure, increased release of vasopressin and ACTH, stimulation of drinking and sodium appetite, and natriuresis. Many, and possibly all, of these effects can be produced by centrally administered angiotensin II or by circulating angiotensin II, which appear to act at common receptor sites located in the circumventricular organs. Whether these effects are normally produced by blood-borne angiotensin II formed by the renal renin-angiotensin system, by angiotensin II formed centrally by the putative brain renin-angiotensin system, or by both, remains to be determined. A large body of information concerning the site and mechanism of these different central actions of angiotensin II is available, and the physiologic significance of these actions is beginning to be understood. Nevertheless, much additional research will be required before the actions of angiotensin II on the brain are completely understood.
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PMID:Actions of angiotensin II on the brain: mechanisms and physiologic role. 632 14

The effect of angiotensin II on the acquisition and extinction of a conditioned avoidance response was examined in rats. Angiotensin II, 1 and 2 micrograms, given intracerebroventricularly facilitated acquisition of the conditioned avoidance response but did not influence extinction. [Sar1, Ile8]-angiotensin II (1 microgram), a specific antagonist of angiotensin II receptors, unexpectedly produced an effect quite similar to that of angiotensin II. Vasopressin (1 microgram) did not influence the rate of acquisition of the conditioned avoidance response but it markedly delayed its extinction. The data are discussed in terms of learning and memory facilitating properties of angiotensin II. This action seems to be independent of an interaction of angiotensin II with its known receptors or of release of vasopressin caused by the peptide.
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PMID:Effect of angiotensin II and vasopressin on acquisition and extinction of conditioned avoidance in rats. 641 15

Angiotensin II (Ang II), peripherally or centrally administered, increases plasma vasopressin concentrations in the rat. Peripherally injected Ang II was unable to effect the release of vasopressin in rats with subfornical organ (SFO) lesions. In contrast, a normal increase of plasma vasopressin levels was induced by centrally injected Ang II. These results suggest that peripherally administered Ang II elicits antidiuretic hormone (ADH) release by stimulating receptors in the SFO, whereas centrally administered Ang II acts at receptors outside the SFO.
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PMID:Vasopressin release to central and peripheral angiotensin II in rats with lesions of the subfornical organ. 650 26

A study was carried out of the effects of iv angiotensin II on vasopressin release and the distribution of vasopressin between platelets and plasma in 12 week old conscious unrestrained SH and WKY rats. Angiotensin II was infused at rates of 31.25 to 500 ng/kg X min for 20 min. There was an enhanced pressor responsiveness to angiotensin II in the SH rats. Angiotensin II caused a moderate increase in plasma vasopressin concentrations, but only at doses which produced maximal pressor responses (250 to 500 ng/kg X min). There were no significant differences in vasopressin responses to angiotensin II in SH compared to WKY rats. Approximately 30% of circulating immunoreactive vasopressin was found in platelets in both SH and WKY rats, and this distribution was not greatly affected by the iv infusion of angiotensin II.
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PMID:Effect of angiotensin II on vasopressin in plasma and platelets in SH and WKY rats. 650 89

The effects of various agents which have been implicated in the regulation of vasopressin release, on the supraoptic neuroendocrine cells were studied intracellularly. L-glutamate (10(-4)M) and gamma-aminobutyric acid (10(-6) M) had potent excitatory and inhibitory actions, respectively. Acetylcholine (10(-6) M) depolarized the membrane and increased the membrane input resistance. Norepinephrine (10(-5) M) produced either excitatory or inhibitory action on the spontaneous firing rate depending on the cell impaled. Morphine (10(-8)-10(-6) M) strongly depressed the spontaneous firing rate whereas it has no noticeable effect on the membrane potential and input resistance. Angiotensin II (10(-5) M) had no effect on any of the cells tested.
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PMID:Pharmacological characterization of the magnocellular neuroendocrine cells of the guinea pig supraoptic nucleus in vitro. 652 56

In male Wistar rats, under osmotic diuresis, the effect of angiotensin II, noradrenaline, vasopressin and aldosterone on urinary kallikrein excretion were evaluated. Angiotensin II did not modify but all the others drugs used increased significantly the urinary kallikrein excretion. In all the groups studied the urinary sodium excretion increased. No modifications were observed in urine flow, glomerular filtration rate, urine osmolality and potassium excretion. The urinary kallikrein excretion was always positively correlated with the urinary flow and urinary sodium excretion. No correlation was observed with the other parameters studied. These findings suggest that noradrenaline, vasopressin and aldosterone are important stimulators of the urinary kallikrein excretion. Probably, kallikrein is one of the mechanisms involved in the regulation of urinary sodium excretion.
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PMID:Effect of angiotensin, noradrenaline, vasopressin and aldosterone on urinary kallikrein excretion in the rat. 656 41

A number of neuropeptides have been found to affect fluid intake when injected directly into the brain of various vertebrate species. These include: angiotensin II and its peptide precursors; the tachykinins Substance P, eledoisin and physalaemin; the opioid peptides met- and leu-enkephalin and beta-endorphin; bombesin; neurotensin; and vasopressin. Some of these stimulate drinking, some inhibit water intake, and the tachykinins have opposite effects on thirst depending on the species tested. Very little is known about the site or mechamism of action of most of these peptides or if their effects on thirst are physiological. The exception is angiotensin II, a peptide hormone that is synthesized in the blood in response to hypovalaemia or hypotension and is involved in many aspects of the regulation of blood volume and pressure. Angiotensin II injected intravenously or intracranially stimulates drinking in all reptiles, birds and mammals tested. In addition to its role as a hormone, angiotensin II may also function as a neurotransmitter or neuromodulator, since all of the enzymes and precursors necessary for its synthesis have been found in the central nervous system.
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PMID:Neuropeptides and thirst. 658 33


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