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)

Hypertonic saline (HS) and angiotensin II (ANG II) administered centrally or peripherally produce a forebrain-mediated central nervous system-(CNS) dependent pressor action. Although the majority of these effects are due to increased central sympathetic drive and inhibition of the cardiac baroreceptor reflex, evidence from peripheral infusions of vasopressin (Vp) receptor antagonists have suggested that part of the blood pressure increase may be due to circulating Vp. We now report that blockade of CNS Vp receptors in rats, via a fourth ventricle infusion of a Vp receptor antagonist, attenuated greater than 70% of the pressor response to lateral ventricle infusion of HS, ANG II, or hypertonic glucose (HG). Intravenous administration of the Vp antagonist could block only 40% of the HS response. When lateral ventricle infusion of HS was performed in rats with a hereditary lack of Vp (diabetes insipidic rats) no pressor response was obtained. Because centrally administered Vp has autonomic nervous system effects that are similar to those induced by HS or ANG II, our results suggest that CNS Vp may provide a link between forebrain acting pressor agents and autonomic nervous system regulation. Finally, HG produced a pressor effect that had an equivalent peak response to HS. However, unlike the HS response, the pressor effect to HG returned to base line within approximately 5 min during a 10-min infusion. Thus there appears to be a quantitative difference in the pressor responses produced by activation of sodium vs. osmoreceptors.
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PMID:Activation of the central vasopressin system: a common pathway for several centrally acting pressor agents. 375 82

Extracellular single unit recordings were obtained to investigate the effects of systemic administration of angiotensin II (ANG II) on the excitability of antidromically identified neurohypophysial neurons in the rat. Records were obtained from 89 oxytocin- or vasopressin-secreting neurons in the hypothalamic supraoptic or paraventricular nuclei. Increased excitability in response to ANG II was observed in 83% of putative vasopressin- and 75% of putative oxytocin-secreting neurons tested in intact animals. Lesion studies to identify the central nervous system site of action for such peripherally administered ANG II showed that, after electrolytic lesion of the rostral subfornical organ (SFO), neurohypophysial neurons demonstrated no increase in excitability in response to this peptide. In an attempt to correlate the synaptic events through which activation of SFO neurons may result in facilitated excitability of neurohypophysial cells, 19 cells were tested with both systemic ANG II and electrical stimulation in the SFO. These studies demonstrated that all cells which showed long-duration increases in excitability in response to electrical stimulation of SFO were also activated by systemic ANG II. It is concluded that the SFO is an essential central nervous system structure in eliciting increases in the excitability of both oxytocin- and vasopressin-secreting neurons in response to systemic ANG II. These effects may involve the activation of SFO efferents that evoke long-duration post-synaptic changes in neurohypophysial cell excitability.
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PMID:Systemic angiotensin acts at subfornical organ to facilitate activity of neurohypophysial neurons. 376 70

The effects of intracerebroventricular (IVT) infusion of angiotensin II (ANG II), the converting enzyme inhibitor SQ 20881, and dopamine were studied in 15 conscious Na-depleted sheep. IVT ANG II (25 ng/min) significantly increased plasma aldosterone (163 +/- 24%) and vasopressin (ADH) (533 +/- 100%). Plasma renin activity (PRA) was decreased to 64 +/- 10% of basal. IVT SQ (1 microgram/min) decreased aldosterone to 70 +/- 10% and ADH to 55 +/- 9% of basal. PRA increased to 124 +/- 10%. There were no significant changes in plasma Na, K, or cortisol levels nor in mean arterial or intracranial pressure after either infusion. Increasing the dose of SQ to 10 micrograms/min resulted in an increased magnitude of change in the same variables. IVT SQ (1 microgram/min) significantly decreased aldosterone level in five nephrectomized sheep. The responses to IVT dopamine (20 micrograms/min) were qualitatively similar to those elicited by IVT SQ. These data support the existence of an endogenous brain renin-angiotensin system (RAS) independent of the renal RAS. ANG II acts centrally to regulate plasma ADH, aldosterone, and PRA levels. The similarity of the responses to SQ and dopamine suggests that a dopaminergic pathway may be involved in these responses.
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PMID:Central effects of angiotensin II and dopamine in sodium-depleted sheep. 388 49

The role of the sympathetic nervous system, angiotensin II (ANG II), and arginine vasopressin (AVP) in maintaining blood pressure (BP) during endotoxic shock was investigated in 117 conscious male Wistar rats. After intravenous injection of 2 mg Escherichia coli endotoxin, mean BP fell within 5 min by approximately 50 mmHg and rose again to approach base-line levels within 90 min. At that time, plasma renin activity, plasma norepinephrine (NE), and vasopressin levels of the endotoxin-treated animals were, respectively, 12-, 10-, and 54-fold (P less than 0.001) higher than those of the controls. The BP effect of either prazosin (0.125 mg iv), captopril (2.5 mg iv), or d(CH2)5Tyr(Me)AVP (5 micrograms iv), a specific antagonist of the vascular effect of AVP, was evaluated over a 30-min observation period starting 90 min after administration of endotoxin or its vehicle. Captopril reduced mean BP from 116 +/- 1.8 to a low of 109 +/- 2.1 (SE) mmHg (P less than 0.05, n = 8) only in rats pretreated with endotoxin, whereas the vasopressin antagonist had no depressor effect even during endotoxemia. The BP drop induced by prazosin in rats exposed to endotoxin (-21 +/- 3.3 mmHg, n = 6) did not significantly differ from that observed in control rats (-14 +/- 3.4 mmHg, n = 6). A dose-response curve to NE, ANG II, and lysine vasopressin was also performed. In endotoxin-treated rats the mean BP response to all agonists was markedly suppressed (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensin II, vasopressin, and sympathetic activity in conscious rats with endotoxemia. 390 75

To assess a role for peripherally administered angiotensin II (ANG II) in regulating vasopressin (antidiuretic hormone, ADH) release, the effects on plasma ANG II and ADH of intraperitoneal injections of ANG II dissolved in various solutions were examined in conscious rats. Plasma ANG II and ADH were determined by radioimmunoassay using the trunk blood collected after decapitation. Injections of 150 mM NaCl containing ANG II (6, 12, or 24 micrograms X 2 ml-1 X 100 g body wt-1) caused dose-related increases in plasma ANG II 15 and 30 min after, but plasma ADH remained unchanged. The lack of effect on plasma ADH of the ANG II dissolved in isotonic saline was also confirmed in another series of experiments in which the solution with a higher ANG II concentration was loaded by much smaller injection volume (14.3 micrograms X 0.1 ml-1 X 100 g-1). However, when given together with 600 mM NaCl, ANG II (8 micrograms X 2 ml-1 X 100 g-1) significantly potentiated the plasma ADH response to the vehicle at 15, 30, and 60 min, without affecting those of plasma osmolality, sodium, and hematocrit. The elevations of plasma ANG II and osmolality brought about by the treatment were comparable with those previously observed in rats deprived of water for 46 h. ANG II was without effect on the plasma ADH responses to the intraperitoneal injections of hypertonic sucrose or mannitol solution that did not alter plasma sodium, although these solutions were equipotent to 600 mM NaCl in augmenting plasma ADH and osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma vasopressin response to peripheral administration of angiotensin in conscious rats. 391 65

After alterations in sodium balance, osmotic reactivity of vasopressin (AVP) release was evaluated in seven conscious dogs during bilateral intracarotid infusions of hypertonic saline. A low-sodium diet reduced plasma sodium concentration by 3%; deoxycorticosterone acetate (30 mg/day for 2 days) elevated the concentration by 1%. Neither treatment altered resting plasma AVP. Hypertonic intracarotid infusions increased jugular plasma osmolality by 20 +/- 2 mosmol/kg independent of manipulations. Plasma AVP values were significantly increased (P less than 0.05) in sodium-depleted dogs compared with values of the control animals. In addition, the osmotic reactivity of AVP release was evaluated during exogenous administration of angiotensin II (ANG II). Intravenous infusion of ANG II (5 ng . kg-1 . min-1) increased plasma concentration of ANG II but did not alter concentration of plasma AVP. The slope for the relationship of jugular plasma osmolality to plasma AVP during hypertonic intracarotid infusions was significantly increased with intravenous infusion of ANG II. Sodium depletion and intravenous ANG II potentiate the relationship of plasma osmolality and plasma AVP when evaluated with intracarotid hypertonic saline infusions in dogs.
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PMID:Effects of sodium depletion and angiotensin II on osmotic regulation of vasopressin. 394 42

The thermoregulatory role of brain angiotensin II (ANG II) was tested by intracerebroventricular (IVT) infusion of ANG II or the converting enzyme inhibitor SQ 20881 (SQ) in 15 conscious sheep. Deep body temperature decreased 0.30 +/- 0.07 degree C (SE) during the 3-h period of IVT ANG II (25 ng/min) infusion (P less than 0.05) and increased 0.50 +/- 0.13 degree C during IVT SQ (1 microgram/min) infusion (P less than 0.01). To determine whether the rise in body temperature after IVT SQ infusion might be the result of a central renin-angiotensin system (RAS), SQ was infused IVT in five conscious sheep 20 h after bilateral nephrectomy. This resulted in a significant rise in body temperature of 0.28 +/- 0.05 degree C (P less than 0.05). When vasopressin antidiuretic hormone (ADH) was infused intravenously at the same time of IVT SQ infusion, the rise in temperature was depressed, but ADH did not lower the temperature below basal. IVT dopamine (20 micrograms/min) increased body temperature by 0.40 +/- 0.04 degree C (P less than 0.01), which was qualitatively similar to the result with IVT SQ. These data support the hypothesis that endogenous brain ANG II may play a role in thermoregulation. Furthermore, plasma ADH level, regulated in part by brain ANG II, is probably not the mediator of that thermoregulation. The similar effects of IVT dopamine and SQ on body temperature strengthen the hypothesis that dopamine may be involved in the central action of brain ANG II.
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PMID:Thermal responses to central angiotensin II, SQ 20881, and dopamine infusions in sheep. 397 11

The effects of administration of angiotensin II (ANG II) and antidiuretic hormone (ADH) on the glomerular filtration rate (GFR, measured as creatinine clearance) were examined in patients with mesangial proliferation. For this study, the patients whose conditions were similar to that of healthy subjects, except for asymptomatic urinary abnormalities and glomerular histological changes, were selected. Both ANG II and ADH administration significantly decreased GFR in the patients and the healthy subjects. Compared to the healthy subjects, a significantly greater drop in GFR was observed in the patients following ANG II infusion with or without SQ14225 administration, but not following ADH infusion. We conclude that mesangial proliferation may modulate an ANG II induced drop in GFR.
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PMID:Role of mesangial proliferation in angiotensin II and antidiuretic hormone induced changes in glomerular filtration rate. 409 35

We recently reported that microinjection of angiotensin II (ANG II) into the nucleus tractus solitarius (NTS) results in an increase in mean arterial pressure (MAP) in urethan-anesthetized rats in a dose range of 50-500 ng. To investigate the mechanism of this response, hexamethonium (20 mg/kg iv) was used to inhibit sympathetic activation. There was a highly significant (P less than 0.001) reduction in the magnitude of the pressor response (4.7 +/- 1.1 mmHg) compared with preblockade ANG II (500 ng) responses (15.5 +/- 1.6 mmHg). A vasopressin antagonist and hypophysectomized rats were used to study the contribution of pituitary vasopressin. Injection of 500 ng ANG II in hypophysectomized rats produced a pressor response (14.8 +/- 3.2 mmHg) indistinguishable from that in intact controls (15.5 +/- 1.6 mmHg). Pretreatment with the vasopressin antagonist d(CH2)5Tyr(Me)AVP (1 microgram iv) in intact rats also had no effect on the magnitude of the pressor response (15.7 +/- 1.7 mmHg). Microinjection of ANG I and II produces an increase in arterial pressure. It is concluded that the angiotensin pressor response in the NTS is mediated by activation of descending sympathetic fibers and is not dependent on release of blood-borne pressor agents from the pituitary.
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PMID:Mechanism of pressor effects by angiotensin in the nucleus tractus solitarius of rats. 608 97

Angiotensin II (ANG II) acts on the brain to elevate blood pressure (BP), stimulate drinking, increase the secretion of vasopressin and corticotropin (ACTH), and inhibit the secretion of renin. The present studies were designed to evaluate the possible physiological significance of these effects. The experiments were performed in conscious dogs with small catheters chronically implanted in both carotid and both vertebral arteries. ANG II was infused into both carotid or both vertebral arteries in doses of 0.1, 0.33, 1.0, and 2.5 ng.kg-1.min-1. Intravertebral ANG II produced dose-related increases in BP that were generally accompanied by increases in heart rate. Intracarotid angiotensin also increased BP but did not change heart rate. Intracarotid ANG II stimulated drinking and, at the highest dose only, increased the secretion of vasopressin, ACTH, and corticosteroids. Intravertebral and intracarotid ANG II suppressed plasma renin activity (PRA). In a parallel series of experiments, the effects of intravenous ANG II, in doses of 2, 5, 10, and 20 ng.kg-1.min-1, were studied. These infusions produced dose-related increases in BP and water intake and suppressed PRA. Only the highest dose of ANG II increased vasopressin or corticosteroid secretion. Analysis of these results in terms of calculated or measured changes in plasma ANG II concentration indicate that the central cardiovascular and dipsogenic actions of angiotensin, as well as the suppression of PRA, can be elicited by concentrations of the peptide that are within the physiological range. On the other hand high, probably supraphysiological, levels of ANG II are required to increase vasopressin or ACTH secretion.
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PMID:Analysis of the actions of angiotensin on the central nervous system of conscious dogs. 628 22


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