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)

The effects of intracerebroventricular (icv) injections of 10 ng angiotensin II (ANG II) on mean arteriolar diameter and spontaneous arteriolar vasomotion were studied in subcutaneous tissue of conscious, restrained hamsters, using the skin fold window chamber preparation. Angiotensin II caused a significant decrease in mean arteriolar diameter which was associated with a significant elevation in the amplitude of vasomotion. The frequency of vasomotion did not change significantly. The central ANG II-induced effects on arteriolar vasomotion were not significantly altered by continuous intravenous (iv) infusion of hexamethonium (1 mg.kg-1.min-1). In contrast, iv bolus injection of the vascular vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP (10 micrograms.kg-1) 5 min prior to icv injection of ANG II significantly attenuated the effects of the neuropeptide on mean arteriolar diameter and the amplitude of vasomotion. These data indicate that central ANG II stimulation enhances arteriolar vasomotion in peripheral subcutaneous tissue of conscious hamsters and that this effect may be mediated by release of vasopressin.
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PMID:Central angiotensin II stimulates arteriolar vasomotion in conscious hamsters. 257 95

The sequential effects of an increased daily NaCl intake on hemodynamics, fluid electrolyte balances, and hormonal responses were evaluated in dogs (n = 7) with fixed circulating levels of angiotensin II (ANG II). During the control period, ANG II was infused at 3 ng.kg-1.min-1 while dogs were maintained on an 8 meq NaCl/day diet. Water intake was fixed at 700 ml/day. Continuously recorded (24 h/day) changes of total body weight (TBW) were used as an index of total body water. Cardiac stroke volume and arterial pressure were recorded, and each beat was digitized to provide hourly and 24-h average cardiac output (CO), mean arterial pressure (MAP), and total peripheral resistance (TPR). After three stable control days, daily salt intake was increased to 120 meq for 7 days. TBW increased gradually to 448 +/- 111 g (2.9%, P less than 0.05) above control by day 3. An 11% expansion of blood volume (P less than 0.05) was found (51CR-labeled red blood cells) on day 2 of high NaCl. CO rose 12% and MAP 20% (P less than 0.05) in parallel with TBW by day 4. By day 7, CO remained only 5% elevated, whereas MAP had stabilized at 20% above control levels. TPR remained significantly elevated from days 3 through 7. A positive Na balance averaging 91 +/- 8 meq (P less than 0.05) occurred on day 1. Plasma Na concentration was increased 2-3 meq/l above control throughout the period of high-salt intake. Plasma renin activity and aldosterone levels decreased to nearly undetectable levels, vasopressin rose slightly, and atrial natriuretic peptide levels increased significantly. Dogs maintained at 8 meq/day NaCl during the same infusion of ANG II showed no changes in MAP, CO, TPR, or TBW. In summary, the salt-induced hypertension was consistently related to small but significant fluid retention, blood volume expansion, elevations of cardiac output, and a gradual increase in TPR.
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PMID:Hemodynamics and blood volume in angiotensin II salt-dependent hypertension in dogs. 258 96

The role of vasopressin (AVP) and angiotensin II (ANG II) in the onset of acute (45 min) aortic coarctation hypertension was studied in conscious rats. Changes in mean carotid pressure (MCP) and heart rate (HR) were measured in four groups of rats. Control rats presented a hypertensive response that attained a plateau 5 min after coarctation and remained near this level throughout the experiment. Rats treated with AVP V1-vascular receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]arginine vasopressin [d(CH2)5Tyr(Me)AVP] presented a prompt rise in MCP similar to the control rats, but in contrast to this group, the MCP started to decline progressively. Rats treated with saralasin presented a delay in the onset of hypertension right after coarctation but slowly attained values similar to those for control rats. In contrast, the rats treated with AVP antagonist plus saralasin showed a blunted MCP elevation throughout the experiment. Reflex bradycardia observed in the rats treated with saralasin or the AVP antagonist plus saralasin was similar to that observed in the control rats, whereas for the group treated only with AVP antagonist, the reflex bradycardia was more intense than for the other three groups, indicating an increased sensitivity of the baroreflex. These data demonstrate that in addition to the mechanical effect of aortic constriction, both ANG II and AVP participate in the onset of acute aortic coarctation hypertension. Moreover, the results indicate that ANG II acts on the prompt (5 min) rise in pressure, whereas AVP is responsible for the maintenance (30-45 min) of the arterial pressure elevation.
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PMID:Acute aortic coarctation hypertension: role of vasopressin and angiotensin II. 258 3

It is known that the pressor response to intravenous angiotensin II (ANG II) is blunted in pregnancy. In the present study we examined the pressor response to intracerebroventricular ANG II to determine whether central ANG II effects are also attenuated in conscious pregnant rats. Two to three days before experimentation, animals were instrumented with arterial and venous catheters and a ventricular guide cannula. Pressor responses to 10, 50, and 100 ng iv of ANG II, and 30, 100, and 300 ng iv of norepinephrine were significantly reduced in pregnant animals. The pressor response to 5, 20, and 50 ng iv of vasopressin was not attenuated in pregnant rats. The pressor response to intracerebroventricular 100 ng ANG II was significantly increased in pregnancy. Blockade of the vasopressin V1 receptor and the sympathetic ganglia indicated that the greater pressor response to intracerebroventricular ANG II in pregnancy may be the result of a larger contribution by the sympathetic nervous system. We conclude that the central effects of ANG II are augmented in pregnancy, suggesting a significant role for central ANG II in blood pressure regulation.
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PMID:Role for central angiotensin II in control of blood pressure during pregnancy. 260 4

The subfornical organ plays a role in a number of the effects of blood-borne angiotensin II (ANG II) including the increase in water drinking and blood pressure and the release of vasopressin from the pituitary. Recently it has been shown that systemically administered ANG II also reduces voluntary alcohol intake. The present study assessed the role of the SFO in alcohol consumption by examining the effects of SFO lesions on voluntary alcohol intake and on the suppression of voluntary alcohol intake by ANG II. Whereas the lesion did not alter alcohol consumption per se, it did significantly attenuate the ability of ANG II to reduce alcohol intake. This effect was not due to a lesion-induced change in the pharmacokinetics of alcohol and was observed only in those animals whose lesions produced a functional deficit, i.e., abolishing the increase in water drinking produced by ANG II. These results indicate that the SFO mediates the effect of systemically administered ANG II on alcohol intake but does not otherwise affect the regulation of alcohol consumption.
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PMID:Systemic angiotensin II acts at the subfornical organ to suppress voluntary alcohol consumption. 262 49

A number of theoretical and practical aspects of acute myocardial infarction suggest a potential role for ACE inhibition in enhancing coronary blood flow and limitation of infarct size. Indeed, the use of ACE inhibitors in acute myocardial infarction could be viewed as a logical intervention in the face of the neuroendocrine response which accompanies the acute phase. During the first 24 h post-infarction, very high plasma concentrations of arginine-vasopressin and catecholamines occur. This is followed by a sharp rise in the concentration of angiotensin II (ANG II) over the next few days. The neuroendocrine response is most marked in those patients with larger infarcts, who frequently develop left ventricular failure. The extent to which these factors influence coronary flow in acute myocardial infarction is unknown, although in chronic heart failure ACE inhibition does not reduce coronary blood flow despite a reduction in rate-pressure product, suggesting a coronary vasodilator effect. However, in the presence of fixed coronary stenoses, the fall in blood pressure and, therefore, of coronary perfusion pressure must be taken into account. Whether or not the use of ACE inhibitors can limit infarct size in man also remains to be determined, although it has been clearly demonstrated that concentrations of ANG II similar to those observed in the early phase of myocardial infarction can cause myocardial cell damage in experimental animals. Post-infarction ventricular enlargement can be reduced by ACE inhibitors. Additionally, ACE inhibitors, through their balanced vasodilator effect, maintain cardiac output whilst reducing filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of angiotensin-converting enzyme inhibition on coronary blood flow and infarct size limitation. 267 35

The effects of intracerebroventricular (icv) injections of angiotensin II (ANG II) on water intake, blood pressure, heart rate, and plasma arginine-vasopressin (AVP) concentration were studied in chronically instrumented adult male Syrian golden hamsters (Mesocricetus auratus). Furthermore, the effects of pharmacological ganglionic blockade, and of vascular AVP receptor blockade, on central ANG II-induced cardiovascular responses were investigated. ANG II (1, 10, and 100 ng, icv) elicited dose-dependent increases in water intake and arterial blood pressure. Heart rate showed a biphasic response with a short initial non dose-dependent tachycardic and a subsequent longer lasting bradycardic phase. Plasma AVP concentration was increased two and a half fold with 100 ng ANG II icv. Both ganglionic blockade and vascular AVP receptor blockade significantly attenuated the central ANG II-induced pressor response. The tachycardic phase of the heart rate response was abolished by ganglionic blockade and the bradycardic phase was significantly diminished by AVP receptor blockade. The results support the hypothesis that brain ANG II may participate in the central control of body fluid volume and in central cardiovascular regulation in conscious hamsters.
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PMID:Central effects of angiotensin II in conscious hamsters: drinking, pressor response, and release of vasopressin. 271 57

Angiotensin II (ANG II) is formed from angiotensin I by the action of angiotensin-converting enzyme located on the luminal surface of vascular endothelial cells. We determined whether binding sites specific for ANG II exist on pulmonary artery and aortic endothelial cells. The binding of 125I-ANG II to pulmonary artery and aortic endothelial cells was time dependent, saturable, and reversible. Scatchard analysis indicated a single class of high-affinity binding sites with equilibrium dissociation constants (Kd) of 0.85 and 0.81 nM and total binding capacities of 70 and 73 fmol/mg protein in pulmonary artery and aortic endothelial cells, respectively. Angiotensin analogues [Sar1,Ile8]ANG II and [Sar1,Ala8]ANG II, as well as angiotensin I and angiotensin III, competitively displaced 125I-ANG II in both pulmonary artery and aortic endothelial cells. The degree of inhibition of 125I-ANG II binding by these angiotensin analogues and antagonists was comparable except that [Sar1,Ala8]ANG II was 65% less potent than the other antagonists in both cell types. The binding of 125I-ANG II in pulmonary artery and aortic endothelial cells was not affected by vasopressin, substance P, or insulin, suggesting the presence of specific angiotensin receptors on these cells. These receptors appear to recognize the general configuration of angiotensin peptide rather than being specific to ANG II with no major differences between endothelial cells from pulmonary arterial or aortic vessels.
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PMID:Angiotensin receptors in pulmonary arterial and aortic endothelial cells. 271

Extracellular recordings in urethane-anesthetized male rats indicated that electrical stimulation of the subfornical organ (SFO) alters the activity of 54 out of 62 phasically firing neurosecretory neurons in the hypothalamic paraventricular nucleus (PVN); 44 cells demonstrate an increase in excitability; 10 cells display a depression in their activity. In 14 out of 38 PVN cells tested, SFO stimulation-evoked excitations were abolished by pretreatment with the angiotensin II (ANG II) antagonist, saralasin (Sar), in the region of the median preoptic nucleus (MnPO). Inhibitory responses (n = 7) were not affected. Microinjection of ANG II into the region of the SFO produced either a facilitation (n = 28) or no effect (n = 6) on the excitability of phasically active PVN neurosecretory cells and the facilitatory effect of 9 out of 23 cells tested was prevented by pretreatment with Sar in the region of the MnPO. All the PVN cells which had excitatory responses to either electrical (n = 7) or chemical (n = 9) stimulation of the SFO that were blocked following the pretreatment could also be activated by intravenous administration of ANG II. Furthermore, this activation was blocked (n = 10) or attenuated (n = 6) by pretreatment with Sar in the region of the MnPO. These results show an involvement of both the MnPO and the SFO for the regulation of excitability of putative vasopressin (VP)-secreting PVN neurons, and suggest that MnPO neurons sensitive to ANG II may relay activation of SFO neurons by circulating ANG II to putative VP-secreting PVN neurons which result in enhanced excitability.
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PMID:Involvement of the median preoptic nucleus in the regulation of paraventricular vasopressin neurons by the subfornical organ in the rat. 275 8

We lesioned the periventricular tissue of the anteroventral portion of the third cerebral ventricle (AV3V) of dogs to evaluate the mechanism that accounts for blunting of the pressor activity of angiotensin II (ANG II). AV3V lesions were done with a microknife using a transbuccal approach; the procedure denervated the organum vasculosum of the laminae terminalis, the nucleus medianus, and the medial preoptic nucleus. Two to four days after surgery, the conscious AV3V-lesioned dogs showed adipsia and their blood contained increased quantities of Na+ (175 +/- 2 meq/l) and an elevated osmolality (352 +/- 5 mosmol/kg). Cardiac rate was faster (131 +/- 8 beats/min) in AV3V-lesioned dogs, but their mean arterial pressure (MAP) was within normal values (99 +/- 4 mmHg). These changes were accompanied by an almost 18-fold increase in the plasma levels of immunoreactive ANG II (irANG II). In contrast, plasma vasopressin (AVP) levels fell to nondetectable values. Pressor responses produced by intravenous infusions of ANG II or injections of norepinephrine (NE) were significantly blunted 3 days after AV3V ablation. Short-term treatment of eight AV3V-lesioned dogs with the synthetic AVP analogue, 1-desamino-8-D-arginine vasopressin, reduced plasma Na+ and irANG II levels. The pressor activity of peripheral infusions of ANG II was restored to prelesion values, whereas pressor responsiveness to NE remained depressed. These data suggest that the blunting of the pressor action of ANG II in AV3V-lesioned dogs is an expression of a disorder in the regulation of renal and behavioral mechanisms maintaining fluid balance and AVP secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alternative mechanism for attenuated pressor responses in AV3V-lesioned dogs. 276 63


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