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)

Observations that angiotensin-(1-7) [ANG-(1-7)] may oppose the vasoconstrictor actions of angiotensin II (ANG II) prompted an investigation of the effects of the heptapeptide on the maintenance of elevated blood pressure in spontaneously hypertensive rats (SHR). ANG-(1-7) (24 micrograms.kg-1.h-1) was infused into the jugular vein of 13-wk-old SHR (n = 64), Wistar-Kyoto (WKY, n = 50), and Sprague-Dawley (SD, n = 18) rats for 2 wk, with the use of osmotic minipumps. Blood pressure, fluid and electrolyte balance, plasma vasopressin, and urinary excretion of prostaglandin E2 and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) were measured at days 2, 7, and 12 of the infusion. In SHR, ANG-(1-7) caused a sustained and significant reduction in plasma vasopressin concentration that was associated with an increase in urinary prostaglandin E2 and 6-keto-PGF1 alpha excretion at day 2 after the commencement of the infusion. These changes were accompanied by diuresis and natriuresis during the first 3 days of infusion in SHR but not in WKY or SD rats. Direct measurements of arterial pressure confirmed the lowering effect of ANG-(1-7) on systolic pressure of SHR on day 2 of treatment with a restoration of the pressure by days 7 and 12. These findings, along with our previous demonstration that ANG-(1-7) is an active depressor peptide in the intact animal, suggest that ANG-(1-7) may play a significant role as a vasodepressor system opposing the hemodynamic actions of ANG II in this genetic form of experimental hypertension.
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PMID:Antihypertensive actions of angiotensin-(1-7) in spontaneously hypertensive rats. 763 63

The components of the Renin-Angiotensin System (RAS) have been found to be expressed in the brain. Angiotensinogen, the high molecular weight precursor of the system, is widely distributed and expressed in areas not related to control of blood pressure and body fluid homeostasis as well. It has been shown that it is regulated by steroid hormones independently from the liver and that it is also regulated in a different manner in several brain areas. Angiotensin II, the effector peptide of the system, may be generated in the brain via the classical pathway, using renin and angiotensin converting enzyme or directly from angiotensinogen by cathepsin G or tonin. N-terminal peptides of angiotensin II have been found in several brain areas with ANG (1-7) involved in vasopressin release however without influence on blood pressure and with ANG III acting as potent as ANG II. Transgenic animals may be used to study the pathophysiology of an activated brain RAS.
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PMID:The brain renin-angiotensin system: molecular mechanisms of cell to cell interactions. 773 73

Stimulation of central angiotensin receptors promotes, among others, drinking behaviour, stimulation of natriuresis and increased release of vasopressin. Angiotensin (ANG II)-containing pathways in the lamina terminalis and the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, brain areas involved in the regulation of body fluid homeostasis, have been described. All these areas express predominantly AT1 receptors. The drinking response and the vasopressin release to centrally administered ANG II are mediated by AT1 receptors, while AT2 receptors exert inhibitory effects. Evidence for the involvement of the catecholaminergic and angiotensinergic pathways in the PVN and SON in mediating the ANG II-induced release of vasopressin is presented. ANG II is released in the PVN upon local osmotic stimulation and water deprivation. Finally, we present evidence that activation of central angiotensinergic receptors, water deprivation, or hypertonicity induce transcription of immediate-early genes and expression of the respective proteins in the lamina terminalis and in the PVN and SON. The summarized data implicate ANG II as a neuromodulator/neurotransmitter in central control of body fluid and electrolyte homeostasis.
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PMID:Angiotensin as neuromodulator/neurotransmitter in central control of body fluid and electrolyte homeostasis. 773 75

We tested the hypothesis that respiration would be stimulated after vasopressin (AVP) V1 receptor blockade because of disinhibition and activation of the renin-angiotensin system. Intravenous infusion of angiotensin II (ANG II) stimulates respiration, presumably centrally, via circumventricular organs. In the present study, the AVP V1 receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine]-Arg8-AVP (PMP; 10 micrograms/kg i.v.) was administered to six awake resting dogs. Measurements were made 30 min prior, and 60 min subsequent, to injection of PMP (protocol 1). In three other protocols, the ANG II blocker saralasin (0.5 microgram.kg-1.min-1 i.v.) was infused starting 20 min before PMP (protocol 2) and 30 min after PMP (protocol 4) and saline was infused (0.2 ml/min) over 90 min as a control (protocol 3). After PMP in protocol 1, alveolar ventilation increased and arterial PCO2 decreased (approximately 3 Torr). ANG II receptor blockade prevented (protocol 2) and reversed (protocol 4) respiratory stimulation by PMP. Despite ventilatory stimulation, plasma renin activity and ANG II were not increased after PMP relative to control (protocol 3). We conclude that AVP acts at V1 receptors to inhibit formation of brain ANG II. Brain ANG II must modulate respiratory control via a circumventricular organ, because systemically administered saralasin, which does not cross the blood-brain barrier, blocked stimulation of respiration.
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PMID:Angiotensin mediates stimulation of ventilation after vasopressin V1 receptor blockade. 792 78

Sinoaortic denervation in the rat is associated with an increased sensitivity of vasopressin neurons in the supraoptic nucleus (SON) to peripheral angiotensin II (ANG II). Lesion studies have indicated that the diagonal band of Broca (DBB) and the perinuclear zone of the SON in the lateral hypothalamus (PNZ) are essential components in the central pathway for the baroreceptor inhibition of vasopressin SON neurons. The present study examined the effect of ibotenate lesions in either the DBB or the lateral hypothalamus, which includes the PNZ, on the responses of SON neurons to peripherally administered ANG II (500 pmol/kg ia). Extracellular recordings obtained from vasopressin SON neurons in pentobarbital-anesthetized rats indicate that DBB and PNZ lesions not only interrupted the baroreceptor-mediated inhibition of SON neurons but also significantly increased the excitatory effects of ANG II on putative vasopressin SON neurons. These results suggest that ibotenate lesions of the DBB and the lateral hypothalamus that include the PNZ affect the ANG II-induced activation of putative vasopressin SON neurons in a manner consistent with results obtained from baroreceptor-denervated rats.
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PMID:Perinuclear zone and diagonal band lesions enhance angiotensin responses of rat supraoptic neurons. 794 32

The transgenic (TG) rat carrying the mouse renin gene (mRen-2d) has provided a unique opportunity to explore central interactions between the brain renin-angiotensin (RAS) and vasopressin (AVP) systems. To evaluate the hypothalamic vasopressin axis in the TG rat, we measured the central nervous system concentrations of AVP and determined the effect of angiotensin II (ANG II) and its NH2-terminal heptapeptide [angiotensin-(1-7)] on blood pressure, heart rate, and AVP release using brain microdialysis. Intracerebroventricular infusion of ANG II or ANG-(1-7) in control rats increased local AVP release from the paraventricular and supraoptic nuclei. The ANG II infusion was associated with a significant increase in blood pressure not observed with ANG-(1-7). In contrast, the angiotensin peptide-induced central AVP responses and the ANG II-induced blood pressure increase were absent in the TG animal. The plasma AVP responses to ANG II and ANG-(1-7) were comparable in the control and TG rats. The TG rats exhibited a 22-fold higher level of AVP in the dorsal lower brain stem but had lower AVP levels in the posterior pituitary and the median eminence compared with control rats. These results suggest that insertion of the mouse renin gene into the rat genome leads to alterations in the AVP axis in terms of AVP peptide content and angiotensin-induced cardiovascular and AVP responses.
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PMID:Differential regulation of central vasopressin in transgenic rats harboring the mouse Ren-2 gene. 809 24

The effects of extracellular Cl- concentration ([Cl-]o) on cultured mesangial cells from spontaneously hypertensive rats (SHR) were examined. Angiotensin II (ANG II)- and vasopressin (VP)-induced cell contraction and Ca2+ transients of SHR mesangial cells were unaffected when the cells were preincubated with 10 mM [Cl-]o, while obvious suppression of the responses to these agents was observed in Wistar-Kyoto (WKY) mesangial cells. Enhanced prostaglandin E2 (PGE2) production was elicited by a decrease in [Cl-]o in WKY mesangial cells. In contrast, PGE2 synthesis by SHR mesangial cells was not enhanced by low [Cl-]o. However, ANG II-stimulated PGE2 production and the attenuation of ANG II-induced cell contraction and Ca2+ transients by the addition of exogenous PGE2 were present equally in both WKY and SHR mesangial cells. Based on these findings, we conclude that the absence of modification of mesangial cell function by [Cl-]o in SHR is due to the inability of low [Cl-]o to enhance PGE2 production. Insensitivity of SHR mesangial cells to changes in [Cl-]o might underlie the dysregulation of renal function in SHR.
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PMID:Modification of mesangial cell function by chloride is attenuated in spontaneously hypertensive rats. 818 91

This study was performed to test the hypothesis that smaller reflex increases in vasopressin, cortisol, adrenocorticotropic hormone (ACTH), and angiotensin II (ANG II) concentrations are produced by hemorrhage in pregnant compared with nonpregnant conscious dogs. Equivalent hemorrhages (1% of the initial blood volume per minute) produced larger decreases in arterial pressure [P < 0.01; 107 +/- 6 to 73 +/- 10 mmHg (pregnant); 109 +/- 6 to 90 +/- 5 mmHg (nonpregnant)] but produced similar increases in plasma vasopressin concentration in the pregnant animals. As a result, the slope of the arterial pressure-to-vasopressin relationship was reduced (P < 0.05). During pregnancy, smaller increases in plasma cortisol concentration and heart rate were also produced for a given decrease in arterial pressure, but the relationship between pressure and ACTH was not significantly affected. In contrast, higher levels of plasma renin activity and plasma ANG II concentration were achieved in the pregnant dogs. In general, the relationships between plasma hormone levels and either left or right atrial pressure were not significantly altered. These results indicate that reflex increases in heart rate, vasopressin, and cortisol concentration are attenuated in pregnant dogs and that this attenuation may contribute to the inability of pregnant animals to achieve normal cardiovascular homeostasis during hemorrhage.
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PMID:Hemorrhage decreases arterial pressure sooner in pregnant compared with nonpregnant dogs: role of baroreflex. 818 41

Microinjection of angiotensin II (ANG II) into the area postrema (AP) of urethan-anesthetized male Sprague-Dawley rats elicited statistically significant increases in mean arterial blood pressure at doses ranging from 10 pg to 500 ng (10 pg, mean +/- SE, 10.8 +/- 1.1 mmHg, P < 0.001; 250 ng, 15.2 +/- 2.6 mmHg, P < 0.001). Heart rate was also significantly increased at doses > 10 pg, although these increases were not dose dependent. Systemic administration of losartan (Dup-753), an AT1 antagonist, was able to significantly reduce the pressor response to 250 ng ANG (post-losartan: 81.9 +/- 9.5% reduction in blood pressure response, P < 0.0001), whereas PD123319, an AT2 antagonist, was without significant effect (P > 0.1). Microinjection of vasopressin (VP) (10 pg-500 ng) into the AP also resulted in statistically significant increases in blood pressure at doses ranging from 10 to 100 pg (10 pg, 7.0 +/- 1.5 mmHg, P < 0.05) and 100-500 ng (250 ng, 12.2 +/- 1.8 mmHg, P < 0.0001). Small but significant changes in heart rate were observed only at 100 pg and 100 ng. Systemic administration of a V1 antagonist significantly attenuated the increases in blood pressure in response to 50, 100, and 250 ng VP (250 ng, post-V1 antagonist: 66.4 +/- 8.6% reduction in blood pressure response, P < 0.001), whereas [desamino,D-Arg8]vasopressin (DDAVP), a V2 agonist, had a depressor effect when microinjected directly into the AP (250 ng, -9.9 +/- 1.6 mmHg, P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular consequences of microinjection of vasopressin and angiotensin II in the area postrema. 821 57

In the course of electrophysiological investigations using iontophoresis, we observed that in specific regions of the forebrain even these minute applications of peptide and steroid hormones can influence systemic blood pressure. In urethan-anesthetized male Wistar rats, with a catheter in the femoral artery, iontophoretic application of the peptide hormones angiotensin II (ANG II), vasopressin (AVP), and atrial natriuretic peptide (ANP) and the steroid hormone aldosterone (ALDO) was effective at locations in the midline septum, the triangularis nucleus of the septum, and the subfornical organ (SFO). Increases in blood pressure (of up to 15 mmHg) were observed after ANG II and AVP, decreases after ALDO, and either an increase or a decrease, depending on the location, after ANP. There was no clear evidence of an antagonistic effect of ANP on ANG II-induced neuronal or blood pressure responses. In addition to demonstrating the potency of these hormones even when they are restricted to tiny volumes of tissue, the present results demonstrate that the medial ventral region of the anterior forebrain may be included in the same baroreceptive circuit as the SFO (and organ vasculosum of the lamina terminalis) and hence be involved in the regulation of blood volume and perhaps in the sensing of and corrective responses to extracellular thirst.
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PMID:Blood pressure effects of iontophoretically applied bioactive hormones in the anterior forebrain of the rat. 823 53


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