UNIPROT:P01185 - FACTA Search

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

Angiotensin II (Ang II), the biologically active component of renin-angiotensin system (RAS), acts through two receptor subtypes, the AT1 and the AT2 receptor. All classic physiological effects of Ang II, such as vasoconstriction, aldosterone and vasopressin release, sodium and water retention and sympathetic facilitation, are mediated by the AT1 receptor. Ang II, via its AT1 receptor, is also involved in cell proliferation, left ventricular hypertrophy, nephrosclerosis, vascular media hypertrophy, endothelial dysfunction, neointima formation and processes leading to athero-thrombosis. Recent investigations have established a role for the AT2 receptor in cardiovascular, brain and renal function as well as in the modulation of various biological processes involved in development, cell differentiation, tissue repair and apoptosis. This review summarizes new insights in the regulation, signalling and (patho-) physiological functions of AT1 and AT2 receptors. An extensive review on angiotensin receptors has been published recently (de Gasparo M et al., Pharmacol Rev 2000; 52: 415-72).
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PMID:Angiotensin AT1/AT2 receptors: regulation, signalling and function. 1279 27

We have previously shown that pretreatment of A-10 vascular smooth muscle cells (VSMC) with angiotensin II (Ang II) attenuated atrial natriuretic peptide receptor-C (ANP-C)-mediated inhibition of adenylyl cyclase without altering [125I]ANP binding. In the present studies, we have investigated the modulation of ANP-C receptor signaling by arginine-vasopressin (AVP). Pretreatment of A-10 VSMC with AVP for 24h resulted in a reduction in ANP receptor binding activity by about 50% (B(max); control cells, 22.9+/-2.5 fmol/mg protein, AVP-treated cells, 11.4+/-1.2 fmol/mg protein). In addition, the expression of ANP-C receptor as determined by immunoblotting was also decreased by about 50% by AVP treatment, which was prevented by GF109203X, an inhibitor of protein kinase C (PKC). The decreased expression of ANP-C receptor was reflected in an attenuation of ANP-C receptor-mediated inhibition of adenylyl cyclase. C-ANP(4-23) [des(Gln(18),Ser(19),Gln(20),Leu(21),Gly(22))ANP(4-23)-NH(2)], a ring deleted peptide of ANP that interacts specifically with ANP-C receptor, inhibited adenylyl cyclase activity by about 30% in control cells, which was completely attenuated in AVP-treated cells. This attenuated inhibition was significantly restored by GF 109203X. In addition, AVP treatment augmented the levels of Gialpha-2 and Gialpha-3 proteins; however, the Gi functions were completely attenuated. The increased expression of Gialpha proteins induced by AVP was inhibited by GF109203X as well as by actinomycin D treatments. In addition, AVP treatment also enhanced the expression of Gsalpha protein and Gsalpha-mediated stimulation of adenylyl cyclase by GTPgammaS, N-ethylcarboxamide adenosine (NECA), and forskolin (FSK), whereas the levels of Gbeta were not altered by AVP treatment. These results indicate that AVP-induced PKC signaling may be responsible for the down-regulation of ANP-C receptor that results in the attenuation of C-ANP(4-23)-mediated inhibition of adenylyl cyclase activity, and suggest a cross-talk between vasopressin V(1) and ANP-C receptor-mediated signaling pathways.
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PMID:Modulation of ANP-C receptor signaling by arginine-vasopressin in A-10 vascular smooth muscle cells: role of protein kinase C. 1283 42

The inhibitory effect of lipopolysaccharides (LPS) on alpha-adrenergic contraction is quite well known, but molecular mechanism of this inhibition is unclear. In the present study, the interaction between alpha-adrenoceptor and vasopressin receptor response, and LPS in rat tail artery was investigated using chemical stimulation. In the presence of LPS, noradrenaline, phenylephrine and arginine-vasopressin, concentration-response curves (CRCs) were shifted to the right with the change in maximal responses. The K(A) and K(B) values calculated in the presence and absence of LPS did not differ significantly. The results strongly suggest that LPS did not change the receptors affinity. The changes in the relationship between receptor occupancy and response to an agonist in the presence of LPS and reduction of K(A)/ED(50) value suggest reduction of receptor reserve. In the presence of angiotensin II (Ang II), CRCs were shifted to the right with significant increase in receptor reserve. Moreover, this effect was still present in LPS-pretreated arteries. The receptor reserve reduced by LPS significantly increased in the presence of Ang II. It suggests that inhibitory effect of LPS is partially reversible. The results strongly suggest that in early endotoxemia, inhibitory effect of LPS may by partially reverted by an increase in activity of renin-angiotensin-aldosterone system.
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PMID:Physiological antagonism of angiotensin II and lipopolysaccharides in early endotoxemia: pharmacometric analysis. 1470 72

In transgenic mice expressing an antisense mRNA against the glucocorticoid receptor (GR), which partially blocks GR expression, impaired glucocorticoid feedback efficacy is accompanied by reduced hypothalamic corticotropin-releasing hormone (CRH) and vasopressin (AVP) activity and reduced peripheral sympathetic tone, indications of a shift in the balance of hypothalamic CRH and sympathetic regulation. As angiotensin II (Ang II) regulates CRH, AVP and sympathetic activity, we studied the expression of Ang II receptors in the hypothalamus and adrenal gland of GR transgenic and wild-type mice, adrenal catecholamines and mRNA for their rate-limiting enzyme, tyrosine hydroxylase (TH). We found that transgenic mice expressed significantly less numbers of Ang II AT(1) receptors in the hypothalamic paraventricular nucleus and median eminence, lower numbers of AT(2) receptors in supraoptic and paraventricular nuclei and lower numbers of AT(2) receptors in the adrenal medulla when compared with wild-type controls. The expression of TH mRNA and the concentration of adrenomedullary epinephrine and norepinephrine were also lower in transgenic mice when compared with wild-type controls. Decreased hypothalamic and adrenal Ang II receptor stimulation as a result of decreased GR expression may explain the decreased hypothalamic CRH and AVP and decreased adrenomedullary and sympathetic activities in this model.
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PMID:Decreased hypothalamic and adrenal angiotensin II receptor expression and adrenomedullary catecholamines in transgenic mice with impaired glucocorticoid receptor function. 1558 74

The renin-angiotensin system (RAS) is one of the best-studied enzyme-neuropeptide systems in the brain and can serve as a model for the action of peptides on neuronal function in general. It is now well established that the brain has its own intrinsic RAS with all its components present in the central nervous system. The RAS generates a family of bioactive angiotensin peptides with variable biological and neurobiological activities. These include angiotensin-(1-8) [Ang II], angiotensin-(3-8) [Ang IV], and angiotensin-(1-7) [Ang-(1-7)]. These neuroactive forms of angiotensin act through specific receptors. Only Ang II acts through two different high-specific receptors, termed AT1 and AT2. Neuronal AT1 receptors mediate the stimulatory actions of Ang II on blood pressure, water and salt intake, and the secretion of vasopressin. In contrast, neuronal AT2 receptors have been implicated in the stimulation of apoptosis and as being antagonistic to AT1 receptors. Among the many potential effects mediated by stimulation of AT2 are neuronal regeneration after injury and the inhibition of pathological growth. Ang-(1-7) mediates its antihypertensive effects by stimulating the synthesis and release of vasodilator prostaglandins and nitric oxide and by potentiating the hypotensive effects of bradykinin. New data concerning the roles of Ang IV and Ang-(1-7) in cognition also support the existence of complex site-specific interactions between multiple angiotensins and multiple receptors in the mediation of important central functions of the RAS. Thus, the RAS of the brain is involved not only in the regulation of blood pressure, but also in the modulation of multiple additional functions in the brain, including processes of sensory information, learning, and memory, and the regulation of emotional responses.
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PMID:The CNS renin-angiotensin system. 1655 51

The objective of the present study was to find out whether brain vasopressin (AVP) and angiotensin II (Ang II) are involved in pressor response to intracerebroventricular (ICV) infusion of interleukin-1 beta (IL-1beta). The experiments were performed on conscious, 12- to 14-week-old Sprague-Dawley rats. Mean arterial blood pressure (MAP) and heart rate (HR) were recorded continuously under baseline conditions and during ICV infusion periods. In the first part of the study, the rats were ICV-infused with one of the following: 0.9% NaCl saline (5 microl/h-control), IL-1beta (100 ng/h), angiotensin AT1 receptor antagonist (losartan 10 microg/h), IL-1beta together with losartan, V1 receptors antagonist (V1ANT), d(CH2)5[Tyr(Me)2,Ala-NH2(9)]AVP, 400 ng/h) or IL-1beta together with V1ANT. Saline infusion did not influence MAP, while administration of IL-1beta elicited a significant but transient increase in MAP. The pressor response to IL-1beta was abolished by losartan but not by V1ANT. On the other hand, combined administration of IL-1beta and V1ANT resulted in increase in HR, which was absent during infusion of IL-1beta alone. In the second part of the study after ICV pretreatment with IL-1beta or 0.9% NaCl (control), the rats received ICV infusion of one of the following: 0.9% NaCl saline, subpressor dose of Ang II (5 ng/15 s) or subpressor dose of AVP (5 ng/15 s). Subpressor doses of Ang II and AVP did not influence MAP and HR in saline-pretreated rats. The same dose of Ang II but not AVP applied in IL-1beta-pretreated rats resulted in a significant increase in MAP. The study provides evidence that IL-1beta through its action in the brain increases sensitivity to central pressor action of Ang II. Additionally, we found that AVP and in particular V1 receptors do not play important role in the central pressor action of IL-1beta, however, they may influence its effect on HR regulation.
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PMID:Centrally administered interleukin-1 beta sensitizes to the central pressor action of angiotensin II. 1676 25

The heart adapts to increased pressure overload by hypertrophic growth of terminally differentiated cardiomyocytes. At the genetic level, the hypertrophic response is characterized by the reprogramming of gene expression, i.e. upregulation of immediate early genes, natriuretic peptide genes and genes encoding structural proteins. In the present study, we characterized the early changes in gene expression with cDNA expression arrays in response to increase in blood pressure produced by arginine8-vasopressin infusion (0.05 microg/kg/min, i.v.) for 30 min and 4 h in conscious normotensive rats. Expression profiling revealed differential expression of 14 genes in the left ventricle, and several novel factors of immediate early genetic response to pressure overload were identified, such as growth arrest and DNA damage inducible protein 45 (GADD45alpha), epidermal fatty acid-binding protein (E-FABP) and Bcl-X. Administration of angiotensin II (Ang II) for 6 h by osmotic minipumps also increased left ventricular GADD45alpha, E-FABP and Bcl-X gene expression. Furthermore, the induction of GADD45alpha and Bcl-X gene expression by Ang II was blocked by angiotensin II type 1 receptor antagonist losartan. In summary, our analysis provided new insights into the pathogenesis of pressure overload-induced hypertrophy by suggesting the existence of novel regulators of the immediate early gene expression program.
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PMID:Early left ventricular gene expression profile in response to increase in blood pressure. 1747 29

The presence of nitric oxide synthase (NOS), the enzyme that catalyses the formation of nitric oxide (NO), in the circumventricular organs and magnocellular neurones suggests an important role of NO in the modulation of vasopressin (AVP) and oxytocin (OT) release. Intracerebroventricular (I.C.V.) injection of angiotensin II (Ang II) stimulates the release of AVP, OT and atrial natriuretic peptide (ANP), with the resultant antidiuretic and natriuretic effects. This study investigated the interaction between nitrergic and angiotensinergic pathways on the release of AVP, OT and ANP and on urinary volume and sodium excretion in water-loaded rats. Unanaesthetized, freely moving, male Wistar rats received two water loads followed by an injection into the lateral ventricle of an inhibitor of NOS (L-NAME), a NO donor [3-morpholinylsydnoneimine chloride (SIN-1) or S-nitroso-N-acetyl penicillamine (SNAP)] or vehicle (isotonic saline) and, 20 min after, they received a second I.C.V. injection of Ang II or vehicle. Injections of L-NAME or Ang II produced an increase in plasma levels of AVP, OT and ANP, a reduction in urinary volume and an increase in sodium excretion. Pretreatment with L-NAME enhanced the Ang II-induced increase in AVP, OT and ANP release, as well as the antidiuresis and natriuresis. Injection of SIN-1 or SNAP did not modify hormonal plasma levels and urinary parameters. In contrast SNAP blocked the AVP, OT and ANP release, as well as antidiuretic and natriuretic responses induced by ANG-II. Thus, the central nitrergic system can act to inhibit AVP, OT and ANP secretion and the antidiuretic and natriuretic effects in response to Ang II.
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PMID:Central nitric oxide blocks vasopressin, oxytocin and atrial natriuretic peptide release and antidiuretic and natriuretic responses induced by central angiotensin II in conscious rats. 1751 44

Angiotensin II (Ang II), aldosterone, and arginine-vasopressin (AVP) are three major neuropeptides or hormones that are important in the control of body fluid regulation. Dehydration during pregnancy induces alterations in maternal-fetal fluid homeostasis. It is still not clear about effects and mechanisms of maternal water deprivation on fetal neuroendocrine and hormonal responses. The present study deprived water from pregnant sheep at near-term for 24 h and 48 h, and determined maternal and fetal blood osmolality and sodium levels before and immediately after water deprivation. Fetal renal excretion and plasma hormones were measured. Fetal forebrain was analyzed for cellular activation marked with Fos and Fos-B. The results showed that maternal and fetal blood osmolality and sodium were increased by water deprivation. Maternal and fetal Ang II, aldosterone, and AVP levels were elevated by 24-h and 48-h water deprivation, while fetal plasma Ang I levels were increased only under the condition of 48-h water deprivation. Intensive Fos and Fos-B expression was detected in the median preoptic nuclei and paraventricular nuclei in the fetal brain following exposure to maternal water deprivation. Double labeling demonstrated that many Fos-positive cells were AVP-containing neurons in the fetal paraventricular nucleus. Together, the results suggest that neuroendocrine and hormonal regulatory mechanisms play a role in the control of body fluid homeostasis, and relatively matured and functional at the last third of gestation, as well as the fetal hypothalamus is functional in the control of the neuropeptide in response to maternal dehydration.
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PMID:Ovine fetal hormonal and hypothalamic neuroendocrine responses to maternal water deprivation at late gestation. 1946 Jun 33

Matrix Gla protein (MGP) expression is increased in cardiac hypertrophy, but the precise mechanisms regulating its expression are unknown. Here we characterized the effect of pressure overload and myocardial infarction in vivo as well as mechanical stretch and hypertrophic agonists in vitro on MGP expression. When angiotensin II (Ang II) was administered by osmotic minipumps, left ventricular (LV) MGP mRNA levels increased significantly from 6 h to 2 weeks, whereas intravenous arginine(8)-vasopressin increased LV MGP mRNA levels within 4 h. During post-infarction remodeling process, MGP mRNA levels were elevated at 24 h (1.3-fold, p<0.05) and the maximal increase was observed at 4 weeks (2.8-fold, p<0.01). Ang II increased MGP mRNA levels 20% (p<0.05) in neonatal rat cardiac myocytes and 40% (p<0.05) in cardiac fibroblasts, whereas endothelin-1 decreased MGP mRNA levels 30% (p<0.01) in myocytes and had no effect in fibroblasts. Cyclic mechanical stretch resulted in reduction of MGP gene expression in both cardiac myocytes and fibroblasts. These results demonstrate that MGP is rapidly upregulated in response to cardiac overload well before the development of LV hypertrophy and post-infarction remodeling process. Our results also suggest that Ang II may be involved in mediating load-induced activation of MGP expression.
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PMID:Upregulation of cardiac matrix Gla protein expression in response to hypertrophic stimuli. 1991 1

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