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)

In this study we investigated the influence of d(CH2)5-Tyr(Me)-[Arg8]vasopressin (AAVP) and [adamanteanacetyl1,0-ET-d-Tyr2,Val4,aminobutyryl6,Arg8,9]-[Arg8]vasopressin (ATAVP), which are antagonists of vasopressin V1 and V2 receptors, and the effects of losartan, a selective angiotensin AT1 receptor antagonist, and CGP42112A, a selective AT2 receptor antagonist, injected into the lateral septal area (LSA) on thirst and hypertension induced by [Arg8]vasopressin (AVP). AAVP and ATAVP injected into the LSA reduced the drinking responses elicited by injecting AVP into the LSA. Both the AT1 and AT2 ligands administered into the LSA elicited a concentration-dependent decrease in the water intake induced by AVP injected into the LSA, but losartan was more effective than CGP42112A. The increase in MAP, due to injection of AVP into the LSA, was reduced by prior injection of AAVP from 18 +/- 1 to 6 +/- 1 mm Hg. Losartan injected into the LSA prior to AVP reduced the increase in MAP to 7 +/- 0.8 mm Hg. ATAVP and CGP42112A produced no changes in the pressor effect of AVP. These results suggest that the dipsogenic effects induced by injecting AVP into the LSA were mediated primarily by AT1 receptors. However, doses of losartan were more effective when combined with CGP42112A than when given alone, suggesting that the thirst induced by AVP injections into LSA may involve activation of multiple AVP and angiotensin II receptor subtypes. The pressor response of AVP was reduced by losartan and by AAVP. CGP42112A and ATAVP did not change the AVP pressor response. These results suggest that facilitator effects of AVP on water intake are mediated through the activation of V1 receptors and that the inhibitory effect requires V2 receptors. The involvement of AT1 and AT2 receptors can be postulated. Based on the present findings, we suggest that the AVP in the LSA may play a role in the control of water and arterial blood pressure balance.
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PMID:Influence of arginine vasopressin receptors and angiotensin receptor subtypes on the water intake and arterial blood pressure induced by vasopressin injected into the lateral septal area of the rat. 1510 40

Angiotensin II (AII), the biologically active component of renin-angiotensin system (RAS), acts through two receptor subtypes, the AT1 and AT2 receptor. All classic physiological effects of AII, such as vasoconstriction, aldosterone and vasopressin release, sodium and water retention and sympathetic facilitation, are mediated by the AT1 receptor. The majority of pilot studies demonstrated the renoprotective effect of RAS blockers via antihypertensive, antiproteinuric, antifibrotic action. In order to establish whether RAS blocker causes antiproteinuric effects or long-term renoprotection in the non-diabetic nephrotic disease, larger prospective, randomized controlled trials are required in the future.
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PMID:[RAS blockade]. 1550 Jan 34

Bilateral carotid occlusion (BCO) increases the sympathetic drive to the circulatory system in conscious intact rats, producing a hypertensive response characterized by two components, i.e., an initial peak followed by a sustained response of lower intensity. The neurohumoral mechanisms involved in the hypertensive response to BCO were evaluated in conscious intact (INTACT) or chronic guanethidine sympathectomized (SYMPX) rats. To accomplish this, the receptor antagonists, prazosin for alpha1-adrenergic receptor, losartan for AT1 angiotensin II receptor and [d(CH2)5Tyr(Me)AVP] for vascular V1 vasopressin receptor were used. A saline control group was studied as well. Conscious rats were equipped with cuffs around the common carotid arteries plus arterial and venous catheters. The results indicate that the sympathetic nervous system is the main mechanism controlling the basal arterial pressure in conscious INTACT rats, whereas in chronically SYMPX rats the renin-angiotensin system plays this role. In INTACT rats prazosin abolished the initial peak and blunted the sustained hypertensive response due to BCO, while the other antagonists exhibited no effect. SYMPX rats did not present the initial peak but displayed an enhanced sustained response, which was blunted by prazosin or the vasopressin antagonist. In conclusion, activation of the sympathetic drive is responsible for both the initial peak and the sustained hypertensive response due to BCO in conscious INTACT rats. On the other hand, vasopressin acting in concert with the sympathetic nervous system, plays a key role in the potentiation of the sustained hypertensive response due to BCO in conscious chronically SYMPX rats.
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PMID:Neurohumoral mechanisms involved in the hypertensive response elicited by bilateral carotid occlusion in conscious intact or chronically sympathectomized rats. 1555 56

Experiments were performed to study the role of angiotensin (Ang) AT1a and AT1b receptor subtypes in osmotic regulation of blood pressure using gene deletion and pharmacological methods. The cardiovascular effects of hypertonic saline (HS) or vasopressin (VP) delivered via vascular catheters were measured in Ang AT1a gene deletion (AT1a-/-) and control (AT1a+/+) mice. Blood pressure (BP) and heart rate (HR) were recorded in conscious mice using direct carotid catheters. Plasma osmolality and VP concentration were also measured. The major finding was that deletion of AT1a receptors resulted in enhanced BP response to osmotic stimulation. This was seen after acute HS injection (20 microl, 20% NaCl). The peak percentage change in mean arterial pressure (MAP) was 15.4+/-1.9% versus 28.1+/-2.4% (AT1a+/+versus AT1a-/-, respectively). Losartan (AT1 antagonist), but not PD123319 (AT2 antagonist), inhibited the HS-induced MAP response, specifically in AT1a-/- mice. Plasma osmolality and VP concentration were elevated after HS injection with no differences noted between groups. Vascular injection of VP (5 ng g-1) increased BP and HR, with similar MAP response between groups. Evidence shows that removal of Ang AT1a receptors results in a significant enhancement in the pressor response to acute osmotic stimulation. Studies of AT1 receptor blockade indicate that complementary Ang AT1b receptors, but not AT2 receptors, may be involved in the osmotic response.
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PMID:Enhanced osmotic responsiveness in angiotensin AT1a receptor deficient mice: evidence for a role for AT1b receptors. 1594 3

We speculated that the influence of lateral preoptic area (LPO) in sodium balance, involves arginine8-vasopressin (AVP) and angiotensin (ANG II) on Na+ uptake in LPO. Therefore, the present study investigated the effects of central administration of specific AVP and ANG II antagonists (d(CH2)5-Tyr (Me)-AVP (AAVP) and [Adamanteanacetyl1, 0-ET-d-Tyr2, Val4, Aminobutyryl6, Arg(8,9)]-AVP (ATAVP) antagonists of V1 and V2 receptors of AVP. Also the effects of losartan and CGP42112A (selective ligands of the AT1 and AT2 angiotensin receptors, respectively), was investigated on Na+ uptake and renal fluid and electrolyte excretion. After an acclimatization period of 7 days, the animals were maintained under tribromoethanol (200 mg/kg body weight, intraperitonial) anesthesia and placed in a Kopf stereotaxic instrument. Stainless guide cannula was implanted into the LPO. AAVP and ATAVP injected into the LPO prior to AVP produced a reduction in the NaCl intake. Both the AT1 and AT2 ligands administered into the LPO elicited a decrease in the NaCl intake induced by AVP injected into the LPO. AVP injection into the LPO increased sodium renal excretion, but this was reduced by prior AAVP administration. The ATAVP produced a decreased in the natriuretic effect of AVP. The losartan injected into LPO previous to AVP decreased the sodium excretion and the CGP 421122A also decreased the natriuretic effect of AVP. The AVP produced an antidiuresis effect that was inhibited by prior administration into LPO of the ATAVP. The AAVP produced no change in the antidiuretic effect of AVP. These results suggest that LPO are implicated in sodium balance that is mediated by V1, V2, AT1 and AT2 receptors.
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PMID:Interaction between arginine vasopressin and angiotensin II receptors in the central regulation of sodium balance. 1619 10

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

Our previous studies have shown that central administration of angiotensin (ANG II) causes arginine vasopressin (AVP) release in the fetus at 70-90% gestation. This is evidence that the hypothalamic-neurohypophysial system is relatively mature before birth. However, few data exist regarding central ANG receptor mechanisms-mediated AVP response during fetal life. To determine roles of brain ANG receptor subtypes in this response, AT1 and AT2 receptor antagonists, losartan and PD123319, were investigated in the brain in chronically prepared ovine fetuses at the last third of gestation. Application of losartan intracerebroventricularly (i.c.v.) at 0.5 mg/kg suppressed central ANG II-stimulated plasma AVP release. Losartan at 5 mg/kg (i.c.v.) demonstrated a significant enhancement of AVP increase to i.c.v. ANG II. Associated with the increase of plasma vasopressin levels, c-fos expression in the hypothalamic neurons was significantly different between the low and high doses of losartan. The low dose losartan markedly reduced the dual immunoreactivity for FOS and AVP in the supraoptic nuclei and paraventricular nuclei after i.c.v. ANG II, whereas the high dose losartan together with ANG II, significantly increased the co-localization of positive FOS in the AVP-containing neurons than that induced by i.c.v. ANG II alone. Central ANG II induced fetal plasma vasopressin increase was not altered by PD123319. The data suggest that losartan in the fetal brain has remarkably different effects based on the doses administrated on central ANG II-related neuroendocrine effects at the late gestation, and that the AT1 mechanism is critical in the regulation of fetal body fluid homeostasis related to plasma AVP levels.
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PMID:Effects of i.c.v. losartan on the angiotensin II-mediated vasopressin release and hypothalamic fos expression in near-term ovine fetuses. 1667 37

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

We studied the in vivo effects of sanguinarine in a hypertensive rat model and its effects on AT1a mRNA expression in kidney tissues. Rats received daily for 14 d sanguinarine 0.1 mg/kg (SangL) and 0.3 mg/kg (SangH), losartan 1 mg/kg by weight (Los), or DMSO (Con). Blood pressures were monitored regularly and urine volume and sodium concentration was measured on days 0, 7, and 14. On day 15, animals were anesthetized (sodium thiopentane, 50 mg/kg), blood samples for aldosterone levels were taken, and kidneys were removed for AT1a mRNA expression. Los and SangH groups showed reduced AT1a mRNA expressions by 4.22- and 5.9-fold, respectively. In the SangL group it was reduced by 2.7-fold. Decreases in systolic blood pressures mirrored decreases in AT1a mRNA expressions in all groups. Los and SangH groups showed reductions in systolic blood pressure of 12.3% and 19.3%, respectively, whereas in the SangL group, it was reduced by 8.07%. Urine output in the Los group increased (228% mean increase from days 0-14), whereas sodium excretion decreased by 69.6% (mean decrease from days 0-14). In the SangL and SangH groups, urine volumes increased significantly by 108.3% and 115% (mean increase from days 0-14), respectively. Urinary sodium excretion increased significantly by 60.9% in the SangH group. We concluded that sanguinarine reduces blood pressure in the Dahl rat because of decreased AT1 receptor expression and reduced aldosterone levels. The action of losartan on increased urinary volume and decreased sodium excretion may be attributed to reduced vasopressin secretion.
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PMID:Sanguinarine downregulates AT1a gene expression in a hypertensive rat model. 1695 16

The study was undertaken to examine the potential cross talk between vasopressin and angiotensin II (ANG II) intracellular signaling pathways. We investigated in vivo and in vitro whether vasopressin-induced water reabsorption could be attenuated by ANG II AT1 receptor blockade (losartan). On a low-sodium diet (0.5 meq/day) dDAVP-treated animals with or without losartan exhibited comparable renal function [creatinine clearance 1.2 +/- 0.1 in dDAVP+losartan (LSDL) vs. 1.1 +/- 0.1 ml.100 g(-1).day(-1) in dDAVP alone (LSD), P > 0.05] and renal blood flow (6.3 +/- 0.5 in LSDL vs. 6.8 +/- 0.5 ml/min in LSD, P > 0.05). The urine output, however, was significantly increased in LSDL (2.5 +/- 0.2 vs. 1.8 +/- 0.2 ml.100 g(-1).day(-1), P < 0.05) in association with decreased urine osmolality (2,600 +/- 83 vs. 3,256 +/- 110 mosmol/kgH(2)O, P < 0.001) compared with rats in LSD. Immunoblotting revealed significantly decreased expression of medullary AQP2 (146 +/- 6 vs. 176 +/- 10% in LSD, P < 0.01), p-AQP2 (177 +/- 13 vs. 214 +/- 12% in LSD, P < 0.05), and AQP3 (134 +/- 14 vs. 177 +/- 11% in LSD, P < 0.05) in LSDL compared with LSD. The expressions of AQP1, the alpha(1)- and gamma-subunits of Na-K-ATPase, and the Na-K-2Cl cotransporter were not different among groups. In vitro studies showed that ANG II or dDAVP treatment was associated with increased AQP2 expression and cAMP levels, which were potentiated by cotreatment with ANG II and dDAVP and were inhibited by AT1 blockade. In conclusion, ANG II AT1 receptor blockade in dDAVP-treated rats on a low-salt diet was associated with decreased urine concentration and decreased inner medullary AQP2, p-AQP2, and AQP3 expression, suggesting that AT1 receptor activation plays a significant role in regulating aquaporin expression and modulating urine concentration in vivo. Studies in collecting duct cells were confirmatory.
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PMID:Interaction between vasopressin and angiotensin II in vivo and in vitro: effect on aquaporins and urine concentration. 2057 79


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