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

Saad, Wilson Abrão; Camargo, Luiz Antônio de Arruda; Cerri, Paulo Sérgio; Simões, Silvio Jorge Coelho; Saad, William Abrão; Garcı́a, Gustavo; Gutierrez, Laura Izabel; Guarda, Ismael Francisco Motta Siqueira; Guarda, Renata Saad

doi:10.1016/j.autneu.2003.08.013

Cited by 11 publications

(4 citation statements)

References 25 publications

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“…Although the increase in water intake in the present study may be related to the blockade of the central AT 2 receptor, the role of the central AT 2 receptors in thirst is not clear. Some studies have suggested that AT 2 receptors are not involved in thirst regulation 28-30 while other studies reported that AT 2 receptor may have a role in thirst in response to water-deprivation 31-34. Higher blood pressure could be responsible for increase in diuresis in the PD-treated obese rats.…”

Section: Discussionmentioning

confidence: 97%

Protective Role of Angiotensin II Subtype 2 Receptor in Blood Pressure Increase in Obese Zucker Rats

2009

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Abstract-Earlier, we reported that there was an increase in angiotensin II type 2 (AT 2 ) receptor expression in the renal proximal tubule, and selective activation of the AT 2 receptor by AT 2 agonist inhibits Na,K-ATPase activity in the proximal tubules and increases urinary Na excretion in obese Zucker rats. We hypothesized that the AT 2 receptor has a protective role against blood pressure increase in obese Zucker rats. To test this hypothesis, we treated obese Zucker rats with the AT 2 receptor antagonist PD123319 (PD; 30 g/kg per minute) using osmotic pumps. Age-matched lean rats and vehicle-treated obese Zucker rats served as controls. On day 15 of the treatment with PD, arterial blood pressure was measured by cannulation of the left carotid artery under anesthesia. Control obese rats exhibited higher mean arterial pressure (122.0Ϯ3.4 mm Hg) compared with lean control rats (97.0Ϯ4.8 mm Hg). The PD treatment of obese rats raised mean arterial pressure further by 13 mm Hg. The plasma renin activity was significantly increased in the PD-treated obese compared with control-obese or lean rats. Western blot analysis revealed that the PD treatment in obese rats caused an Ϸ3-fold increase in the renin expression in the kidney cortex but had no effect on the expression of the cortical angiotensin II type 1 and AT 2 receptors. The present study suggests that the renal AT 2 receptors provide a protective role against blood pressure increase in obese Zucker rats, and this protective effect, in part, could be because of the ability of the AT 2 receptors to keep the kidney renin expression low in obese rats.

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Section: Discussionmentioning

confidence: 97%

Protective Role of Angiotensin II Subtype 2 Receptor in Blood Pressure Increase in Obese Zucker Rats

2009

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“…Renin, Ang II, and Ang III are potent dipsogens and avid stimulation of thirst belongs to the most spectacular effects of these peptides. Several studies indicate that the dipsogenic action of Ang II engages AT1R in the median preoptic nucleus and lateral septal area [ 200 – 203 ]. The dipsogenic effect is adjusted to the actual blood volume and hemodynamic conditions and can be partly damped by the parallel inhibition of thirst by an enhanced input from baroreceptors and cardiopulmonary receptors.…”

Section: Renin-angiotensin Systemmentioning

confidence: 99%

Dysregulation of the Renin-Angiotensin System and the Vasopressinergic System Interactions in Cardiovascular Disorders

2018

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Purpose of ReviewIn many instances, the renin-angiotensin system (RAS) and the vasopressinergic system (VPS) are jointly activated by the same stimuli and engaged in the regulation of the same processes.Recent FindingsAngiotensin II (Ang II) and arginine vasopressin (AVP), which are the main active compounds of the RAS and the VPS, interact at several levels. Firstly, Ang II, acting on AT1 receptors (AT1R), plays a significant role in the release of AVP from vasopressinergic neurons and AVP, stimulating V1a receptors (V1aR), regulates the release of renin in the kidney. Secondly, Ang II and AVP, acting on AT1R and V1aR, respectively, exert vasoconstriction, increase cardiac contractility, stimulate the sympathoadrenal system, and elevate blood pressure. At the same time, they act antagonistically in the regulation of blood pressure by baroreflex. Thirdly, the cooperative action of Ang II acting on AT1R and AVP stimulating both V1aR and V2 receptors in the kidney is necessary for the appropriate regulation of renal blood flow and the efficient resorption of sodium and water. Furthermore, both peptides enhance the release of aldosterone and potentiate its action in the renal tubules.SummaryIn this review, we (1) point attention to the role of the cooperative action of Ang II and AVP for the regulation of blood pressure and the water-electrolyte balance under physiological conditions, (2) present the subcellular mechanisms underlying interactions of these two peptides, and (3) provide evidence that dysregulation of the cooperative action of Ang II and AVP significantly contributes to the development of disturbances in the regulation of blood pressure and the water-electrolyte balance in cardiovascular diseases.

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“…While the extent of contraction was assessed at 10, 20 and 30 min after addition of AVP, because the relative degree of contraction did not change between conditions over the three time points, only the 30-min time point is shown. As shown in figure 2, [d(CH 2 ) 5 1 ,Tyr(Me) 2 ,Arg 8 ]-vasopressin, a peptide antagonist specific for the V 1 receptor [8,9,10], abolished AVP-induced reduction in RMIC area, while [d(CH 2 ) 5 1 , D -Ile 2 ,Ile 4 ,Arg 8 )]vasopressin, a peptide antagonist specific for the V 2 receptor [8,9,10], was without effect on the AVP response. Nifedipine (10 µ M ), an inhibitor of L -type calcium channels, reduced AVP-induced contraction (fig.…”

Section: Resultsmentioning

confidence: 99%

Mechanism of Vasopressin-Induced Contraction of Renal Medullary Interstitial Cells

Hughes¹,

Kohan

2006

Nephron Physiol

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Background/Aims: Previous studies have identified a contractile function for renomedullary interstitial cells (RMIC). Such studies focused on the mechanism of endothelin-1-induced RMIC contraction; however, vasopressin (AVP) was also noted to contract RMIC. Since AVP-induced RMIC contraction may be relevant to the medullary effects of AVP on urinary concentration, these initial observations have been extended to examination of the mechanism of AVP-induced RMIC contraction. Methods: Cultured rat RMIC were exposed to AVP and other agents, and examined using video microscopy. Results: AVP caused a slowly developing and dose-dependent reduction in RMIC surface area. AVP-induced RMIC contraction was abolished by blockade of V₁, but not V₂, receptors. Nifedipine and nickel reduced AVP-stimulated RMIC contraction, indicating that this effect is dependent upon dihydropyridine-sensitive calcium channels. H7, a protein kinase C inhibitor, completely abrogated AVP action, while the nitric oxide synthase inhibitor, NMMA, had no effect. Indomethacin enhanced AVP-induced RMIC contraction, and addition of PGE₂ together with indomethacin reduced AVP action. Conclusion: These data indicate that AVP potently contracts RMIC via V₁ receptor stimulation of PKC and intracellular calcium accumulation, and that AVP-stimulated prostaglandin production downregulates the contractile effect of AVP on RMIC. AVP modulation of RMIC contraction may be involved in the regulation of urinary concentration.

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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

Cited by 11 publications

References 25 publications

Protective Role of Angiotensin II Subtype 2 Receptor in Blood Pressure Increase in Obese Zucker Rats

Protective Role of Angiotensin II Subtype 2 Receptor in Blood Pressure Increase in Obese Zucker Rats

Dysregulation of the Renin-Angiotensin System and the Vasopressinergic System Interactions in Cardiovascular Disorders

Mechanism of Vasopressin-Induced Contraction of Renal Medullary Interstitial Cells

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