Vasopressin and angiotensin receptors of the medial septal area in the control of mean arterial pressure induced by vasopressin

Author:

Pavan de Arruda Camargo Gabriela Maria1,Abrão Saad Wilson2,de Arruda Camargo Luiz Antônio3

Affiliation:

1. Department of Physiology, Paulista State University, UNESP, gabriela.camargo@ gmail.com

2. Department of Physiology, Paulista State University, UNESP, Department of Physiology, Federal University of São Carlos, UFSCAR, University of Taubaté, UNITAU, University of Araraquara, UNIARA

3. Department of Physiology, Paulista State University, UNESP, Department of Physiology, Federal University of São Carlos, UFSCAR, Department of Physiology, Federal University of São Carlos, UFSCAR

Abstract

Introduction. Brain arginine 8-vasopressin (AVP), through the V1a- and V2-receptors, is essential for the maintenance of mean arterial pressure (MAP). Central AVP interacts with the components of the renin-angiotensin system, which participate in MAP regulation. This study aimed to determine the effects of V1a-, V2- and V1a/V2-AVP selective antagonists and AT1- and AT2-angiotensin II (Ang II) selective antagonists on the MAP induced by AVP injected into the medial septal area (MSA) of the brain. Materials and methods. Male Holtzman rats with stainless steel cannulae implanted into the MSA were used in experiments. Direct MAP was recorded in conscious rats. Results. AVP administration into the MSA caused a prompt and potent pressor response in a dose-dependent fashion. Pretreatment with the V1a- and V2-antagonists reduced, whereas prior injection of the V1a/V2-antagonist induced a decrease in the MAP that remained below the baseline. Both AT 1- and AT2-antagonists elicited a decrease, while simultaneous injections of two antagonists were more effective in decreasing the MAP induced by AVP. Conclusion. These results indicate there is a synergism between the V1a- and V2-AVP and AT1and AT2-Ang II receptors in the MSA in the regulation of MAP.

Publisher

Hindawi Limited

Subject

Endocrinology,Internal Medicine

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