
Vasopressin and angiotensin receptors of the medial septal area in the control of mean arterial pressure induced by vasopressin
Author(s) -
Gabriela Maria Pavan de Arruda Camargo,
Wilson Abrão Saad,
Luiz Antônio de Arruda Camargo
Publication year - 2008
Publication title -
jraas. journal of the renin-angiotensin-aldosterone system/journal of the renin-angiotensin-aldosterone system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.457
H-Index - 46
eISSN - 1752-8976
pISSN - 1470-3203
DOI - 10.1177/1470320308095260
Subject(s) - vasopressin , mean arterial pressure , medicine , endocrinology , angiotensin ii , receptor , antagonist , arginine , vasopressin receptor , renin–angiotensin system , blood pressure , chemistry , heart rate , amino acid , biochemistry
. Brain arginine 8 -vasopressin (AVP), through the V 1a - and V 2 -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 V 1a -, V 2 - and V 1a /V 2 -AVP selective antagonists and AT 1 - and AT 2 -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 V 1a - and V 2 -antagonists reduced, whereas prior injection of the V 1a /V 2 -antagonist induced a decrease in the MAP that remained below the baseline. Both AT 1 - and AT 2 -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 V 1a - and V 2 -AVP and AT 1 and AT 2 -Ang II receptors in the MSA in the regulation of MAP.