Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

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

Authors: Pavan de Arruda Camargo, GM  Abrao Saad, W  De Arruda Camargo, LA 
Citation: Pavan de Arruda Camargo GM, etal., J Renin Angiotensin Aldosterone Syst. 2008 Sep;9(3):133-8.
Pubmed: (View Article at PubMed) PMID:18957383
DOI: Full-text: DOI:10.1177/1470320308095260

INTRODUCTION: 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.

Annotation

Gene Ontology Annotations
Objects Annotated

Additional Information

 
RGD Object Information
RGD ID: 2301925
Created: 2008-11-07
Species: All species
Last Modified: 2008-11-07
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.