ROLE OF THE BRAIN RENIN-ANGIOTENSIN SYSTEM IN THE MAINTENANCE OF BLOOD-PRESSURE IN CONSCIOUS SPONTANEOUSLY HYPERTENSIVE AND SINOAORTIC BARORECEPTOR-DENERVATED RATS

Citation
Jra. Paull et al., ROLE OF THE BRAIN RENIN-ANGIOTENSIN SYSTEM IN THE MAINTENANCE OF BLOOD-PRESSURE IN CONSCIOUS SPONTANEOUSLY HYPERTENSIVE AND SINOAORTIC BARORECEPTOR-DENERVATED RATS, Clinical and experimental pharmacology and physiology, 24(9-10), 1997, pp. 667-672
Citations number
25
Categorie Soggetti
Pharmacology & Pharmacy",Physiology
ISSN journal
03051870
Volume
24
Issue
9-10
Year of publication
1997
Pages
667 - 672
Database
ISI
SICI code
0305-1870(1997)24:9-10<667:ROTBRS>2.0.ZU;2-3
Abstract
1, Evidence suggesting an involvement of the brain renin-angiotensin s ystem (RAS) in the development/maintenance of hypertension in spontane ously hypertensive rats (SHR) relies, in part, on early experimental d ata reporting centrally mediated antihypertensive effects of saralasin , However, recent data using non-peptide AT(1) receptor antagonists do es not always support this theory because these compounds usually do n ot lower blood pressure when given centrally, 2, In the present study we have re-assessed the central effects of saralasin in conscious SHR as well as in sinoaortic baroreceptor-denervated (SAD) rats, Both of t hese models exhibit heightened sensitivity to the central presser effe cts of angiotensin II (AngII) and, thus, any potential antihypertensiv e activity would provide functional evidence of activated brain RAS me chanisms in these models, 3, In SHR, saralasin failed to lower mean ar terial pressure (MAP) when given intracerebroventricularly (i.c.v.) as bolus or infusion doses that blocked the centrally mediated presser e ffect of AngII, 4, In SAD rats, there was a marked impairment of the b aroreceptor-heart rate reflex function and enhanced centrally mediated presser responses to AngII. However, i.c.v. saralasin infusions again did not alter MAP. 5, Collectively these results suggest that the cen tral RAS is not involved in the maintenance of MAP in SHR and SAD rats , both of which are models exhibiting a functional hyperresponsiveness to AngII.