Determination of role of sympathetic and renin-angiotensin systems in Goldblatt hypertension with urapidil and captopril.
The objective of this study was to determine the sympathetic and renin-angiotensin contributions to the control of blood pressure and renal blood flow (RBF) in conscious normotensive and Goldblatt hypertensive dogs. Urapidil (2 mg/kg), an alpha-adrenoceptor antagonist, and then captopril (0.2 mg/kg) were administered acutely intravenously (i.v.) to instrumented normotensive and two-kidney, one clip Goldblatt hypertensive dogs. Urapidil decreased mean arterial blood pressure (MAP) in the hypertensive (n = 11) and normotensive dogs (n = 9). Contralateral RBF was unchanged in the hypertensive, but was increased in the normotensive dogs. Captopril caused a further fall in MAP of the hypertensives and increased RBF. MAP of the normotensives was further decreased and RBF increased by captopril. Urapidil increased plasma renin activity in the normotensives, but not in the hypertensives, whereas heart rate was increased and renal vascular resistance was decreased in both groups. In nine hypertensive dogs, captopril alone (0.2 mg/kg i.v.) had a smaller effect on MAP and RBF than after alpha blockade. These results indicate that the combined influence of the sympathetic and renin-angiotensin systems accounts for a major portion of the MAP increase in two-kidney, one clip Goldblatt hypertension, and elimination of their influence causes profound hypotension and renal vasodilatation.[1]References
- Determination of role of sympathetic and renin-angiotensin systems in Goldblatt hypertension with urapidil and captopril. Zimmerman, B.G. J. Hypertens. (1984) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
