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Tohoku J Exp Med. 1992 Jan;166(1):147-54. doi: 10.1620/tjem.166.147.

Renal hemodynamics in canine DOCA-salt hypertension: effect of calcium channel blockade.

The Tohoku journal of experimental medicine

B G Zimmerman, P C Raich

Affiliations

  1. Department of Pharmacology, University of Minnesota, Minneapolis 55455.

PMID: 1357781 DOI: 10.1620/tjem.166.147
Free Article

Abstract

Systemic arterial blood pressure (BP), renal blood flow (RBF), and renal vascular resistance (RVR) were followed for 3-4 wks during the progression of DOCA-salt hypertension in the conscious dog. Accompanying the gradual increase in BP was an increase in RBF; however, RVR was unchanged. The hypertension was totally reversed 5-7 days after cessation of DOCA-salt treatment, but the increase in RBF persisted, presumably as a result of renal hypertrophy. Renal adrenoceptor blockade with prazosin (6 dogs) and prazosin plus idazoxan (4 dogs) caused a comparable decrease in BP in the normotensive and DOCA-salt hypertensive dog; however, RVR was decreased only in the normotensive. Similar results were obtained during ganglionic blockade with hexamethonium. The i.v. infusion of diltiazem for 1 wk restored BP of the hypertensive dog to a normotensive level, and hexamethonium given i.v. had little further effect on either BP or RVR. These results suggest a non-neurogenically mediated mechanism of canine DOCA-salt hypertension that is susceptible to calcium channel blockade.

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