This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sano, T. Articles by Tarazi, R. C. Search for Related Content PubMed PubMed Citation Articles by Sano, T. Articles by Tarazi, R. C.

Circulation, Vol 75, 618-626, Copyright © 1987 by American Heart Association

ARTICLES

Differential structural responses of small resistance vessels to antihypertensive therapy

T Sano and RC Tarazi

Regression of left ventricular hypertrophy after control of blood pressure has been documented with some antihypertensive agents but not with others. To determine whether similar differences in regression of wall thickening also occur in resistance vessels during treatment, matched groups of spontaneously hypertensive rats (SHR) were treated for 12 weeks with either hydralazine (H) or captopril and hydrochlorothiazide (C-D) and they were compared with untreated SHR and Wistar-Kyoto rats (WKY). Perfusion pressure was then determined in the hindlimbs of pithed rats under conditions of constant blood flow (4.0 ml/min) and maximal vasodilation (hemodilution to 22% hematocrit combined with continuous nitroprusside and papaverine infusion). This perfusion pressure, which has been validated as an index of thickening (hypertrophy) of resistance vessels walls, averaged 26.8 +/- 0.4(SE) mm Hg in untreated WKY (n = 12) and 37.6 +/- 0.4 mm Hg in untreated SHR (n = 11) (p less than .01). Treatment with H or C-D controlled blood pressure equally in SHR, but the two drugs had significantly different effects on both left ventricular hypertrophy and resistance vessels. Perfusion pressure was reduced from 37.6 +/- 0.4 mm Hg to 34.0 +/- 0.5 mm Hg (p less than .01) with C-D but only to 36.5 +/- 0.5 mm Hg with H (NS). Left ventricular weight was significantly reduced by C-D (2.02 +/- 0.02 vs 2.63 +/- 0.05 mg/g, p less than .01) but only to 2.44 +/- 0.05 mg/g by H.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				P. A. Thurmann, N. Stephens, A. M. Heagerty, P. Kenedi, G. Weidinger, and N. Rietbrock Influence of Isradipine and Spirapril on Left Ventricular Hypertrophy and Resistance Arteries Hypertension, September 1, 1996; 28(3): 450 - 456. [Abstract] [Full Text]

				R. Tatchum-Talom, N. Niederhoffer, F. Amin, T. Makki, P. Tankosic, and J. Atkinson Aortic Stiffness and Left Ventricular Mass in a Rat Model of Isolated Systolic Hypertension Hypertension, December 1, 1995; 26(6): 963 - 970. [Abstract] [Full Text]