Many studies have documented regression of
left ventricular hypertrophy following blood pressure control by some
antihypertensive agents but not by others. To determine whether similar differences in regression of wall thickening also occur in resistance vessels during treatment, matched control groups of spontaneously hypertensive rats (SHR) were treated for 12 weeks with either
hydralazine or
captopril + hydrochlorothiazide and compared with untreated SHR and Wistar-Kyoto rats (WKY). Perfusion pressure was then determined in the hind-limbs of pithed rats under conditions of constant blood flow (4.0 ml/min) and maximal vasodilatation as an index of thickening (
hypertrophy) of resistance vessel walls. Treatment with
hydralazine or
captopril + hydrochlorothiazide controlled blood pressure equally in SHR but had significantly different effects on both
left ventricular hypertrophy and resistance vessels. Perfusion pressure was reduced from 37.4 +/- 0.5 mmHg to 33.9 +/- 0.5 mmHg (P < 0.01) with
captopril + hydrochlorothiazide but only marginally to 35.9 +/- 0.3 mmHg with
hydralazine (P < 0.05 at some levels of flow and P > 0.05 at others). Left ventricular weight was significantly reduced by
captopril + hydrochlorothiazide (2.02 +/- 0.02 versus 2.63 +/- 0.05 mg/g, P < 0.01) but only to 2.44 +/- 0.05 by
hydralazine. Significant correlations were found both before and following treatment between perfusion pressure and left ventricular weight (r = 0.59, P < 0.01) but not between either of these two parameters and arterial pressure. Thus, despite equal blood pressure control, thickening of resistance vessel walls regressed more with
captopril + hydrochlorothiazide than with
hydralazine, suggesting that vascular
hypertrophy-like
left ventricular hypertrophy is not determined by blood pressure levels alone.