Regression of hypertrophy in small resistance vessels

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.