L-TYPE CALCIUM CHANNELS MODULATE THE REGRESSION OF LEFT VENTRICULAR HYPERTROPHY AFTER ACE-INHIBITION IN GENETIC HYPERTENSION

Abstract

The aim of this study was to investigate the possible link between the regression of the left ventricular mass induced by ACE-inhibition and L-type calcium channels. For this purpose, an evaluation of both L-type calcium channels and AT1receptor patterns in the left ventricular tissue of adult spontaneously hypertensive rats (SHR) was made before and after long-term treatment with ramipril. An abnormal density of both dihydropyridine and AT1receptors was observed in SHR at 24 weeks, compared to age-matched control Wistar–Kyoto (WKY) rats (dihydropyridine receptorBmax: 1.30±0.09vs1.14±0.06 pmol mg−1proteins,P<0.001; AT1receptorBmax: 1.35±0.07vs2.62±0.08,P<0.001 pmol mg−1proteins). A treatment for 10 weeks with ramipril induced a significant decrease in the left ventricular mass index of SHR, as well as a significant decrease in dihydropyridine receptor density (Bmax: 0.96±0.01vs1.39±0.08 pmol mg−1proteins,P<0.001) and a significant increase in AT1receptor density (Bmax: 3.08±0.26vs2.78±0.09 pmol mg−1proteins, ramipril-treated SHRvsvehicle-treated SHR,P<0.001). These results suggest that the decrease in left ventricular mass after treatment with ramipril may be dependent on changes in L-type calcium channels other than the direct effect on circulating and tissue angiotensin II (ang II) levels: involvement of calcium channels and subsequent calcium influx into cardiac cells could be proposed as an additional mechanism for the regression of left ventricular mass after ACE-inhibition.