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(Hypertension. 1995;26:118-123.)
© 1995 American Heart Association, Inc.

Articles

Effects of Low and High Doses of Fosinopril on the Structure and Function of Resistance Arteries

Damiano Rizzoni; Maurizio Castellano; Enzo Porteri; Giorgio Bettoni; Maria Lorenza Muiesan; Angelo Cinelli; Enrico Agabiti Rosei

From Cattedra di Semeiotica e Metodologia Medica, UOP Scienze Mediche, University of Brescia (Italy).

Correspondence to Prof Enrico Agabiti Rosei, Cattedra di Semeiotica e Metodologia Medica, Scienze Mediche, University of Brescia, c/o 1a Medicina, Spedali Civili, 25100 Brescia, Italy.

Abstract It has been suggested that angiotensin-converting enzyme inhibitors may induce a significant regression of cardiovascular hypertrophy not only through blood pressure reduction but also as a possible consequence of growth factor inhibition. The aim of this study was to evaluate the effects of the angiotensin-converting enzyme inhibitor fosinopril, given either at a hypotensive high dose or a nonhypotensive low dose, on structural and functional alterations of mesenteric resistance arteries and on cardiac mass in spontaneously hypertensive rats (SHR) and control Wistar-Kyoto rats. Fosinopril was administered in the drinking water from 6 to 12 weeks of age. Rats were killed at 12 weeks, and the ratio of heart weight to body weight was measured. Mesenteric arterioles were dissected and mounted on a micromyograph (Mulvany's technique). Vascular morphology (media-lumen ratio, media thickness) and endothelial function (response to acetylcholine) were then assessed. During the 6 weeks of treatment, systolic pressure in SHR treated with high-dose fosinopril was significantly lower compared with that in untreated SHR, whereas no difference was observed with low-dose fosinopril. In SHR treated with both high-dose and low-dose fosinopril, a statistically significant reduction of vascular structural alterations, in terms of both media-lumen ratio and media thickness, was observed. The ratio of heart weight to body weight was reduced only in SHR treated with high-dose fosinopril. An improvement in the endothelium-dependent relaxation to acetylcholine was observed in SHR treated with high-dose fosinopril compared with untreated SHR, whereas in SHR treated with low-dose fosinopril no improvement in endothelial function was detected. In conclusion, low-dose fosinopril selectively prevented the structural but not functional vascular alterations in SHR, thus suggesting a possible interference of angiotensin-converting enzyme inhibitors with growth factors, at least in the peripheral vasculature.

Key Words: angiotensin-converting enzyme inhibitors • endothelium-derived relaxing factor • vascular resistance • hypertrophy • fosinopril • acetylcholine • rats, inbred SHR • endothelium

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