Effects of α-Adrenoceptor Antagonists on Striated Muscle Microcirculation of Conscious Rats

Abstract

Recent studies have shown an important role for the microcirculation in the pathogenesis and maintenance of hypertension (Bohlen 1989; Schmid-Schonbein & Chien 1986).The greatest increase in vascular resistance occurs in the smallest arteries and arterioles, of which the most important are those in skeletal muscle (Evenwel et al. J983). Mechanisms that cause elevated microvascular resistance are not yet completely understood but arteriolar diameters have been shown to be decreased (Bohlen 1983; Le Noble et al. 1990), perhaps because of a decrease in vascular wall: lumen ratio or an increase in microvascular tone. Furthermore, the absolute number of arterioles may be decreased , either temporarily (functional rarefaction) or permanently (anatomical or structural rarefaction). Adrenergic mechanisms play an important role in the regulation of vascular diameter and tone in general. There are several reports indicating that various vessel types are subserved by different a-adrenoceptor populations (Alabaster & Davey 1984; De Mey & Vanhoutte 1981; Heusch et al. 1984; Langer & Hicks 1984), and differences in aadrenoceptor subtype distribution might be involved in differential regulation of vascular tone at distinct vascular levels and in various beds (Faber 1988; Faber et al. 1988). Regulation of peripheral resistance via microvascular effects is essential for the explanation of the antihypertensive effects of o-adrenoceptor antagonists. Therefore , we investigated the effects of specific aland az-adrenoceptor antagonists on microvessels of the cutaneous maximus muscle of conscious spontaneously hypertensive rats (SHR).