Effect of sympathetic nerves on composition and distensibility of cerebral arterioles in rats.

Abstract

1. The goals of this study were to examine the effects of chronic sympathetic denervation on the mechanics and composition of cerebral arterioles in normotensive Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). 2. We used an in vivo method to examine the mechanics of pial arterioles in 10- to 12-month-old, anaesthetized WKY and SHRSP that had undergone unilateral removal of the superior cervical ganglion at 1 month of age. Bilateral craniotomies were performed in each rat to expose pial arterioles in the innervated and denervated cerebral hemispheres. Arterioles were deactivated with EDTA. Incremental distensibility and stress-strain relationships were calculated from measurements of pial arteriolar pressure (servo null), diameter and cross-sectional area of the arteriolar wall. Point counting stereology was used to quantify volume density and cross-sectional area of individual components in the arteriolar wall. 3. Chronic sympathetic denervation reduced cross-sectional area of the arteriolar wall by 16 +/- 2% (mean +/- S.E. of mean; P less than 0.05) in WKY and 44 +/- 3% in SHRSP. During maximal dilatation with EDTA, incremental distensibility was reduced and the stress-strain curve was shifted to the left in denervated arterioles of SHRSP, but not WKY. These findings indicate that sympathetic denervation in SHRSP attenuates the development of hypertrophy in pial arterioles and reduces arteriolar distensibility. The ratio of non-distensible (collagen and basement membrane) to distensible (smooth muscle, elastin and endothelium) components was reduced in denervated arterioles in SHRSP, but not WKY. 4. Thus, sympathetic nerves have trophic effects on cerebral arterioles in WKY and, to a greater degree, in SHRSP. Sympathetic nerves also contribute to increases in distensibility of cerebral arterioles in SHRSP, but not WKY. The increase in arteriolar distensibility is accompanied by a disproportionate increase in the more compliant elements of cerebral arterioles.