Carotid arterial changes produced by a centrally mediated antihypertensive agent in hypertensive rats.

We studied the effects of centrally mediated reduction of sympathetic outflow on the mechanical properties of the carotid arterial wall in spontaneously hypertensive rats (SHR) as compared with matched Wistar-Kyoto rats (WKY). Ascending aortic pressure and flow were recorded in open-chest anesthetized rats, and the systemic arterial compliance (SAC) was calculated. Intravenous injection of rilmenidine induced a transient increase in blood pressure (BP) in WKY and SHR, followed by a long-lasting reduction in SHR, together with a decrease in cardiac output (CO) and heart (HR) and a significant increase in SAC. Serial measurements of internal carotid artery diameter made with a newly described echo-tracking technique showed a significant, rapid, and long-lasting constriction in both strains. In this set of experiments, the carotid compliance was determined from the arterial volume-pressure relation under control conditions and after administration of intravenous (i.v.) rilmenidine. In both WKY and SHR, carotid compliance increased, but the increase was observed only at the higher transmural pressure ranges and not at the operating systemic BP of the corresponding animals. Simultaneous recordings of the carotid arterial diameter made with the echo-tracking technique indicated that these compliance changes occurred in the presence of carotid arterial constriction at any given value of transmural pressure. Distensibility was increased in a higher pressure range: from 100 to 200 mm Hg transmural pressure. The centrally mediated antihypertensive agent rilmenidine produced carotid arterial constriction independent of BP changes and, in in vivo in situ carotid preparations, arterial constriction was associated with a decrease in the stiffness of the arterial wall.