Role of endothelium in the mechanical response of the carotid arterial wall to calcium blockade in spontaneously hypertensive and Wistar-Kyoto rats

Abstract

Objectives: Calcium blockade has been reported to inhibit the contraction of the vascular smooth muscle and the liberation of vasoactive substances by endothelial cells. We tested the effects of calcium blockade on the mechanical properties of the carotid artery in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) in the presence and in the absence of endothelium.

Methods: The pressure-volume relationships of isolated carotid arteries were recorded in situ in SHR (n = 20) and WKY rats (n = 20) before and after calcium blockade by local incubation with clentiazem.

Results: With intact endothelium, calcium blockade induced a significant shift in the pressure-volume curve in both strains, volume being significantly higher after calcium blockade than under control conditions. In WKY rats the carotid mechanical properties were similar after calcium blockade and after abolition of the smooth muscle tone by potassium cyanide (KCN) poisoning. In SHR the carotid compliance measured after incubation with clentiazem was significantly lower than that measured after KCN poisoning. Removal of the endothelium induced a significant shift in the pressure-volume curve towards the volume axis in both strains, and an increase in carotid compliance. Local incubation with clentiazem or KCN did not induce further modifications of the pressure-volume relationship either in WKY rats or in SHR. Furthermore, in SHR and WKY rat carotid arteries, the pressure-volume relationship and the compliance measured after incubation with clentiazem were identical in the presence and in the absence of endothelium.

Conclusions: In WKY rat and SHR carotid arteries, acute calcium blockade increases the arterial compliance independently of the endothelium integrity. Furthermore, part of the compliance enhancement induced by the calcium antagonist could be related to an antagonizing mechanism of the production of endothelial constricting factor or factors.