Endothelium-dependent mechanical properties of the carotid artery in WKY and SHR. Role of angiotensin converting enzyme inhibition.

Author:

Levy B I1,Benessiano J1,Poitevin P1,Safar M E1

Affiliation:

1. Institut National de la Santé et de la Recherche Médicale, Hôpital Lariboisière, Paris, France.

Abstract

An experimental model of in situ isolated carotid arteries has been used to evaluate the static mechanical properties of the arterial wall in 12-week-old Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). The effects of endothelium removal and of local incubation with the converting enzyme inhibitor lisinopril (ICI Pharma 209000) on the carotid compliance (CC) were compared with the effects of total abolition of the vascular smooth muscle tone by potassium cyanide. CC measured for pressures ranging from 50 to 175 mm Hg had maximal values (0.22 +/- 0.07 microliter/mm Hg and 0.13 +/- 0.03 microliter/mm Hg, respectively, for WKY and SHR, p less than 0.001) for pressure values close to the operating pressures in both groups. Maximal values of CC were increased by 35% and 45% in WKY and SHR, respectively, after potassium cyanide poisoning (p less than 0.01). The endothelium removal induced a significant increase in CC compared with their control values (+37%, p less than 0.01, and +25%, p less than 0.01, respectively, in WKY and SHR). CC measured after endothelium removal did not significantly differ from its values measured after potassium cyanide poisoning in normotensive animals. In contrast, in hypertensive animals, CC was significantly lower after endothelium, removal than after potassium cyanide poisoning (p less than 0.01). In the presence of intact endothelium, local incubation with converting enzyme inhibitor increased CC by 23% (p less than 0.05) in WKY rats and by 14% (p less than 0.01) in SHR. In contrast, after endothelium removal, converting enzyme inhibitors did not significantly increase further CC in either strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Physiology

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