[Effects of chronic administration of captopril on vascular reactivity of the rat aorta].

UNLABELLED

The vascular endothelial function is altered in certain vascular pathology such as arterial hypertension. However, the endothelial effect of the pharmacologic treatment of this pathology with angiotensin converting enzyme (ACE) inhibitor is poorly understood. To evaluate the effects of long-term treatment of captopril on the rat aortic vascular reactivity, 2 groups of spontaneously hypertensive rats (SHR) (n = 6) were studied for 12 weeks: the first group was treated with captopril (CAP) (2 g/l of water) while group 2 (OCAP) received no treatment. A third group without hypertension was considered as control group (CTL). At the end of the experiments, isolated aortic rings were studied in organ chambers for endothelial and smooth muscle vascular reactivity. The endothelial-dependent relaxations (EDR) to cumulative doses of acetylcholine, histamine or adenosine diphosphate were significantly decreased in the aortic segments of CTL compared to CAP (p < 0.05). Aortic segments from OCAP group demonstrated intermediate EDR responses between CAP and CTL groups. Smooth muscle relaxation to sodium nitroprusside was comparable among the 3 groups. Maximal smooth muscle contraction to progressive doses of norepinephrine was significantly higher in the CTL group compared to the hypertensive groups.

CONCLUSION

Spontaneously hypertensive rats have an increased basal vascular tone. The increased EDR observed with hypertension partially compensates this hypercontractility. Chronic hypertension treatment with captopril partially normalizes EDR responses in the rat aorta suggesting the lost of the endothelial compensatory mechanism by ACE inhibitors.