Differential responses of the heart and vasculature to chronic blood pressure reduction in essential hypertension.
BACKGROUND: In subjects with hypertension, converting enzyme inhibitors and calcium entry blockers may decrease arterial stiffness independently of blood pressure changes, but the heterogeneity of response of the arterial tree has never been taken into account. MATERIAL AND METHODS: In 31 subjects with hypertension, we determined through the use of Doppler echographic techniques the compliance and distensibility of the common carotid and femoral arteries and of the abdominal aorta, the radial artery wall thickness, and cardiac mass. In a double-blind randomized study, the converting enzyme inhibitor ramipril and the calcium entry blocker nitrendipine were studied and compared during 12 weeks treatment, then 4 weeks after treatment was stopped. RESULTS: The two drugs caused significantly different plasma levels of active renin, angiotensin I, and norepinephrine but the same effects on blood pressure, cardiac mass, radial artery wall thickness, and stiffness indices. In contrast, the effect of treatment differed substantially according to the site of cardiovascular measurements. Although cardiac mass decreased significantly in parallel with blood pressure reduction, no change in radial artery wall thickness occurred. Carotid compliance and distensibility increased significantly, even after drug treatment was stopped, whereas little or no change was observed for the femoral artery and the abdominal aorta. CONCLUSION: This study provides evidence that the changes in cardiovascular structure and function with ramipril and nitrendipine treatment are poorly influenced by their different mechanisms of action but highly dependent on the site of measurements. The results suggest that local autocrine-paracrine mechanisms act synergistically with blood pressure to produce cardiovascular changes.[1]References
- Differential responses of the heart and vasculature to chronic blood pressure reduction in essential hypertension. Lafleche, A., Gautier, S., Topouchian, J., Wilmet, C.S., Girerd, X., Safar, M.E., Benetos, A. Clin. Pharmacol. Ther. (1998) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
