CORONARY HEMODYNAMICS IN AGING SPONTANEOUSLY HYPERTENSIVE AND NORMOTENSIVE WISTAR-KYOTO RATS

Citation
D. Susic et al., CORONARY HEMODYNAMICS IN AGING SPONTANEOUSLY HYPERTENSIVE AND NORMOTENSIVE WISTAR-KYOTO RATS, Journal of hypertension, 16(2), 1998, pp. 231-237
Citations number
31
Categorie Soggetti
Peripheal Vascular Diseas
Journal title
ISSN journal
02636352
Volume
16
Issue
2
Year of publication
1998
Pages
231 - 237
Database
ISI
SICI code
0263-6352(1998)16:2<231:CHIASH>2.0.ZU;2-S
Abstract
Objective io delineate hypertension-related and age-related changes in coronary hemodynamics and to assess the role of myocardial (i.e. left ventricular) hypertrophy and cardiac fibrosis in inducing progressive deterioration of coronary flow reserve associated both with hypertens ion and with aging. Methods Systemic and coronary hemodynamics (using radionuclide-labeled microspheres), right ventricular, left ventricula r, and aortic mass indexes, and ventricular hydroxyproline concentrati ons tan estimate of collagen) in normotensive Wistar-Kyoto and spontan eously hypertensive rats aged 22, 35, and 65 weeks were determined. Re sults Spontaneously hypertensive rats of all ages had greater left ven tricular and aortic masses, greater collagen concentrations in both ve ntricles, a lower coronary flow reserve, and greater minimal coronary vascular resistance after administration of dipyridamole than did Wist ar-Kyoto rats. Despite spontaneously hypertensive rats having only lef t ventricular hypertrophy, coronary hemodynamics were impaired to the same extent in both ventricles. Progressive increases in myocardial co llagen concentration, decreases in coronary flow reserve, and increase s in minimal coronary vascular resistance were observed in rats of bot h strains with aging. A positive correlation and linear regression bet ween myocardial collagen concentration and minimal vascular resistance were found for both ventricles of rats of both strains. Conclusions B oth aging and hypertension adversely affected the coronary circulation ; furthermore, these effects appeared to be additive. Cardiac fibrosis , but not hypertrophy, might play a role in progressive deterioration of coronary hemodynamics in aging and hypertension and could provide a n explanation for the diastolic dysfunction encountered clinically in older patients with hypertension. (C) 1998 Rapid Science Ltd.