Why the study?
Does early and chronic renin-angiotensin system (RAS) blockade improve left and right ventricular coronary vasodilatation reserve in experimental models of hypertension and chronic heart failure?
Does early and chronic renin-angiotensin system (RAS) blockade improve left and right ventricular coronary vasodilatation reserve in experimental models of hypertension and chronic heart failure?
RAS blockade improves coronary vasodilatation reserve in experimental models of hypertension and heart failure, primarily by preventing pericoronary fibrosis and vascular remodeling.
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Hypothesis-generating in experimental hypertension and CHF; leaves open clinical translation of RAS blockade for coronary reserve.
The aim of the present study was to investigate left and right ventricular (LV and RV, respectively) coronary vasodilatation reserve (CVR; fluorescent microsphere technique) in rats with hypertension (spontaneously hypertensive rats (SHR)) or congestive heart failure (CHF) and the effects of early and chronic renin-angiotensin system (RAS) blockade thereupon. 2. In adult SHR, both LV and RV CVR were impaired, especially in the non-hypertrophied RV, the main factor involved being coronary vascular remodelling. Blockade of the RAS normalized both LV and RV CVR, mainly through the prevention of hypertension and suppression of the resulting pericoronary fibrosis. 3. In postischaemic CHF rats, there was an early and severe degradation of LV and RV CVR that developed before any significant vascular remodelling and appeared to be linked to the deterioration of cardiac hypertrophy and haemodynamics. This degradation in CVR further worsened over the longer term due to late-developing pericoronary fibrosis and endothelial dysfunction. Blockade of the RAS had no early effects on LV and RV CVR, but improved RV CVR over the long term, mainly by limiting RV hypertrophy and by preventing the development of pericoronary fibrosis and coronary endothelial dysfunction. 4. In kallikrein-kinin system-deficient mice, CVR was not different from that of wild-type mice, suggesting that this system is not implicated in normal CVR regulation.
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Richer et al. (2001) studied this question.
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