Why the study?
Does candesartan cilexetil improve left ventricular capillarity and reduce hypertrophy in stroke-prone spontaneously hypertensive rats?
Does candesartan cilexetil improve left ventricular capillarity and reduce hypertrophy in stroke-prone spontaneously hypertensive rats?
AT1-receptor blockade with candesartan cilexetil induces regression of cardiomyocyte hypertrophy and improves left ventricular capillarity via neoangiogenesis in a hypertensive rat model.
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Should not change clinical practice; extends preclinical data on AT1 blockade in hypertensive rat hearts.
The effect of the angiotensin II type 1 receptor blockade, candesartan cilexetil (TCV116), on the capillarity of the innermost region of the left ventricular subendocardium were studied in stroke-prone spontaneously hypertensive rats (SHRSP). The rats were fed for 32 days on chow that contained TCV116, the average dose being 0.96 mg/kg/day. Compared with values from control SHRSP, the systolic blood pressure, left ventricular weight and cross-sectional area of cardiomyocytes decreased. A significant increase in the total capillary density was coupled with a decrease of capillary domain areas in all capillary portions. The proportion of venular capillary portions, which was low in control SHRSP, increased significantly, suggesting neoangiogenesis of capillaries. The results indicate that AT1-receptor blockade caused regression of the hypertrophied cardiomyocytes and improved capillarity of the left ventricular wall.
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Xie et al. (1999) studied this question.
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