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Cardiomyopathy produced in rats with acute renal hypertension.

Acute renal hypertension was produced in Sprague-Dawley female rats by the AL between the origins of the renal arteries. These were compared with an LN group. A sham group in which the ligature was placed but not tied was also prepared. MAP was recorded, and the animals were sacrificed at 1, 2, or 4 days after surgery. The hearts were examined histologically, and the lesions, consisting of focal or confluent necrosis of myocardial fibers with mononuclear cellular infiltrate, were scored. In the AL group the intensity of the lesions increased with time. The score on day 1 was 0.92 +/- 0.09; on day 2, 1.37 +/- 0.08; and on day 4, 1.75 +/- 0.01. Values at comparable intervals in the LN group were 0.14 +/- 0.04, 0.27 +/- 0.12, and 0.09 +/- 0.07, respectively (p less than 0.001). No coronary lesions were found. Arterial pressures were significantly elevated in the AL group but not in the LN or sham groups. Ventricular water and potassium were unchanged with the exception of a significant decrease of [K+] in the AL group 2 days after ligation. It is concluded that rats with acute renal hypertension develop cardiac necrosis, with a secondary fall in myocardial [K+]. The possibility that this is due to endogenous renin-angiotensin will require further study.