Myocardial morphology in spontaneously hypertensive and aortic‐constricted rats

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Abstract
The cellular and subcellular adaptations in the myocardium of spontaneously hypertensive rats (SHR) were compared with those in Kyoto‐Wistar normotensive rats with cardiac hypertrophy induced by constriction of the abdominal aorta (ACR). Hypertensive blood pressure levels were attained at eight weeks of age in SHR and coincided with the surgically‐induced pressure‐overload in ACR at this age. Specimens from the subepicardial and subendocardial regions of the myocardium from glutaraldehyde‐perfused‐fixed hearts of 16‐week‐old animals were compared.Spontaneous hypertension and aortic constriction are associated with significant and comparable increases in heart rate, blood pressure, heart weight, and left ventricular muscle fiber diameter. While the cardiomegaly in both models was accompanied by a decrease in capillary density, the decrement was greater in the aortic‐constricted rats. Stereological analysis of cardiocytes revealed an increase in myofibril/cell‐volume, and a decrease in mitochondria/myofibril‐volume ratios in both models of cardiomegaly. In addition, double intercalated discs and subsarcolemmal foci containing abundant sarcoplasm with numerous small mitochondria, free filaments and Golgi complexes were commonly observed in both experimental groups. Cell diameter increased by a larger increment in the subendocardium than in the subepicardium, but capillary density was similar in these two regions. While aortic constriction was associated with dilatation of T‐tubules and the non‐specialized junctions of the intercalated disc, the myocardial ultrastructure of SHR was characterized by a greater number of lipid droplets and an increased folding of the intercalated discs comprising the subendocardial region.These findings suggest that data based on surgically‐induced pressure‐overload should be extrapolated cautiously to cardiomegaly associated with spontaneous hypertension. The differences between the adaptations in the two models may be due to either (1) the rate at which hypertrophy occurs or (2) some other, possibly genetic, factors unique to SHR.