The adult rat's ventricular myocardium is able to increase its mass markedly while maintaining its unit quality. It does so by maintaining constant the design of the sarcomeres: an increase in length is accomplished by the addition of sarcomeres in series; an increase in tension production is accomplished by the addition of more cross-sectional area of a uniform quality. This was shown by the almost constant concentration of the contractile protein, actomyosin, as well as by the histologic evidence of the constancy in the sarcomere lengths. Functional support was obtained by the finding of an identity in the parameters of the length-tension curves; the curves differed only in the absolute magnitude of the tensions, a difference that completely disappeared when suitable corrections were made for the size of the muscle. The electrical parameters also indicated a lack of change in the quality of the excitatory membrane phenomena. However, some data were presented that suggest that the myocardium may show altered properties dependent on the age of the animal. No evidence was found in support of the concept of detrimental consequences at least with this degree of cardiomegaly. It is rather concluded that this degree of cardiomegaly is accomplished without change in the basic architecture, properties, or concentration of the contractile mechanism.

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Canrenone, a metabolic product of spironolactone, which competes with ouabain for binding to Na-K-ATPase at the digitalis receptor site and by itself inhibits Na-K-ATPase, was administered intramuscularly to reduced renal mass-saline drinking hypertensive and reduced renal mass-distilled water drinking normotensive rats for 8 days. Reduced renal mass-saline hypertension in the rat, is a low renin, volume expanded form of hypertension. Rats with this type of hypertension have been shown to have depressed arterial Na-K pump activity and increased Na-K pump inhibitory activity in their plasma. Canrenone treatment caused a progressive decrease in blood pressure in the hypertensive rats and this was associated with normalization of Na-K pump activity in arteries. Water and salt intake and excretion did not change. On the other hand, canrenone progressively increased blood pressure in the normotensive rats and this was associated with positive inotropy in isolated papillary muscles. These findings suggest that the depressed pump activity and the pump inhibitor play a role in reduced renal mass-saline hypertension in the rat and that the rise in blood pressure in the normotensive rats probably reflects canrenone's ability, by itself, to inhibit Na-K-ATPase.

The myocardial DNA, RNA, actomyosin, and total protein concentrations were determined in rat ventricles ranging between 251 and 1635 mg. Three phases of myocardial growth were evident. Phase 1 (ventricular weights less than 550 mg): DNA concentrations remained relatively constant with increasing ventricular weight. The increasing total DNA per ventricle suggests continuing mitotic activity. Phase 2 (ventricular weights between 550 and 1000 mg): total DNA per ventricle remained relatively constant; with ventricular growth there was a progressive decrease in DNA concentrations. This would be the phase of true myocardial hypertrophy. Phase 3: DNA concentrations continued to slowly decrease although the total DNA per ventricle increased. It would appear that this is the result of a renewed synthesis of DNA.In phases 1 and 2, the RNA concentrations progressively decreased, although the RNA/DNA ratio was increasing. This ratio appeared to reach its maximum value by the end of phase 2 and remain relatively constant in phase 3. Thus in phase 3, the concentrations of DNA and RNA simultaneously decreased to maintain this constant ratio. The ventricular total protein and ventricular actomyosin levels did not change over this range of ventricular weights.

In vitro tension development is significantly reduced in surviving left ventricular columnae carneae and ATP treated glycerol extracted fibers of ovariectomized albino rats. This reduction in contractility is paralleled by decrease in ventricular actomyosin content. Heart-body weight ratio, myocardial water content and total protein concentration are not abnormal. No changes in excitability or refractoriness of surviving bundles of castrate animals were found. Treatment with alpha estradiol, 0.1 µg/day, returned tension production and actomyosin concentration to the normal range. It is concluded that the contractile system of cardiac muscle, like that of the uterus, is dependent on estrogen. These data suggest a general action of the hormone on contractile protein synthesis in all types of muscle and have important implications regarding cardiac and other muscular functions.