Why the study?
Does coarctation of one renal artery alter Ca-activated specific actomyosin ATPase activity in Goldblatt rats?
Does coarctation of one renal artery alter Ca-activated specific actomyosin ATPase activity in Goldblatt rats?
In Goldblatt rats, moderate hypertrophy is associated with a progressive reduction in specific actomyosin ATPase activity, serving as an adaptive mechanism that parallels decreased myocardial shortening velocity.
Indicates potential adaptive response in rodent pressure overload; leaves open translation to human myocardial dysfunction or therapies.
Left ventricular myocardia of Goldblatt rats with an average increase in arterial blood pressure to about 200 mm Hg showed a progressive reduction of the Ca-activated specific acotmyosin ATPase activity 4 -12 weeks after the coarctation of one renal artery, as compared with controls of the same age. During the same period, a significant increase in the concentration of contractile proteins was noticeable, whereas the content of nonprotein substances and of water corresponded to the control values. The hydroxyproline concentration, as a measure of the collagen tissue content, increased only after 24 weeks. The time course of the specific ATPase activity was closely parallel to the decrease in the unloaded myocardial shortening velocity, as estimated at the same stage by our group. This is in accordance with the assumption of a fundamental relationship between the two values. The reduced rate of energy turnover and of the shortening velocity is regarded as an adaptive mechanism which, however, has a negative effect in advanced hypertrophy when further diminution takes place. The decrease in the specific enzymatic activity of actomysin is not necessarily linked to a large increase in myocardial mass, but is already apparent at moderate degrees of hypertrophy (34%).
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Medugorac et al. (1976) studied this question.
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