Aortic perfusion pressure, protein synthesis, and protein degradation.

An increase in aortic pressure from 60 to 120 mm Hg accelerated protein synthesis and inhibited protein degradation in isolated rat hearts perfused as Langendorff preparations. This elevation of aortic pressure raised intraventricular pressure development, coronary flow, and oxygen consumption. The effect of aortic pressure on protein turnover was dissociated from intraventricular pressure development, contractile activity, and oxygen consumption by use of beating-drained and arrested-drained preparations. Results of other experiments argued against coronary flow as a determinant of rates of protein synthesis and degradation. These results indicated that effects of elevated aortic pressure on protein turnover were caused by stretch of the ventricular wall via its engorgement with blood, the so-called erectile properties of the heart or "garden-hose effect." These effects on protein turnover may be of importance in initiating hypertrophy of the heart secondary to pressure or volume overload.