Based on previous studies, the myosins of rat ventricular myocardium have been separated by PGE into three isoenzymes, ie, V1, V2 and V3, whose electrophoretic mobility becomes slower and ATPase activity becomes lower in that order. Furthermore, under some physiological or pathological conditions, the rat ventricular myosin isoenzyme pattern changes in parallel with changes in myosin ATPase activity . Our results show that cardiac hypertrophy develops in Goldblatt rats (Table 1). In addition, the myosin isoenzymes were separated from the left ventricular myocardium and identified as V1, V2 and V3 in control and Goldblatt rats.
In Goldblatt rats, increased V3 and decreased V1 concentrations were observed (P<0.01). We have previously shown that there is no significant difference in the degree of myocardial contractility between hypertensive and normal rats, but that the maximum velocity of muscle shortening (dT/dt max) was significantly decreased in the former group. In a previous review, myocardial hypertrophy secondary to pressure overload was divided into physiological and pathological classes . The former is defined as “hypertrophy accompanied by a normal or augmented contractile state in which the maximum rate at which myosin hydrolyzes ATP and the maximum velocity of muscle shortening are either normal or elevated”. You are always offered finest quality buy cheap alegra at the pharmacy you can fully trust and enjoy being its customer. Why wouldn’t you, if it offers lowestprices in the industry and fast delivery that can be free for someorders?