Certain prostaglandins (PGE2, PGF2 alpha, PGI2) are potent inhibitors of rat heart (Na+ + K+)-ATPase, though the relationship to their inotropic effects remains uncertain.
Prostaglandin inhibition of rat cardiac Na/K-ATPase is hypothesis-generating; leaves open links to inotropy and human relevance.
The ability of prostaglandins (PG) D2, E1, E2, F2 alpha and I2 (2.8 X 10(-11) to (2.8 X 10(-7) M) to modify Ca2+, Mg2+ and (Na+ + K+)-ATPase activities of rat heart sarcolemmal membrane fractions was examined. Administration of PGE2, PGF2 alpha, and PGI2 reduced basal (Na + + K+)-ATPase activity by up to 30, 80, and 80%, respectively. PGE1 and PGD2 were ineffective at any concentration. Neither Mg2+ -ATPase nor Ca2+ -ATPase was affected by PG treatment. Kinetic analysis revealed that the (Na+ + K+)-ATPase activity reducing ability of PGE2, PGF2 alpha and PGI2 was of a complex nature involving a reduction in Vmax and an elevation of the respective K values for either substrate or activator. These results demonstrate that some PG's are potent inhibitors of rat heart (Na+ + K+)-ATPase. These PG's produced varied inotropic influences on isolated heart preparations and it is uncertain whether their myocardial actions are dependent on enzyme inhibition.
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Karmazyn et al. (1981) studied this question.
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