Control of the L-Type Ca~(2+) Current by the NO-cGMP Cascade in Isolated Cardiomyocytes of Normotensive and Spontaneously Hypertensive Rats

摘要

The NO-cGMP cascade, which inhibits cal-cineurin/NFAT via PKG-mediated inhibition of Ca~(2+) currents, is an important protective mechanism in SHRs [7, 8]. The obtained data show that the NO-cGMP cascade alone is insufficient for suppressing isoproterenol-activated L-type Ca~(2+) currents. Combined action of the NO-cGMP system and acetylcholine is a necessary condition for the currents to return to their basal values. Moreover, the modulators of the NO-cGMP system per se do not change the amplitude of isoproterenol-acti-vated L-type Ca~(2+) currents, and acetylcholine only partly eliminates the activating effect of isoproterenol and cannot decrease the currents to their basal values. Therefore, a combined effect of the NO-cGMP system and acetylcholine is necessary to suppress L-type Ca~(2+) currents.