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Dual roles of CNP on intracellular calcium and atrial dynamics NPRB-phosphodiesterase-calcium signaling


, : Dual roles of CNP on intracellular calcium and atrial dynamics NPRB-phosphodiesterase-calcium signaling. FASEB Journal 16(5): A841, March 22

Effects of particulate guanylyl cyclase-coupled natriuretic peptide receptor (NPR)-B-cGMP signaling on the contractility, cAMP and (Ca2+)i transients were investigated in beating rabbit atria and atrial myocytes under basal and adenylyl cyclase (AC) activated conditions. C-type natriuretic peptide (CNP), a specific activator for NPR-B, inhibited atrial dynamics with an increase in cGMP but not cAMP production in a basal condition. CNP inhibited (Ca2+)i transients in single beating atrial myocytes. In contrast, in a condition of AC activation with forskolin, CNP augmented the stimulated atrial contractility concomitantly with a further increase in cAMP production and myocytic (Ca2+)i transients. The augmentation of the stimulated contractility and (Ca2+)i transients was reversed and the augmented cAMP increase was blocked by the combined treatment with an inhibitor of cGMP-inhibited phosphodiesterase (PDE3), milrinone. An inhibitor of cGMP-stimulated phosphodiesterase (PDE2), erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA), attenuated the CNP-induced inhibitions in (Ca2+)i transients and contractility in the presence or absence of forskolin plus milrinone. These data provide direct evidence for cAMP level-dependent distinct roles of NPR-B-activated cGMP for the regulation of atrial dynamics, cAMP production and (Ca2+)i transients.

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