Abstract
This study was to define the role of CNP-activated particulate (p) guanylyl cyclase (GC)-cGMP-phosphodiesterase (PDE) 3 signaling in the regulation of atrial cAMP levels, contractile and secretory functions in the cardiac atrium from hyperthyroid rabbit. Experiments were performed in perfused beating rabbit atria. CNP (0.1 μM) increased cGMP and cAMP efflux by 176.72 ± 17.69 and 55.31 ± 10.02%, respectively, in the atria from sham-treated control rabbits. CNP decreased atrial stroke volume and myocytic ANP release by 54.21 ± 7.33 and 60.85 ± 3.79%, respectively. Pretreatment with milrinone blocked CNP-induced increase in cAMP but without significant changes in atrial dynamics and ANP release. In the atria from hyperthyroid rabbit, CNP-induced increase in cGMP levels was accentuated, while CNP-induced increase in cAMP was attenuated. The gain of cAMP, i.e., change in cAMP efflux concentration in terms of cGMP was attenuated in the atrium from hyperthyroid rabbit compared to sham. CNP rather increased atrial stroke volume instead of decrease. CNP-induced decrease in atrial myocytic ANP release was attenuated. Pretreatment with milrinone blocked CNP-induced increase in cAMP levels concomitantly with a decrease in atrial stroke volume. These data demonstrate that dysfunction of pGC-cGMP-PDE3-cAMP signaling is involved in the pathophysiology of hyperthyroid heart. Supported by NSFC (No30570669).
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