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1 Department of Physiology, Jeonbug National University Medical School and Institute for Medical Sciences, Jeonju, Republic of Korea
2 Department of Herbal Resources, Wonkwang University Professional Graduate School of Oriental Medicine, Iksan, Republic of Korea
* To whom correspondence should be addressed. E-mail: kwcho{at}moak.chonbuk.ac.kr.
Changes in cyclic nucleotide production and atrial dynamics have been known to modulate atrial natriuretic peptide (ANP) release. Although cardiac atrium expresses histamine receptors and contains histamine, the role of histamine in the regulation of ANP release has to be defined. The purpose of the present study was to define the effect of histamine on the regulation of ANP release in perfused beating rabbit atria. Histamine decreased ANP release concomitantly with increases in cAMP efflux and atrial dynamics in a concentration-dependent manner. Histamine-induced decrease in ANP release was a function of an increase in cAMP production. Blockade of histamine H2 receptor with cimetidine but not of H1receptor with triprolidine abolished the responses of histamine. Cell permeable cAMP analog, 8-Br-cAMP, mimicked the effects of histamine, and the responses were dose-dependent and blocked by a protin kinase A (PKA) selective inhibitor, KT5720. Nifedipine failed to modulate histamine-induced decrease in ANP release. Protein kinase nonselective inhibitor, staurosporine blocked histamine-induced changes in a concentration-dependent manner. KT5720 and Rp-adenosine 3',5'-cyclic monophosphorothioate, another PKA selective inhibitor, attenuated histamine-induced changes. These results suggest that histamine decreases atrial ANP release by H2 receptor-cAMP signaling via PKA-dependent and -independent pathways.
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