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NEUROHUMORAL CONTROL OF CIRCULATION AND HYPERTENSION

Histamine inhibits atrial myocytic ANP release via H₂ receptor-cAMP-protein kinase signaling

¹Department of Physiology, Institute for Medical Sciences, Jeonbug National University Medical School, Jeonju 561-180; and ²Department of Herbal Resources, Wonkwang University Professional Graduate School of Oriental Medicine, Iksan 570-749, Korea

Submitted 29 October 2002 ; accepted in final form 22 April 2003

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 H₁ receptor 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 protein 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.

atrial natriuretic peptide; histamine receptors; L-type calcium channels

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