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Am J Physiol Heart Circ Physiol 279: H2879-H2888, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 6, H2879-H2888, December 2000

Distinct roles for L- and T-type Ca2+ channels in regulation of atrial ANP release

Jin Fu Wen1, Xun Cui1, Jin Sub Ahn2, Suhn Hee Kim1, Kyung Hwan Seul1, Sung Zoo Kim1, Young Kyung Park2, Ho Sub Lee3, and Kyung Woo Cho1,3

Departments of 1 Physiology and 2 Urology, Institute for Medical Sciences, Jeonbug National University Medical School, Jeonju 561-180; and 3 Department of Physiology, College of Oriental Medicine, Wonkwang University Medicinal Resources Research Center, Iksan 570-749, Korea

Atrial secretion of atrial natriuretic peptide (ANP) has been shown to be regulated by atrial workload. Although modulating factors for the secretion of ANP have been reported, the role for intracellular Ca2+ on the secretion of ANP has been controversial. The purpose of the present study was to define roles for L- and T-type Ca2+ channels in the regulation of ANP secretion in perfused beating rabbit atria. BAY K 8644 (BAY K) increased atrial stroke volume and pulse pressure. BAY K suppressed ANP secretion and ANP concentration in terms of extracellular fluid (ECF) translocation concomitantly with an increase in atrial dynamics. BAY K shifted the relationship between ANP secretion and ECF translocation downward and rightward. These results indicate that BAY K inhibits myocytic release of ANP. In the continuous presence of BAY K, diltiazem reversed the effects of BAY K. Diltiazem alone increased ANP secretion and ANP concentration along with a decrease in atrial dynamics. Diltiazem shifted relationships between ANP secretion and atrial stroke volume or ECF translocation leftward. The T-type Ca2+ channel inhibitor mibefradil decreased atrial dynamics. Mibefradil inhibited ANP secretion and ANP concentration in contrast with the L-type Ca2+ channel inhibitor. These results suggest that activation of L- and T-type Ca2+ channels elicits opposite effects on atrial myocytic release of ANP.

atria; atrial natriuretic peptide; secretion


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