title: Distinct roles for L- and T-type Ca(2+) channels in regulation of atrial ANP release.
abstract: 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 Ca(2+) on the secretion of ANP has been controversial. The purpose of the present study was to define roles for L- and T-type Ca(2+) 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 Ca(2+) channel inhibitor mibefradil decreased atrial dynamics. Mibefradil inhibited ANP secretion and ANP concentration in contrast with the L-type Ca(2+) channel inhibitor. These results suggest that activation of L- and T-type Ca(2+) channels elicits opposite effects on atrial myocytic release of ANP.
authors.affiliation: Department of Physiology, Institute for Medical Sciences, Jeonbug National University Medical School, Jeonju 561-180, Korea.
authors.forename: J F
authors.initials: JF
authors.lastname: Wen
authors.forename: X
authors.initials: X
authors.lastname: Cui
authors.forename: J S
authors.initials: JS
authors.lastname: Ahn
authors.forename: S H
authors.initials: SH
authors.lastname: Kim
authors.forename: K H
authors.initials: KH
authors.lastname: Seul
authors.forename: S Z
authors.initials: SZ
authors.lastname: Kim
authors.forename: Y K
authors.initials: YK
authors.lastname: Park
authors.forename: H S
authors.initials: HS
authors.lastname: Lee
authors.forename: K W
authors.initials: KW
authors.lastname: Cho
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000378:metabolism*; D012634:Bodily Secretions / Q000187:drug effects; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000502:physiology*; D020747:Calcium Channels, T-Type / Q000502:physiology*; D004110:Diltiazem / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism; D006325:Heart Atria / Q000378:metabolism; D066298:In Vitro Techniques; D020748:Mibefradil / Q000494:pharmacology; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D011817:Rabbits; D013318:Stroke Volume / Q000187:drug effects
chemical_list: D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D020747:Calcium Channels, T-Type; D020748:Mibefradil; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009320:Atrial Natriuretic Factor; D004110:Diltiazem