title: Osmoregulation of atrial myocytic ANP release: osmotransduction via cross-talk between L-type Ca2+ channel and SR Ca2+ release.
abstract: Hyperosmolality has been known to increase ANP release. However, its physiological role in the regulation of atrial myocytic ANP release and the mechanism by which hyperosmolality increases ANP release are to be defined. The purpose of the present study was to define these questions. Experiments were performed in perfused beating rabbit atria. Hyperosmolality increased atrial ANP release, cAMP efflux, and atrial dynamics in a concentration-dependent manner. The osmolality threshold for the increase in ANP release was as low as 10 mosmol/kgH2O (approximately 3%) above the basal levels (1.55 +/- 1.71, 17.19 +/- 3.11, 23.15 +/- 5.49, 54.04 +/- 11.98, and 62.00 +/- 13.48% for 10, 20, 30, 60, and 100 mM mannitol, respectively; all P < 0.01). Blockade of sarcolemmal L-type Ca2+ channel activity, which increased ANP release, attenuated hyperosmolality-induced increases in ANP release (-13.58 +/- 4.68% vs. 62.00 +/- 13.48%, P < 0.001) and cAMP efflux but not atrial dynamics. Blockade of the Ca2+ release from the sarcoplasmic reticulum, which increased ANP release, attenuated hyperosmolality-induced increases in ANP release (13.44 +/- 7.47% vs. 62.00 +/- 13.48%, P < 0.01) and dynamics but not cAMP efflux. Blockades of Na+-K+-2Cl- cotransporter, Na+/H+ exchanger, and Na+/Ca2+ exchanger had no effect on hyperosmolality-induced increase in ANP release. The present study suggests that hyperosmolality regulates atrial myocytic ANP release and that the mechanism by which hyperosmolality activates ANP release is closely related to the cross-talk between the sarcolemmal L-type Ca2+ channel activity and sarcoplasmic reticulum Ca2+ release, possibly inactivation of the L-type Ca2+ channels.
authors.affiliation: Department of Physiology, Institute for Medical Sciences, Jeonbug National University Medical School, Republic of Korea.
authors.forename: Jing Yu
authors.initials: JY
authors.lastname: Jin
authors.forename: Jin Fu
authors.initials: JF
authors.lastname: Wen
authors.forename: Dan
authors.initials: D
authors.lastname: Li
authors.forename: Kyung Woo
authors.initials: KW
authors.lastname: Cho
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000502:physiology*; D000242:Cyclic AMP / Q000378:metabolism; D006325:Heart Atria / Q000378:metabolism; D066298:In Vitro Techniques; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism*; D009543:Nifedipine / Q000494:pharmacology; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D011817:Rabbits; D011863:Radioimmunoassay; D020239:Receptor Cross-Talk / Q000502:physiology*; D012433:Ryanodine / Q000494:pharmacology; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*; D019831:Sodium-Calcium Exchanger / Q000378:metabolism; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism; D028021:Sodium-Potassium-Chloride Symporters / Q000378:metabolism; D019284:Thapsigargin / Q000494:pharmacology; D014882:Water-Electrolyte Balance / Q000502:physiology*
chemical_list: D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D047428:Protein Kinase Inhibitors; D019831:Sodium-Calcium Exchanger; D017923:Sodium-Hydrogen Exchangers; D028021:Sodium-Potassium-Chloride Symporters; D012433:Ryanodine; D019284:Thapsigargin; D009320:Atrial Natriuretic Factor; D000242:Cyclic AMP; D009543:Nifedipine; D002118:Calcium