title: The role of voltage-dependent calcium channels in angiotensin-stimulated glomerulosa cells.
abstract: The concept that voltage-dependent Ca2+ influx is essential in the aldosterone stimulating action of angiotensin II (AII) has been recently challenged by the demonstration of the dihydropyridine (DHP) insensitive 'capacitative' Ca2+ uptake mechanism. The DHP-sensitivity of AII-induced aldosterone secretion is still to be explained. In rat glomerulosa cells the lag phase of AII-induced depolarization is more than 30 s, and there is no enhanced Ca2+ influx within the first min of stimulation. Yet we observed that DHPs as well as diltiazem influenced also the peak of cytoplasmic Ca2+ signal, although the peak (approximately 12 s) is attributed to Ca2+ release alone. Nifedipine reduced the Ca2+ transient induced by AII even after complete inhibition of Ca2+ channel activity. Recalling the loose attachment of InsP3 receptors (IP3R) to the plasma membrane, and the homology between the cytosolic domain of IP3R and the Ca2+ release channel (ryanodine receptor) of skeletal muscle, we proposed that DHP-sensitive L-type Ca2+ channels (DHP receptors) influence InsP3-induced Ca2+ release rather than Ca2+ influx in AII-stimulated cells. Although the dominant isoform is the neuroendocrine (D) one, the skeletal muscle isoform of L-type voltage-dependent Ca2+ channel is also expressed in rat glomerulosa cells. This isoform may be a candidate for protein-protein interaction between DHPR and subplasmalemmal IP3R, similarly to that occurring between DHP receptors and ryanodine receptors in skeletal muscle.
authors.affiliation: Dept. of Physiology, Semmelweis University of Medicine, Budapest, Hungary.
authors.forename: A
authors.initials: A
authors.lastname: Spät
authors.forename: T
authors.initials: T
authors.lastname: Rohács
authors.forename: A
authors.initials: A
authors.lastname: Horváth
authors.forename: G
authors.initials: G
authors.lastname: Szabadkai
authors.forename: P
authors.initials: P
authors.lastname: Enyedi
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism / Q000502:physiology*; D020746:Calcium Channels, L-Type; D002132:Calcium Radioisotopes; D003593:Cytoplasm / Q000378:metabolism; D004095:Dihydropyridines / Q000494:pharmacology; D004110:Diltiazem / Q000494:pharmacology; D004594:Electrophysiology; D053496:Inositol 1,4,5-Trisphosphate Receptors; D008345:Manganese / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D015384:Zona Glomerulosa / Q000502:physiology*
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D020746:Calcium Channels, L-Type; D002132:Calcium Radioisotopes; D004095:Dihydropyridines; D053496:Inositol 1,4,5-Trisphosphate Receptors; D018160:Receptors, Cytoplasmic and Nuclear; D000804:Angiotensin II; D008345:Manganese; C038806:1,4-dihydropyridine; D004110:Diltiazem; D011188:Potassium; D002118:Calcium