title: Differential regulation of cytosolic calcium between afferent arteriol ar smooth muscle cells from mouse kidney.
abstract: Using a combination of whole-cell patch-clamping and calcium microspectrofluorimetry we have examined the calcium regulation and calcium-activated electrical currents in smooth muscle cells along mouse renal afferent arterioles. In cells located at a distance up to 50microm from the glomerular vascular pole, guanosine 5'-[gamma-thio]triphosphate, (GTP[tau -S], 100micromol/l) and angiotensin II (1micromol/l) evoked internal calcium mobilization and oscillations of intracellular calcium concentration. Membrane depolarization up to +30mV did not increase cytosolic free calcium in these cells, which displayed calcium-activated chloride currents. In cells located more distant than 100microm from the glomerular vascular pole, GTP[tau -S] did not increase cytosolic calcium at negative membrane potentials. Depolarization of these cells to 0mV or positive membrane potentials increased intracellular calcium in a dihydropyridine-sensitive manner. These cells responded to angiotensin II with single calcium transients and also displayed calcium-activated chloride currents. These findings suggest that intracellular calcium is differentially regulated between afferent arteriolar smooth muscle cells from mouse kidney: in smooth muscle cells which are distant from the glomerular vascular pole, cytosolic calcium is increased primarily via calcium influx through potential-operated calcium channels, whilst in cells which are close to the vascular pole intracellular calcium is elevated predominantly via mobilization from internal stores. Both cell types are equipped with receptors for angiotensin II and possess calcium-activated chloride channels.
authors.affiliation: Institut für Physiologie I, Universität Regensburg, Universitätsstrasse 31, D-93040 Regensburg, Germany.
authors.forename: H
authors.initials: H
authors.lastname: Scholz
authors.forename: A
authors.initials: A
authors.lastname: Kurtz
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000166:cytology / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D002120:Calcium Channel Agonists / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism*; D004594:Electrophysiology; D066298:In Vitro Techniques; D015640:Ion Channel Gating / Q000502:physiology; D007668:Kidney / Q000098:blood supply* / Q000166:cytology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D002120:Calcium Channel Agonists; D015220:Calcium Channels; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D002118:Calcium