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| Item type: | Article | ||||||||||||||||||||||||||||||||||||||||
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| Journal or Publication Title: | Proceedings of the National Academy of Sciences of the United States of America = PNAS | ||||||||||||||||||||||||||||||||||||||||
| Publisher: | National Academy of Sciences | ||||||||||||||||||||||||||||||||||||||||
| Volume: | 86 | ||||||||||||||||||||||||||||||||||||||||
| Number of Issue or Book Chapter: | 9 | ||||||||||||||||||||||||||||||||||||||||
| Page Range: | pp. 3423-3427 | ||||||||||||||||||||||||||||||||||||||||
| Date: | 1989 | ||||||||||||||||||||||||||||||||||||||||
| Institutions: | Biology, Preclinical Medicine > Institut für Physiologie > Prof. Dr. Armin Kurtz | ||||||||||||||||||||||||||||||||||||||||
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| Classification: |
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| Dewey Decimal Classification: | 500 Science > 570 Life sciences 600 Technology > 610 Medical sciences Medicine | ||||||||||||||||||||||||||||||||||||||||
| Status: | Published | ||||||||||||||||||||||||||||||||||||||||
| Refereed: | Yes, this version has been refereed | ||||||||||||||||||||||||||||||||||||||||
| Created at the University of Regensburg: | Unknown | ||||||||||||||||||||||||||||||||||||||||
| Item ID: | 26981 |
Abstract
Simultaneous patch-clamp and fura-2 measurements were used to investigate the electrical properties and receptor-mediated changes of intracellular calcium in renal juxtaglomerular cells. Here we report the presence of voltage-activated inward and outward rectifying potassium currents and the inhibition of the anomalous inward rectifying potassium current by angiotensin II (ANG-II). This action of ...
Abstract
Simultaneous patch-clamp and fura-2 measurements were used to investigate the electrical properties and receptor-mediated changes of intracellular calcium in renal juxtaglomerular cells. Here we report the presence of voltage-activated inward and outward rectifying potassium currents and the inhibition of the anomalous inward rectifying potassium current by angiotensin II (ANG-II). This action of ANG-II was mimicked by guanosine 5'-[gamma-thio]triphosphate but not by cAMP, cGMP, inositol 1,4,5-trisphosphate, or phorbol ester, suggesting that ANG-II inhibits the potassium channel directly by means of a guanine nucleotide-binding regulatory protein or by means of an unusual type of second messenger. Blocking of the inward rectifier was paralleled by membrane depolarization, but we obtained no evidence for calcium entry due to voltage-gated calcium channels in juxtaglomerular cells. Instead, under voltage clamp, ANG-II and guanosine 5'-[gamma-thio]triphosphate induced release of calcium from intracellular stores followed by a sustained phase of transmembrane calcium influx and oscillations of intracellular Ca2+ concentrations. Changes in intracellular Ca2+ concentrations were found to depend on the extracellular Ca concentration--i.e., the sustained elevation was abolished in absence of extracellular Ca, and the frequency of repetitive calcium release was directly related to the extracellular concentration of calcium. Moreover, an elevation of extracellular Ca concentration by itself induced release of intracellular calcium in the absence of other stimuli. Changes in intracellular Ca2+ concentrations were accompanied by prominent calcium-activated chloride currents, and this mechanism is inferred to be responsible for the inhibitory role of calcium in renin secretion. Intracellular application of cAMP but no cGMP inhibited ANG-II and guanosine 5'-[gamma-thio]triphosphate induced calcium mobilization in juxtaglomerular cells, being consistent with the facilitatory effects of elevated cAMP levels of renin release. The frequency of ANG-II induced oscillations was also markedly attenuated at depolarized membrane potentials suggesting effective negative feedback control of ANG-II-induced depolarization on repetitive Ca2+ transients induced by the hormone.
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