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This Article Full Text Full Text (PDF) All Versions of this Article: 289/1/F127    most recent 00397.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (12) Citing Articles via Google Scholar Google Scholar Articles by Facemire, C. S. Articles by Arendshorst, W. J. Search for Related Content PubMed PubMed Citation Articles by Facemire, C. S. Articles by Arendshorst, W. J.

Calmodulin mediates norepinephrine-induced receptor-operated calcium entry in preglomerular resistance arteries

Department of Cell and Molecular Physiology and Program in Integrative Vascular Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina

Submitted 1 November 2004 ; accepted in final form 2 February 2005

Although L-type voltage-dependent calcium channels play a major role in mediating vascular smooth muscle cell contraction in the renal vasculature, non-L-type calcium entry mechanisms represent a significant component of vasoactive agonist-induced calcium entry in these cells as well. To investigate the role of these non-voltage-dependent calcium entry pathways in the regulation of renal microvascular reactivity, we have characterized the function of store- and receptor-operated channels (SOCs and ROCs) in renal cortical interlobular arteries (ILAs) of rats. Using fura 2-loaded, microdissected ILAs, we find that the L-type channel antagonist nifedipine blocks less than half the rise in intracellular calcium concentration ([Ca²⁺]_i) elicited by norepinephrine. SOCs were activated in these vessels using the sarco/endoplasmic reticulum Ca²⁺ ATPase (SERCA) inhibitors cyclopiazonic acid and thapsigargin and were dose dependently blocked by the SOC antagonists Gd³⁺ and 2-aminoethoxydiphenyl borate (2-APB) and the combined SOC/ROC antagonist SKF-96365. Gd³⁺ had no effect on the non-L-type Ca²⁺ entry activated by 1 µM NE. A low concentration of SKF-96365 that did not affect thapsigargin-induced store-operated Ca²⁺ entry blocked 60–70% of the NE-induced Ca²⁺ entry. Two different calmodulin inhibitors (W-7 and trifluoperazine) also blocked the NE-induced Ca²⁺ entry. These data suggest that in addition to L-type channels, NE primarily activates ROCs rather than SOCs in ILAs and that this receptor-operated Ca²⁺ entry mechanism is regulated by calmodulin. Interestingly, 2-APB completely blocked the NE-induced non-L-type Ca²⁺ entry, implying that SOCs and ROCs in preglomerular resistance vessels share a common molecular structure.

receptor-operated channel; store-operated channel; vascular smooth muscle

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