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Cellular Calcium Regulation in Hypertension

Hermsmeyer, K. ; Erne, P.

In: American Journal of Hypertension, 1989, vol. 2, no. 8, p. 655-658

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    Title
    • Cellular Calcium Regulation in Hypertension
    Author
    • Hermsmeyer, K.. Chiles Research Institute, Providence Medical Center and Departments of Medicine and Cell Biology, Oregon Health Science University, Portland, Oregon, and Department of Pharmacology and The Cardiovascular Center, University of Iowa, Iowa City, Iowa.
    • Erne, P.. Chiles Research Institute, Providence Medical Center and Departments of Medicine and Cell Biology, Oregon Health Science University, Portland, Oregon, and Department of Pharmacology and The Cardiovascular Center, University of Iowa, Iowa City, Iowa.
    Document Type
    • Postprint
    Language
    • English
    Published in
    • American Journal of Hypertension, 1989, vol. 2, no. 8, p. 655-658. Oxford University Press
    Other Version
    OAI-PMH Identifier
    • oai:doc.rero.ch:293809
    Summary
    In vascular muscle cells, two distinct types of functionally important calcium (Ca2++) channels, called transient (T) and sustained (L), are differentiated by dihydropyridine calcium antagonists (CaA). We studied the ratio of T/L Ca2++ channels in isolated, spontaneously contracting azygous venous cells of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) by quantitating Ca2++ currents and intracellular Ca2++ release. While total transmembranous Ca2++ current was not different between the two strains, the proportion of Ca2++ currents carried by L-type channels was enhanced in vascular muscle cells from SHR. We have recently compared subcellular distribution of intracellular free Ca2++ concentration in the same cells, at rest and during stimulation, by quantitation with a digital photon-counting camera. Fura-2 fluorescence intensity showed that Ca2++ release was principally from sarcoplasmic reticulum and that cells from SHR had higher levels of Ca2++ upon calcium channel stimulation, especially at the cell periphery. These findings suggest fundamental differences in SHR and WKY vascular muscle cells implicating the importance of changes in calcium channels, modulation of Ca2++ release, and Ca2++ uptake in SHR hypertension. Am J Hypertens 1989;2:655-658