This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Perry, P. A. Articles by Webb, R. C. Search for Related Content PubMed PubMed Citation Articles by Perry, P. A. Articles by Webb, R. C. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CAFFEINE CALCIUM COMPOUNDS CALCIUM, ELEMENTAL SODIUM CHLORIDE Medline Plus Health Information High Blood Pressure

Hypertension, Vol 17, 603-611, Copyright © 1991 by American Heart Association

ARTICLES

Agonist-sensitive calcium stores in arteries from steroid hypertensive rats

PA Perry and RC Webb
Department of Physiology, University of Michigan Medical School, Ann Arbor.

The present study characterizes cellular calcium stores that are sensitive to norepinephrine and caffeine in arteries from deoxycorticosterone acetate hypertensive rats. Mesenteric arteries from normotensive and hypertensive rats were excised and cut into helical strips for isometric force recording. In calcium-free solution, phasic contractile responses to norepinephrine (5.9 x 10(-9) to 5.9 x 10(-6) M), but not caffeine (0.3-30 mM), were greater in hypertensive arteries. D-600, a calcium channel blocker, or removal of the endothelium did not alter phasic contractions to norepinephrine or caffeine. In contrast, contractions to both norepinephrine and caffeine were inhibited by ryanodine, a drug that depletes calcium from intracellular stores. An inhibitor of phospholipase C (2-nitro-4- carboxyphenyl N,N-diphenylcarbamate) attenuated contractions to norepinephrine but not those to caffeine. The augmented response to norepinephrine in hypertensive rats did not occur early after implantation of the mineralocorticoid, suggesting that this vascular change may not play a role in the development of high blood pressure in this experimental model. The augmented response to norepinephrine was reduced in mineralocorticoid-treated rats maintained on a low sodium diet, and these rats had blood pressures in the normotensive range. Because contractile responses to caffeine were not enhanced in arteries from hypertensive rats, we conclude that the cellular store for calcium is not enlarged compared with that in normotensive arteries. In contrast, the mobilization of calcium from cellular stores by norepinephrine is augmented in mineralocorticoid hypertension. This augmented response may be linked to altered phospholipase C activity and thus to an augmented action of inositol trisphosphate that releases calcium from intracellular sites.

This article has been cited by other articles:

				F. R.C. Giachini, C.-W. Chiao, F. S. Carneiro, V. V. Lima, Z. N. Carneiro, A. M. Dorrance, R. C. Tostes, and R. C. Webb Increased Activation of Stromal Interaction Molecule-1/Orai-1 in Aorta From Hypertensive Rats: A Novel Insight Into Vascular Dysfunction Hypertension, February 1, 2009; 53(2): 409 - 416. [Abstract] [Full Text] [PDF]

				G. Jiang, S. Cobbs, J. D. Klein, and W. C. O'Neill Aldosterone Regulates the Na-K-2Cl Cotransporter in Vascular Smooth Muscle Hypertension, May 1, 2003; 41(5): 1131 - 1135. [Abstract] [Full Text] [PDF]

				M. E Ullian The role of corticosteroids in the regulation of vascular tone Cardiovasc Res, January 1, 1999; 41(1): 55 - 64. [Full Text] [PDF]

				M. E. Ullian and L. G. Walsh Corticosterone Metabolism and Effects on Angiotensin II Receptors in Vascular Smooth Muscle Circ. Res., October 1, 1995; 77(4): 702 - 709. [Abstract] [Full Text]