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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

A key role for Na+/K+-ATPase in the endothelium-dependent oscillatory activity of mouse small mesenteric arteries

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Author(s):
Giachini, F. R. C. [1, 2] ; Carneiro, F. S. [1, 2] ; Lima, V. V. [1, 2] ; Carneiro, Z. N. [1] ; Brands, M. W. [1] ; Webb, R. C. [1] ; Tostes, R. C. [1, 2]
Total Authors: 7
Affiliation:
[1] Med Coll Georgia, Dept Physiol, Augusta, GA 30912 - USA
[2] Univ Sao Paulo, Fac Med, Dept Farmacol, Sao Paulo - Brazil
Total Affiliations: 2
Document type: Journal article
Source: Brazilian Journal of Medical and Biological Research; v. 42, n. 11, p. 1058-1067, NOV 2009.
Web of Science Citations: 5
Abstract

Oscillatory contractile activity is an inherent property of blood vessels. Various cellular mechanisms have been proposed to contribute to oscillatory activity. Mouse small mesenteric arteries display a unique low frequency contractile oscillatory activity (1 cycle every 10-12 min) upon phenylephrine stimulation. Our objective was to identify mechanisms involved in this peculiar oscillatory activity. First-order mesenteric arteries were mounted in tissue baths for isometric force measurement. The oscillatory activity was observed only in vessels with endothelium, but it was not blocked by L-NAME (100 µM) or indomethacin (10 µM), ruling out the participation of nitric oxide and prostacyclin, respectively, in this phenomenon. Oscillatory activity was not observed in vessels contracted with K+ (90 mM) or after stimulation with phenylephrine plus 10 mM K+. Ouabain (1 to 10 µM, an Na+/K+-ATPase inhibitor), but not K+ channel antagonists [tetraethylammonium (100 µM, a nonselective K+ channel blocker), Tram-34 (10 µM, blocker of intermediate conductance K+ channels) or UCL-1684 (0.1 µM, a small conductance K+ channel blocker)], inhibited the oscillatory activity. The contractile activity was also abolished when experiments were performed at 20°C or in K+-free medium. Taken together, these results demonstrate that Na+/K+-ATPase is a potential source of these oscillations. The presence of α-1 and α-2 Na+/K+-ATPase isoforms was confirmed in murine mesenteric arteries by Western blot. Chronic infusion of mice with ouabain did not abolish oscillatory contraction, but up-regulated vascular Na+/K+-ATPase expression and increased blood pressure. Together, these observations suggest that the Na+/K+ pump plays a major role in the oscillatory activity of murine small mesenteric arteries. (AU)

FAPESP's process: 06/01773-0 - RhoA/Rho-cinase signaling pathway in the vascular smooth muscle from mice with angiotensin II-induced hypertension: interaction with reactive oxygen species, interleukin-6 (IL-6) and JAK/STAT activation
Grantee:Rita de Cassia Aleixo Tostes Passaglia
Support type: Scholarships abroad - New Frontiers