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

F. R.C. Giachini, F. S. Carneiro, V. V. Lima, Z. N. Carneiro, Michael W Brands, R Clinton Webb, R. C. Tostes

Research output: Contribution to journalArticle

6 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)1058-1067
Number of pages10
JournalBrazilian Journal of Medical and Biological Research
Volume42
Issue number11
DOIs
StatePublished - Dec 8 2009

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Mesenteric Arteries
Endothelium
Adenosine Triphosphatases
Phenylephrine
Ouabain
Blood Vessels
Tetraethylammonium
Force measurement
NG-Nitroarginine Methyl Ester
Blood pressure
Blood vessels
Epoprostenol
Activity Cycles
Indomethacin
Nitric Oxide
Protein Isoforms
Baths
Pumps
Tissue
Western Blotting

Keywords

  • Na/K-ATPase pump
  • Oscillatory activity
  • Ouabain
  • Small mesenteric arteries

ASJC Scopus subject areas

  • Biophysics
  • Neuroscience(all)
  • Biochemistry
  • Physiology
  • Immunology
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Cell Biology

Cite this

A key role for Na+/K+-ATPase in the endothelium-dependent oscillatory activity of mouse small mesenteric arteries. / Giachini, F. R.C.; Carneiro, F. S.; Lima, V. V.; Carneiro, Z. N.; Brands, Michael W; Webb, R Clinton; Tostes, R. C.

In: Brazilian Journal of Medical and Biological Research, Vol. 42, No. 11, 08.12.2009, p. 1058-1067.

Research output: Contribution to journalArticle

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AU - Carneiro, F. S.

AU - Lima, V. V.

AU - Carneiro, Z. N.

AU - Brands, Michael W

AU - Webb, R Clinton

AU - Tostes, R. C.

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AB - 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.

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