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Detail of "90880-94-7"

  • CAS Number:
  • 90880-94-7
  • Name:
  • 51005-20-0

  • Molecular Structure:
  • Formula:
  • HNO

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Reference

Vasodilator responses to acetylcholine, bradykinin, and substance P are mediated by a TEA-sensitive mechanism
Vasodilator responses to acetylcholine, bradykinin, and substance P are mediated by a TEA-sensitive mechanism. Champion, Hunter C.; Kadowitz, Philip J. (Department of Pharmacology, Tulane University School of Medicine, New Orleans, LA 70112, USA). American Journal of Physiology, 273(1, Pt. 2), R414-R422 (English) 1997 American Physiological Society. CODEN: AJPHAP. ISSN: 0002-9513. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) The effects of tetraethylammonium (TEA), a K+ channel antagonist, on vasodilator responses were investigated in the hindquarters vascular bed of the cat under const.-flow conditions. After administration of TEA in a total dose of 60 mg/kg into the hindquarters perfusion circuit, vasodilator responses to acetylcholine, bradykinin, and substance P were reduced, whereas vasodilator responses to the NO donors, diethylamine-NO complex, S-nitroso-N-acetylpenicillamine, and sodium nitroprusside, and to prostaglandin E1, albuterol, vasoactive intestinal polypeptide, isradipine, and levcromakalim were not altered. The inhibitory effect of TEA on responses to the endothelium-dependent vasodilators was reversible with time, and vasoconstrictor responses to norepinephrine, U-46619, angiotensin II, and BAY K 8644 were enhanced by the K+ channel antagonist. 90880-94-7 is the cas registry number. This chemical is also mentioned in this article. Although TEA had no sustained effect on baseline systemic arterial and hindquarters perfusion pressures, the NO synthase inhibitor, Nw-nitro-L-arginine Me ester, increased these pressures in the presence of TEA. The results of the present investigation suggest that TEA attenuates vasodilator responses to acetylcholine, bradykinin, and substance P by inhibiting the release of endothelium-derived relaxing factor. These data suggest that the acetylcholine-, bradykinin-, and substance P-stimulated release of endothelium-derived relaxing factor may involve the opening of a TEA-sensitive K+ channel in the endothelium in the hindlimb vascular bed of the cat, but that a TEA-sensitive mechanism is not involved in the maintenance of baseline tone in this vascular bed. .
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