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Titolo:
Mechanisms of NO-resistant relaxation induced by acetylcholine in rabbit renal arteries
Autore:
Kwon, SC;
Indirizzi:
Yonsei Univ, Coll Med, Dept Physiol, Seoul 120752, South Korea Yonsei Univ Seoul South Korea 120752 Physiol, Seoul 120752, South Korea
Titolo Testata:
JOURNAL OF VETERINARY MEDICAL SCIENCE
fascicolo: 1, volume: 63, anno: 2001,
pagine: 37 - 40
SICI:
0916-7250(200101)63:1<37:MONRIB>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTHELIUM-DEPENDENT HYPERPOLARIZATION; RAT HEPATIC-ARTERY; SMOOTH-MUSCLE; POTASSIUM CHANNELS; CAROTID-ARTERY; NITRIC-OXIDE; BED; RELEASE;
Keywords:
ATP; K+ channel; rabbit renal artery;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Citazioni:
20
Recensione:
Indirizzi per estratti:
Indirizzo: Kwon, SC Yonsei Univ, Coll Med, Dept Physiol, Seoul 120752, South Korea Yonsei Univ Seoul South Korea 120752 Seoul 120752, South Korea
Citazione:
S.C. Kwon, "Mechanisms of NO-resistant relaxation induced by acetylcholine in rabbit renal arteries", J VET MED S, 63(1), 2001, pp. 37-40

Abstract

The effects of K+ channel blockers and P-2Y receptor agonist/antagonist onthe vasorelaxation mediated by endothelium-derived hyperpolarizing factor (EDHF) were investigated in the rabbit renal artery. Acetylcholine (ACh, 1 nM-10 muM) induced endothelium-dependent relaxation of arterial rings precontracted with norepinephrine (NE, 1 muM) in a concentration-dependent manner. N-G-nitro-L-arginine (L-NAME, 0.1 mM), an inhibitor of NO synthase, partially inhibited the ACh-induced endothelium-dependent relaxation. The ACh-induced relaxation was only partially inhibited by L-NAME whereas combined addition of L-NAME and 30 mM KCl completely inhibited the relaxation. The ACh-induced relaxation observed in the presence of L-NAME was significantly reduced by a combination of iberiotoxin (0.1 muM) and apamin (1 muM), and almost completely blocked by 4-aminopyridine (5 mM). The ACh-induced relaxation was antagonized by P-2Y receptor antagonist, cibacron blue (10 and 100 muM) in a concentration-dependent manner. Furthermore, ADP(beta)S, a potent P-2Y agonist, induced the endothelium-dependent relaxation, and this relaxation was markedly reduced by either the combination of iberiotoxin and apamin or by cibacron blue alone. In conclusion, ACh may activate the release of ATP from endothelial cells which in turn activates a P-2Y receptor on theendothelial cells followed by a release of EDHF, resulting in a vasorelaxation via a mechanism that involves activation of both the voltage-gated K+ channels and the Ca2+-activated K+ channels.

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Documento generato il 04/12/20 alle ore 13:11:22