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Titolo:
Mechanisms of acetylcholine-induced vasorelaxation in high K+-stimulated 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: 41 - 44
SICI:
0916-7250(200101)63:1<41:MOAVIH>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR ENDOTHELIUM; NITRIC-OXIDE; CHANNELS; CELLS;
Keywords:
acetylcholine; nitric oxide; rabbit renal artery; vasorelaxation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Citazioni:
13
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 acetylcholine-induced vasorelaxation in high K+-stimulated rabbit renal arteries", J VET MED S, 63(1), 2001, pp. 41-44

Abstract

To characterize the mechanisms of acetylcholine (ACh)-induced vasorelaxation in rabbit renal arteries precontracted with high K+ (100 mM), muscle tension and cytosolic free Ca2+ concentration ([Ca2+](i)) were measured simultaneously in the fura-2-loaded arterial strips. In the artery with endothelium, high K+ increased both [Ca2+](i) and muscle tension. Addition of ACh (10 muM) during high-K+ induced contraction significantly relaxed the muscle and induced additional increase in [Ca2+](i). In the presence of NG-nitro-L-arginine (L-NAME, 0.1 mM), ACh increased [Ca2+](i) without relaxing the muscle. In the artery without endothelium, high KC increased both [Ca2+](i) and muscle tension although ACh was ineffective, suggesting that ACh acts selectively on endothelium to increase [Ca2+](i). 4-DAMP (10 nM) or atropine (0.1 muM) abolished the ACh-induced increase in [Ca2+](i) and relaxation. However, pirenzepine (0.1 muM), AF-DX 116 (1 muM) and tropicamide (1 muM) were ineffective. The ACh-induced increase of [Ca2+](i) and vasorelaxation was significantly reduced by 3 muM gadolinium, 10 muM lanthanum or 10 muM SKF96365. These results suggest that, in rabbit renal artery, ACh-evoked relaxation of 100 mM K+-induced contractions is mediated by the release of endothelial NO. ACh may stimulates the M-3 subtype of muscarinic receptor in the endothelial cells, resulting in the opening of the nonselective cation channels followed by an increase of [Ca2+](i) and stimulation of NO synthase.

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Documento generato il 04/12/20 alle ore 13:18:27