ArticleBritish journal of pharmacology2003
Acetylcholine-induced vasodilation may depend entirely upon NO in the femoral artery of young piglets.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Noninvasive measure of microvascular nitric oxide function in humans using very low-frequency cutaneous laser Doppler flow spectra.Microcirculation (New York, N.Y. : 1994)Trial
- Endothelial TRPV4-Cx43 signalling complex regulates vasomotor tone in resistance arteries.The Journal of physiology · 2025Article
- Acetylcholine activates a regenerative vasodilator mechanism that is sensitive to nitric oxide production.Frontiers in physiology · 2025Article
- Endothelial TRPV4/Cx43 Signaling Complex Regulates Vasomotor Tone in Resistance Arteries.bioRxiv : the preprint server for biology · 2024Article
- Nitric oxide and prostaglandin inhibition during acetylcholine-mediated cutaneous vasodilation in humans.Microcirculation (New York, N.Y. : 1994) · 2008Article
- Combination of Ca2+ -activated K+ channel blockers inhibits acetylcholine-evoked nitric oxide release in rat superior mesenteric artery.British journal of pharmacology · 2006Article
- Evaluation of bioavailability of nitric oxide in coronary circulation by direct measurement of plasma nitric oxide concentration.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Prostacyclin release and receptor activation: differential control of human pulmonary venous and arterial tone.British journal of pharmacology · 2004Article
- Developmental changes in myoendothelial gap junction mediated vasodilator activity in the rat saphenous artery.The Journal of physiology · 2004Article
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1 To characterize agonist-induced relaxation in femoral artery rings from young piglets, we compared the effect of a NOS-inhibitor N(omega)-nitro-L-arginine (L-NOARG), an NO-inactivator oxyhaemoglobin (HbO) and a soluble guanyl cyclase(sGC)-inhibitor 1H-[1,2,4]Oxadiazolo-[4,3,-alpha]quinoxalin-1-one (ODQ) on acetylcholine(ACh)-induced relaxation. The involvement of K(+) channel activation was studied on relaxations induced by ACh, the two NO donors sodium nitroprusside (SNP) and diethylamine (DEA) NONOate, and the cell membrane permeable guanosine 3'5' cyclic monophosphate (cGMP) analogue 8-Br-cGMP. 2 Full reversal of phenylephrine-mediated precontraction was induced by ACh (1 nM-1 microM) (pD(2) 8.2+/-0.01 and R(max) 98.7+/-0.3%). L-NOARG (100 microM) partly inhibited relaxation (pD(2) 7.4+/-0.02 and R(max) 49.6+/-0.8%). The L-NOARG/indomethacin(IM)-resistant response displayed characteristics typical for endothelium-derived hyperpolarizing factor (EDHF), being sensitive to a combination of the K(+) channel blockers charybdotoxin (CTX) (0.1 microM) and apamin (0.3 microM). 3 ODQ (10 microM) abolished relaxations induced by ACh and SNP. L-NOARG/IM-resistant relaxations to ACh were abolished by HbO (20 microM). 4 Ouabain (1 microM) significantly inhibited ACh-induced L-NOARG/IM-resistant relaxations and relaxations induced by SNP (10 microM) and 8-Br-cGMP (0.1 mM). A combination of ouabain and Ba(2+) (30 microM) almost abolished L-NOARG/IM-resistant ACh-induced relaxation (R(max) 7.7+/-2.5% vs 23.4+/-6.4%, with and without Ba(2+), respectively, P<0.05). 5 The present study demonstrates that in femoral artery rings from young piglets, despite an L-NOARG/IM-resistant component sensitive to K(+) channel blockade with CTX and apamin, ACh-induced relaxation is abolished by sGC-inhibition or a combination of L-NOARG and HbO. These findings suggest that relaxation can be fully explained by the NO/cGMP pathway.
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