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In vitro simultaneous measurements of relaxation and nitric oxide concentration in rat superior mesenteric artery
Author(s) -
Simonsen Ulf,
Wadsworth Roger M.,
Buus Niels Henrik,
Mulvany Michael J.
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.271aa.x
Subject(s) - acetylcholine , nitric oxide , chemistry , vasodilation , snap , endocrinology , medicine , nitric oxide synthase , relaxation (psychology) , endothelium , anesthesia , biophysics , biology , computer graphics (images) , computer science
1 The relationship between nitric oxide (NO) concentration measured with an NO‐specific microelectrode and endothelium‐dependent relaxation was investigated in isolated rat superior mesenteric artery contracted with 1 μM noradrenaline. 2 Acetylcholine (10 μM) induced endothelium‐dependent simultaneous increases in luminal NO concentration of 21 ± 6 nM, and relaxations with pD 2 values and maximum of 6.95 ± 0.32 and 97.5 ± 0.7 % ( n = 7 ), respectively. An inhibitor of NO synthase, N G ‐nitro‐L‐arginine (L‐NOARG, 100 μM) inhibited the relaxations and increases in NO concentration induced by acetylcholine. 3 Oxyhaemoglobin (10 μM) reversed the relaxations and increases in NO concentrations induced by acetylcholine, S ‐nitroso‐ N ‐acetylpenicillamine (SNAP) and S ‐morpholino‐sydnonimine (SIN‐1), but not the relaxations induced with forskolin. Oxyhaemoglobin also decreased the NO concentration below baseline level. 4 In the presence of L‐NOARG (100 μM), a small relaxation to acetylcholine (10 μM) of noradrenaline‐contracted segments was still seen; oxyhaemogobin inhibited this relaxation and decreased the NO concentration by 14 ± 4 nM ( n = 4 ). 4 The NO concentration‐relaxation relationship for acetylcholine resembled that for SNAP and SIN‐1 more than for authentic NO. Thus while 7‐17 nM NO induced half‐maximal relaxations in response to SNAP or SIN‐1, 378 ± 129 nM NO ( n = 4) was needed for half‐maximal relaxation to authentic NO. 5 The present study provides direct evidence that the relaxation of the rat superior mesenteric artery with the endothelium‐dependent vasodilator acetylcholine is correlated to the endogeneous release of NO. The study also suggests that NO mediates the L‐NOARG‐resistant relaxations in this artery, and that there is a basal NO release.