Premium
Endothelium‐dependent modulation of resistance vessel contraction: studies with N G ‐nitro‐ l ‐arginine methyl ester and N G ‐nitro‐ l ‐arginine
Author(s) -
Bennett Michael A.,
Watt Pamela A.C.,
Thurston Herbert
Publication year - 1992
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1992.tb12792.x
Subject(s) - nitroarginine , mesenteric arteries , acetylcholine , contractility , chemistry , endocrinology , contraction (grammar) , endothelium , medicine , myograph , vasodilation , nitric oxide , pharmacology , biophysics , nitric oxide synthase , biology , artery
1 The effect of N G ‐nitro‐ l ‐arginine methyl ester ( l ‐NAME) and N G ‐nitro‐ l ‐arginine ( l ‐NOARG) on noradrenaline (NA)‐induced contractility and acetylcholine (ACh)‐induced endothelium‐dependent relaxation was studied in rat mesenteric resistance arteries. 2 Third order branches of mesenteric arteries were dissected and mounted on two forty micron wires in a Mulvany myograph. 3 Incubation with l ‐NAME and l ‐NOARG (10 μ m ) caused a time‐dependent shift in the 50% response to NA (ED 50 ) (0.01 μ m ‐10 μ m ) but was not associated with an increase in the maximum contractile response. 4 l ‐NAME and l ‐NOARG (10 μ m ) caused a time‐dependent inhibition of ACh (1 μ m )‐induced relaxation with a maximum effect after 120 min. 5 Following endothelium removal, incubation with either l ‐NAME or l ‐NOARG caused no significant shift in the ED 50 , although the residual relaxation response to ACh (1 μ m ) was further attenuated. 6 Incubation with the cylco‐oxygenase inhibitor, indomethacin, enhanced the relaxation to ACh and reduced the inhibitory effects of l ‐NAME and l ‐NOARG. 7 In conclusion, l ‐NAME and l ‐NOARG are potent inhibitors of acetylcholine‐induced endothelium‐dependent relaxation in mesenteric resistance arteries. The shift in ED 50 associated wtih these inhibitors suggests a probable role for the endothelium in modulating the contractility of the resistance vasculature.