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  • Title: Vasomotor responses of canine coronary arterial rings to NG-monomethyl-L-arginine and N omega nitro L-arginine methyl ester.
    Author: Winn MJ, Asante NK, Ku DD.
    Journal: J Pharmacol Exp Ther; 1993 Jan; 264(1):265-70. PubMed ID: 8423529.
    Abstract:
    The actions of NG-monomethyl-L-arginine (L-NMMA) and N omega-nitro L-arginine methyl ester (L-NAME) on canine coronary arterial rings were compared with effects on rat aortic rings. After incubation of rat aortic rings with indomethacin (5 x 10(-6) M) and preconstriction with phenylephrine (10(-7) M), L-NMMA (2.5 x 10(-4) M) caused an increase in tension when endothelium remained intact (+1.1 +/- 0.2 g). L-NMMA had no effect when endothelium was absent. After incubation of canine coronary arterial rings with indomethacin and preconstriction with prostaglandin F2 alpha (10(-6) M), L-NMMA (2.5 x 10(-4) M) increased tension (+39.9 +/- 7.9% of PGF2 alpha-induced constriction) when endothelium was intact, but L-NMMA caused a significant reduction in tension when endothelium was removed (Emax -52.2 +/- 10.3%; P < .05). The reduction in tension after L-NMMA was greater in the absence of indomethacin (Emax -79.8 +/- 4.1%; P < .05). It has been suggested previously that biotransformation of L-NMMA to L-arginine may have contributed to vasorelaxation; L-arginine is the endogenous substrate of nitric oxide synthase. However L-arginine (10(-3) M) did not affect the fall in tension produced by L-NMMA (Emax -69.0 +/- 14.2% in the absence of indomethacin). We also found that incubation with the protein synthesis inhibitor, cycloheximide, did not block the L-NMMA-induced fall in vascular tension; in fact, it increased the magnitude of the relaxant effect (-95.4 +/- 2.5%, experiments performed without indomethacin).(ABSTRACT TRUNCATED AT 250 WORDS)
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