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Biomedical subjects

L E Ward

Publications and source records attributed to L E Ward.

At least 19 recordsLinked to original sources
PubMed1996

Nitric oxide reduces basal efflux of catecholamines from perfused dog adrenal glands.

Norepinephrine, epinephrine, dopamine, and both the free and extended forms of [met]enkephalin spontaneously efflux from adrenal glands under basal conditions. The present study was done to determine whether nitric oxide has a regulatory role in these effluxes. Isolated adrenal glands (n = 63) from mongrel dogs were perfused retrogradely with Krebs-Ringer solution. In some experiments NG-monomethyl-L-arginine (3 x 10(-4) M), an inhibitor of nitric oxide synthesis, was added to the perfusate. In other experiments one of the nitric oxide donors, 3-morpholinosydnonimine (10(-7) M or 10(-5) M) or sodium nitroprusside (10(-6) M or 10(-4) M) was added. Norepinephrine, epinephrine, dopamine and their metabolites 3,4-dihydroxyphenylglycol and 3,4-dihydroxyphenylacetic acid in perfusates were quantitated by high performance liquid chromatography with electrochemical detection and in some experiments the [met]enkephalins were determined by radioimmunoassay. In the presence of NG-monomethyl-L-arginine, the basal effluxes of norepinephrine, epinephrine, and dopamine were significantly increased from control, but the effluxes of the free and extended forms of the [met]enkephalins were not changed. The effects of NG-monomethyl-L-arginine on catecholamine efflux were reversed in the presence of L-arginine (10(-3) M). Sodium nitroprusside (10(-6) M) inhibited effluxes of norepinephrine and epinephrine and 3-morpholinosydnonimine had no effect on these effluxes. Dopamine efflux appeared to be under different controls from those of norepinephrine and epinephrine since dopamine efflux was unaffected by sodium nitroprusside and was decreased over time by 3-morpholinosydnonimine (10(-7) M). It is concluded that endogenously produced nitric oxide inhibits the basal efflux of norepinephrine, epinephrine, and dopamine from isolated dog adrenal glands; this inhibition appears to be near maximal for norepinephrine and epinephrine but not for dopamine.

Adrenal Glands↗
PubMed1995

Effluxes of 3,4-dihydroxyphenylalanine, 3,4-dihydroxyphenylglycol, and norepinephrine from four blood vessels during basal conditions and during nerve stimulation.

Effluxes of 3,4-dihydroxyphenylalanine, 3,4-dihydroxyphenyglycol, and norepinephrine from four superfused canine blood vessels (saphenous and portal veins and mesenteric and pulmonary arteries) were studied under basal conditions and during nerve stimulation. From quantification of the compounds a series of indices of activities at neuroeffector junctions are proposed. These are (a) basal overflow of 3,4-dihydroxyphenylglycol as an index of vesicular-cytoplasmic translocation of norepinephrine, (b) the increase in 3,4-dihydroxyphenyglycol overflow attributable to nerve stimulation as an index of neuronal reuptake of norepinephrine released by stimulation, (c) the sum of the increases in overflows of norepinephrine and 3,4-dihydroxyphenylglycol attributable to nerve stimulation as an index of evoked release of norepinephrine, and (d) the efflux of 3,4-dihydroxyphenylalanine as an index of the activity of tyrosine hydroxylase, the rate-limiting enzyme in the synthesis of norepinephrine. There were clear differences between these indices in the vessels. Correlation coefficients of the indices among vessels indicated that a high tissue norepinephrine level was associated with high biosynthetic capacity and high vesicular-cytoplasmic exchange but not with high release. There was no evidence suggesting feedback inhibition of synthesis by neuroplasmic norepinephrine--whether arising from vesicular-cytoplasmic translocation or from reuptake from the junctional cleft. The major value of these indices will probably be in determining the integrated effects of pharmacologic agents at neuroeffector junctions in different blood vessels.

Animals↗