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Biomedical subjects

N Miki

Publications and source records attributed to N Miki.

At least 199 records · Page 11Linked to original sources
PubMed1980

Inhibition of N-methyl-N'-nitro-N-nitrosoguanidine-activated guanylate cyclase by anticarcinogenic agents.

Recent studies have demonstrated that nitroso chemical carcinogens markedly activate guanylate cyclase, which catalyzes the production of guanosine 3',5'-monophosphate (cyclic GMP). We therefore examined the effect of inhibitors of carcinogenic compounds on guanylate cyclase activation by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). An antioxidant group of anticarcinogenic compounds was effective. Disulfiram and phenethyl isothiocyanate exhibited the most potent inhibition. Inhibitor constants (Ki) for disulfiram and phenethyl isothiocyanate were 1.2 x 10(-5) M and 4.9 x 10(-5) M, respectively. Sodium diethyldithiocarbamate, phenyl isothiocyanate, butylated hydroxyanisole and ethoxyquin showed moderate inhibitory effects. Sodium selenide decreased the MNNG-activated guanylate cyclase activity to about 30%, and it was inhibitory at the low concentration of 10(-5) M. The present data suggest that one of the mechanisms by which anticarcinogenic compounds exert their effect may in part be related to the inhibition of guanylate cyclase.

Animals↗
PubMed1979

Chlorpromazine inhibits episodic growth hormone secretion in the rat.

Effects of chlorpromazine (CPZ) on plasma GH and prolactin levels were observed in conscious rats provided with chronic indwelling right atrial cannulae. The administration of CPZ (200 micrograms/100 g b.w. iv) suppressed episodic plasma GH burst and resulted in significant elevations of plasma prolactin levels. These were also observed in rats in which two types of hypothalamic deafferentation, i.e. anterior and complete, had been carried out. The data suggest that CPZ acts within the medial basal hypothalamus and inhibits episodic plasma GH secretion. In addition, it is inferred that catecholamines are involved in the generation of episodic plasma GH burst.

Animals↗
PubMed1978

Effect of sodium ion on levels of cyclic adenosine 3',5'-monophosphate in guinea pig cerebral slices.

Accumulation of cyclic AMP was studied in guinea pig cerebral slices when Na+ levels in the bathing medium were varied or agents which affect tissue Na+ content were added. When NaCl was gradually replaced with Tris-HCl or choline chloride, cyclic AMP formation was progressively enhanced. ;when Na+ was below 30 mM, cyclic AMP formation reached the maximum (approximately 30 fold), but this increment was not blocked by tetrodotoxin. The stimulatory effect of high K+ was nearly linear over 120 mM and became much more prominent when Na+ also was not blocked by tetrodotoxin. Ouabain (10(-4) M), electrical pulses and glutamate (5 x 10(-3) M), each stimulated cyclic AMP formation about 17-, 7- and 5-fold, respectively. Tetrodotoxin (2 x 10(-6) M) completely blocked the effects of electrical pulses and partially blocked the effects of glutamate and oubain. It is suggested that the increase of cyclic AMP in cerebral cortical slices may be related to the decrease in Na+ gradient across the cell membrane.

Animals↗
PubMed1977

Stimulation of immunoreactive somatostatin release from hypothalamic synaptosomes by high (K+) and dopamine.

Effects of high (K+) and dopamine on the release of immunoreactive somatostatin from isolated hypothalamic synaptosomes were studied in rats. High (K+) (60 mM) and dopamine (10(-6) M) in the incubation media stimulated the release of immunoreactive somatostatin and the former effect was completely abolished by the removal of Ca++ from the media. These suggest that hypothalamic somatostatinergic synaptosomes preserved at least one of the important basic properties of secretory cells. Although it is of interest to note that dopamine stimulated the release of somatostatin. Its physiological significance awaits further studies.

Animals↗