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Biomedical subjects

H Moritoki

Publications and source records attributed to H Moritoki.

66 records · Page 4Linked to original sources
PubMed1976

Effects of methylxanthines and imidazole on the contractions of guinea-pig ileum induced by transmural stimulation.

Methylxanthines (10(-5) to 10(-3)M) were found to increase the amplitude of contractions of guinea-pig ileum induced by transmural stimulation but to inhibit those induced by acetylcholine or histamine. The order of the abilities of methylxanthines to augment the contractile responses was theobromine greater than caffeine greater than theophylline. When the contractions were completely suppressed by reduction of the calcium content in the medium or by addition of cyclic AMP, methylxanthines restored the responses effectively, just as does addition of calcium. Methylxanthines also accelerated the release of acetylcholine from the ileum associated with stimulation. Imidazole (3 X 10(-5) to 10(-3) M) had an essentially similar effect to methylxanthines in potentiating the contractile responses and in augmenting the release of acetylcholine. The present results indicate that the potentiating effects of methylxanthines and imidazole are due to an action on the nerve terminals, not on the postsynaptic membranes or contractile elements. Therefore, it si concluded that theit potentiating actions are due to facilitation of the movement of calcium in the nerve terminals on excitation, resulting in increased release of acetylcholine, and are not due to the effect of cyclic AMP formed as a result of their inhibitory actions on phosphodiesterase.

Animals↗
PubMedDate not supplied

Possible association of decrease of ATP-induced vascular relaxation with reduction of cyclic GMP during aging.

The effect of aging on the ATP-induced relaxation of rat thoracic aorta was examined. Haemoglobin, methylene blue and NG-nitro L-arginine, and removal of the endothelium inhibited or reversed the relaxation induced by ATP. The relaxant response of the aorta to ATP was greatest in the preparations from 4-week-old rats. As the age of rats increased to 45 and 105 weeks, the concentration-response curve for ATP was shifted to the right with reduction of maximal relaxation. ATP elevated cyclic GMP levels. This action was endothelium-dependent and inhibited by methylene blue, haemoglobin and NG-nitro L-arginine. With an increase in age of the rats from 4 weeks to 45 weeks, ATP-stimulated cyclic GMP production was attenuated, and in the aorta from 105-week-old rats cyclic GMP level was no longer elevated by ATP. In contrast to the age-associated marked change in cyclic GMP levels, cyclic AMP production was not affected by aging. It is suggested that age-related changes in ATP-induced relaxation and cyclic GMP formation occur mainly at the level of the vascular smooth muscle. Alterations in soluble guanylate cyclase, at step(s) distal to the guanylate cyclase, or in cyclic GMP-phosphodiesterase might contribute.

Adenosine Triphosphate↗
PubMedDate not supplied

Role of endotoxin in L-arginine-induced relaxation of rat thoracic aorta mediated by muscle-derived nitric oxide.

The contribution of endotoxin to the L-arginine-induced relaxation of the endothelium-denuded rat thoracic aorta, which appears to be mediated by nitric oxide synthase in the vascular smooth muscle, was investigated. Special attention was paid to the time course of the phenomenon and its dependence on the concentration of endotoxin. In the absence of endotoxin, L-arginine induced scarcely any relaxation of the arteries. Treatment of the arteries with endotoxin initiated relaxation in response to 10 microM L-arginine with lag periods of 2-4 hours. The degree of relaxation increased on repeated applications of L-arginine, to reach a consistent level after several hours. Increase in the concentration of endotoxin shortened the lag period, enhanced the degree of relaxation and lowered the threshold concentration of L-arginine required to relax the arteries. In endotoxin-primed arteries, L-arginine, at concentrations necessary to induce relaxation, stimulated the cyclic GMP production. Prophylactic application of actinomycin D or dexamethasone, which inhibits the induction of nitric oxide synthase, prevented the induction by endotoxin of the L-arginine-induced relaxation and cyclic GMP formation. Polymyxin B, which inhibits the action of endotoxin, also prevented the development of the endotoxin-sensitized relaxation and the cyclic GMP formation induced by L-arginine. When the Krebs solution was prepared using deionized water, the amount of endotoxin in the reservoir was above the level required to initiate the L-arginine-induced relaxation and cyclic GMP formation. These results suggest that endotoxin triggered the time-dependent development of the L-arginine-induced relaxation by expressing nitric oxide synthase in the vascular smooth muscle.

Amino Acid Oxidoreductases↗