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Biomedical subjects

R Inoki

Publications and source records attributed to R Inoki.

At least 91 records · Page 5Linked to original sources
PubMed1976

[Analgesics and the kallikrein-kinin system].

The mechanism of analgesic actions of aspirin, aminopyrine and morphine was investigated in reference to the kallikrein-kinin system and the results suggested that the analgesic actions of these agents are definitely related with the peripheral kallikrein-kinin activity. The central action of kinin appears to differ from the peripheral action.

Aminopyrine↗
PubMed1975

[Effects of adrenergic agents on secretion of salivary kallikrein in the submandibular gland of the dog].

The effects of sympathetic nerve stimulation and administrations of sympathomimetics on the secretion of salivary kallikrein induced by stimulation of Chorda tympani were examined quantitatively and qualitatively in the dog submandibular gland. Both sympathetic stimulation and administrations of sympathomimetics such as norepinephrine, epinephrine, and isoproterenol caused increased secretion of salivary kallikrein. Among these effects, those of the sympathetic stimulation, norepinephrine, and epinephrine were not completely abolished by pretreatment with phenoxybenzamine or propranolol, but the effect of isoproterenol was abolished by pretreatment with propranolol, and was hardly influenced by pretreatment with phenoxybenzamine. From these results, it would appear that secretion of salivary kallikrein may be mediated through adrenergic alpha- and beta-receptors. On the other hand, in contrast with the activities of the salivary kallikrein secreted by Chorda tympani stimulation or administration of isoproterenol which were not inhibited by SBTI, the activities of the salivary kallikrein secreted by sympathetic stimulation as well as administration of norepinephrine or epinephrine were markedly inhibited by SBTI. From these results, it is concluded that secretion of glandular kallikrein is due either to Chorda tympani stimulation or is mediated through adrenergic beta-receptor, while secretion of plasma kallikrein is mediated through adrenergic alpha-receptor.

Animals↗
PubMed1971

Effects of nicotine on salivary amylase secretion from rabbit parotid gland.

1. The effects of nicotine on amylase secretion induced by auriculo-temporal nerve stimulation were studied.2. Nicotine caused a transient increase in secretion as well as flow rate of amylase.3. No difference in nicotine action was found between acute sympathetic decentralization of the gland and acute denervation.4. The increase in amylase secretion due to nicotine was not inhibited by phenoxybenzamine, bretylium and chronic denervation, but was prevented by hexamethonium, propranolol and adrenalectomy.5. The increase in flow rate due to nicotine was not inhibited by propranolol, chronic denervation and adrenalectomy, but was prevented by hexamethonium, phenoxybenzamine and bretylium.6. These results show that the action of nicotine in increasing amylase secretion is neither a direct action on the ganglion nor on the nerve terminal of the cervical sympathetic nerve, but is an indirect action of catecholamines released from the adrenal medulla on the post-junctional receptors.7. The study also suggests that the initial acceleration of salivary flow due to nicotine is characterized by a mechanism different from that of amylase secretion.

Adrenal Medulla↗