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Biomedical subjects

K Kariya

Publications and source records attributed to K Kariya.

At least 145 records · Page 8Linked to original sources
PubMed1982

Relationship between central actions of bradykinin and prostaglandins in the conscious rat.

Intraventricular injection of bradykinin produced a dose-dependent increase in the mean arterial blood pressure of conscious rats. With 5 nmol of bradykinin, a dual pressor response was observed, which was associated with a biphasic behavioral change. With repeated hourly injections of bradykinin, tachyphylaxis developed to the pressor and central nervous system (CNS) stimulating effect. Indomethacin, given intraventricularly, reduced the hypertension and the behavioral excitation caused by bradykinin in a dose-dependent manner. When prostaglandin E2 was injected into the cerebral ventricles, it induced hypertension and behavioral sedation similar to the secondary response to bradykinin. These results suggest that bradykinin has a dual action on the CNS, and this is mediated by prostaglandin-related systems in the brain.

Animals↗
PubMed1981

Regional distribution of kininase in rat brain.

Kininase activity, which inactivates kinins, was measured in seven regions of the rat brain (i.e., the cerebral cortex, cerebellum, striatum, midbrain, hippocampus, hypothalamus, medulla oblongata), and in the spinal cord with a bioassay method using bradykinin as the substrate. Specific kininase activities in the cerebellum and striatum were higher than those in the other five regions or the spinal cord. Angiotensin-converting enzyme activity, which was measured fluorometrically using Hip-His-Leu as substrate, showed high activity in the striatum and cerebellum. These findings suggest that the presence of high concentrations of peptidases plays a role in the degradation of kinins and/or other peptides in these areas.

Animals↗
PubMed1981

Central action of bradykinin (I). Electroencephalogram of bradykinin and its degradation system in rat brain.

Both in vivo and in vitro experiments were performed to elucidate the relationship between the action of bradykinin (BK) and the possibility of release of pharmacologically active fragments from BK in the rat brain. In in vivo experiments, the activities of electroencephalogram (EEG) increased immediately after the intracerebral administration of 5 nmole BK. The effect was prolonged by intracerebral pretreatment of o-phenanthroline which inhibits plasma kininases. In vitro experiments, o-phenanthroline inhibited partially purified enzyme of rat brain which released fragments of BK possessing phenylalanine, serine, proline and/or arginine as N-terminal amino acids. Only arginine and minute amounts of phenylalanine were observed after the incubation with o-phenanthroline. The evidence suggests that the inhibition of the enzyme by o-phenanthroline resulted in a prolongation of the excited phase produced by BK on the EEG and on behavior. Supporting evidence indicates that Ser-Pro containing fragments derived from BK are concerned with the sedative phase of BK which was observed after the excitative stage.

Animals↗