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Biomedical subjects

K Honda

Publications and source records attributed to K Honda.

At least 685 records · Page 38Linked to original sources
PubMed1983

[Heterogeneity in drug sensitivity of human tumors in the human tumor colony-forming assay].

The human tumor colony-forming assay was used to compare chemosensitivity among tumor cells within a primary tumor, between primary tumor and its metastasis, and between different metastases. The results indicate that the reported discrepancies of in vitro and in vivo results in clinical trials with TCFA for predicting of resistance or sensitivity to cytostatic drugs may be due to therapeutic heterogeneity among tumor colony-forming units within a primary tumors and between primary tumor and metastases, and that the results from a metastatic lesion may have more profound implications in planning treatment of other metastatic lesions of the same patient.

Antineoplastic Agents↗
PubMed1982

Enhancement of [3H]dopamine release and its [3H]metabolites in rat striatum by nicotinic drugs.

Recent evidence has identified directly muscarinic acetylcholine receptor (m-ACh R) and nicotinic acetylcholine receptor (n-ACh R) in the brain utilizing receptor binding assay. Several studies suggest that release of dopamine (DA) in the striatum is regulated by presynaptic receptors present on dopaminergic terminals. In the present study, the effects of cholinergic drugs on [3H]DA release were examined using micropunched tissue and synaptosomes obtained from rat striatum. ACh (5 x 10(-4) M) significantly increased spontaneous [3H]DA release, and the overflow was partially inhibited by D-tubocurarine (1 mM) but not atropine. Nicotine, lobeline, coniine and spartein, nicotinic agonists, significantly increased spontaneous and 25 mM K + evoked [3H]DA release almost in a dose-dependent manner. In contrast, oxotremorine (2 x 10(-4) M), muscarinic agonist, did not any change in [3H]DA efflux. Furthermore, the metabolites of [3H]DA were separated by column chromatography. The main metabolite of [3H]DA in the spontaneous release from rat striatal synaptosomes was [3H]DOPAC (3,4-dihydroxyphenylacetic acid). Lobeline (5 x 10(-5) M) accelerated the outflow of [3H]DOPAC and [3H]OMDA metabolites (O-methylated and deaminated metabolites). These results could give rise to the suggestion that there was n-ACh R on the dopaminergic nerve terminals in the striatum and n-ACh R might have related to a directly excitatory effect on the DA release.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Studies on 125I-alpha bungarotoxin binding sites in rat brain.

The distribution and properties of 125I-alpha bungarotoxin (125I-alpha BTX) binding in rat brain using micropunched tissue homogenates were examined with a binding technique. Highest level of 125I-alpha BTX binding was observed in the hypothalamus, followed by hippocampus, cortex, globus pallidus, nucleus caudatus and nucleus accumbens. Although high levels of 3H-quinuclidinyl benzilate (3H-QNB) binding in the striatum were found at dorso-lateral sites and low levels in the central regions, the level of 125I-alpha BTX binding within the striatum was almost equal. There was no significant correlation between 125I-alpha BTX binding and choline uptake which could be useful as a marker for functional cholinergic nerve terminals. The inhibition of specific 125I-alpha BTX binding to the hippocampal homogenates by nicotine, d-tubocurarine and other nicotine drugs was studied. The results of these studies suggest that alpha BTX binding sites in the brain are not likely the binding sites of nicotine or the physiological ACh R sites.

Animals↗
PubMed1982

Antihypertensive and adrenoceptor blocking properties of new sulfonamide-substituted phenylethylamines.

Studies on the structure-activity relationship using 9 new 3-sulfamoylphenylethylamines revealed that YM-09538, YM-09649 and YM-09686 were competitive antagonists at both beta- and post-synaptic alpha-receptors. The following order of adrenoceptor blocking activities was obtained : propranolol greater than labetalol greater than YM-09538 greater than YM-09649 greater than YM-09686 for beta-receptors and prazosin greater than YM-09686 greater than YM-09649 greater than YM-09538 greater than phentolamine greater than labetalol for postsynaptic alpha-receptors. In contrast to phentolamine, three YM-compounds showed low affinities for presynaptic alpha-receptors similar to prazosin and labetalol. These antagonists except propranolol effectively lowered blood pressure in conscious SHR and their relative effectiveness parallels the postsynaptic alpha-blocking activity. At hypotensive doses, phentolamine markedly and prazosin, YM-09686 and YM-09649 moderately increased heart rate, whereas YM-09538 and labetalol failed to increase the rate. These results indicate that the postsynaptic alpha-blocking activity of YM-compounds contributes to their hypotensive activities and that both beta-blocking and low presynaptic alpha-blocking activities contribute to attenuation of the tachycardia.

Animals↗