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Biomedical subjects

H Kajiyama

Publications and source records attributed to H Kajiyama.

At least 55 records · Page 3Linked to original sources
PubMed1986

Pharmacokinetics and pharmacodynamics of captopril in patients undergoing continuous ambulatory peritoneal dialysis.

Pharmacokinetics and pharmacodynamics of captopril were studied in 5 continuous ambulatory peritoneal dialysis (CAPD) patients (including 2 hypertensive patients) after single oral administration of 50 mg captopril. The pharmacokinetic parameters for plasma free unchanged captopril were time to maximal concentration 1.1 +/- 0.3 h, maximal plasma concentration 387 +/- 75 ng X ml-1, elimination half-life 1.0 +/- 0.3 h, and the area under the concentration-time curve 711 +/- 144 ng X h X ml-1. For plasma total captopril (the sum of free unchanged captopril and its disulfide compounds) the values were time to maximal concentration 3.5 +/- 0.6 h and maximal plasma concentration 2,777 +/- 429 ng X ml-1. Captopril was detected in the dialysis fluid in all CAPD patients. Blood pressures in the 2 hypertensive CAPD patients were lower at 24 h after than before captopril administration. These results suggest that captopril may be eliminated by CAPD. In addition, there is a possibility that the antihypertensive effects of captopril may be prolonged in hypertensive CAPD patients.

Adult↗
PubMed1982

The increase of cardiac beta 1-subtype of beta-adrenergic receptors in adult rats following neonatal 6-hydroxydopa treatment.

An analysis of Hofstee plots of specific [3H]dihydroalprenolol ([3H]DHA) binding in the presence of various concentrations of practolol showed that KD and Bmax in beta 1-subtype adrenoceptors were 19.2-fold lower and 2.76-fold higher than those in beta 2-subtype in adult rat hearts, respectively. Neonatal treatment with 6-hydroxydopa produced a significant increase only in Bmax in beta 1-adrenoceptors without changing Bmax and KD in beta 2-receptors. "Up' regulation in the density of beta 2-type of adrenoceptors seems to be caused by the 6-hydroxydopa-induced sympathetic lesion.

Animals↗
PubMed1982

Alteration in sensitivity to isoproterenol and acetylcholine in the rat heart after repeated administration of isoproterenol.

Alteration of sensitivity to the inotropic responses to isoproterenol and acetylcholine (ACh) and of saturation constants for the specific binding of [3H]dihydroalprenolol and [3H]quinuclidinyl benzilate to particulate fractions were investigated in rat hearts chronically treated with isoproterenol. The EC50 value for the inotropic response to isoproterenol in the atria of rats injected i.p. with isoproterenol (0.01 or 0.1 mg/kg) twice a day for 10 days, was 9.0-fold higher than in controls. Isoproterenol (0.17 mg/kg i.p.)-induced stimulation of cardiac ornithine decarboxylase activity was significantly (P less than .05) attenuated in atria from animals of the treated groups. Scatchard analysis of specific binding of [3H]dihydroalprenolol revealed that repeated isoproterenol injection produced a significant decrease in the maximum number of binding sites (Bmax), but not in the dissociation constant (KD) for this antagonist. In comparison to the isoproterenol-induced changes in beta adrenergic positive inotropic response, repeated treatment with isoproterenol decreased 2-fold the EC50 value for the negative inotropic response to ACh in isolated atria. Scatchard analysis of specific [3H]quinuclidinyl benzilate binding, however, indicated a significant (P less than .01) decrease in Bmax. Repeated isoproterenol injections also elicited a significant increase in cardiac weight. It is suggested that repeated administration of isoproterenol induces a decrease in density of beta adrenergic receptors which may in part underlie a cardiac hyposensitivity to isoproterenol and an increase in the number of muscarinic ACh receptors and inotropic responsiveness to ACh.

Acetylcholine↗
PubMed1981

Alteration in dopaminergic and muscarinic cholinergic receptors after subchronic treatment with haloperidol in the developing rat brain.

Influence of subchronic treatment with haloperidol (0.5 to 5.0 mg/kg for 10 days, twice a day) on sensitivity of both central dopaminergic (DA) and muscarinic cholinergic (ACh) receptors was behaviorally and neurochemically investigated 4 days after withdrawal stage of the drug in the developing rat aged 28 days. An i.p. injection of apomorphine 0.2 mg/kg induced locomotor stimulation more effectively in haloperidol-treated animals than in controls. Scatchard analysis of the specific [3H]spiperone binding to the striatal membranes showed that haloperidol treatment produced an increase in the maximal number of binding sites (Bmax) without alteration in a dissociation constant (KD). Pilocarpine (100 and 150 mg/kg) was less effective in inducing catalepsy in the treated animals than in controls, although the treatment did not induce any alteration in saturation parameters of specific [3H]quinuclidinyl benzilate ([3H]QNB) binding to the homogenates of striatum, mesolimbic area and hippocampus. It is suggested that a decrease in Bmax in the striatal [3H]spiperone binding by chronic haloperidol treatment underlies DA receptor hypersensitivity in developing rats. Behavioral muscarinic hyposensitivity caused by chronic haloperidol may not to be due to alteration in the striatal [3H]QNB binding.

Animals↗
PubMed1980

Hypersensitivity of cardiac beta-adrenergic receptors after neonatal treatment of rats with 6-hydroxydopa.

The cardiac beta-adrenergic response to noradrenaline (NA) was investigated in the rat neonatally s.c. treated with 6-hydroxydopa (6-OHDOPA, 75 mg/kg, 0, 2 and 4 days after birth). 6-OHDOPA treatment significantly (P < 0.05) reduced the NA content by 32% of the control in whole heart and markedly potentiated the isoproterenol (0.17 mg/kg, i.p.)-induced stimulation of ornithine decarboxylase activity which had been blocked by a preceding i.p. injection of propranol (10 mg/kg) at the adult stage. Scatchard analysis of the specific [3H]-dihydroalprenolol ([3H]DHA0 binding indicated that 6-OHDOPA induced an increase in the maximum number of specific binding sites of [3H]DHA but did not alter the dissociation constant. In addition, 6-OHDOPA treatment resulted in a potentiation of the positive inotropic response to NA but not to isoproterenol in isolated atria. It is suggested that 6-OHDOPA treatment produces an increased density of beta-adrenergic receptor sites relevant to the hypersensitivity of beta-receptors to NA.

Animals↗
PubMed1979

Decrease in muscarinic cholinergic response of the rat heart following treatment with 6-hydroxydopa.

Pretreatment with 6-hydroxydopa (6-OHDOPA) at birth produced a decrease in the number of [3H]quinuclidinyl benzilate ([3H]QNB) binding sites in adult rat heart homogenates. The treatment caused hyposensitivity to acetylcholine (ACh) but did not alter the maximal negative inotropic action of ACh in isolated atria of the rat. These results suggest that 6-OHDOPA affects the negative inotropic response to ACh by modifying the receptor number or through an effect on a step between receptor activation and biological response.

Acetylcholine↗