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Biomedical subjects

H Koike

Publications and source records attributed to H Koike.

At least 343 records · Page 19Linked to original sources
PubMed1981

Effects of captopril on urinary excretion of prostaglandins and electrolytes in spontaneously hypertensive rats.

Captopril was administered to spontaneously hypertensive rats (SHR) and the acute and long-term effects on the urinary excretion of Na, K, prostaglandin (PG)E2 and PGF2 alpha were studied. Captopril (30 mg and 100 mg/kg p.o.) increased urine volume, urinary Na and K excretion on the 1st and 2nd days of its administration. The urinary K/Na ratio was decreased in the captopril-treated groups on the 1st to 3rd day. Urinary PGE2 excretion in the captopril 100 mg/kg group was significantly increased compared to that in the control group (210.6 +/- 31.4 vs. control 123.2 +/- 8.4 ng/day) on the 1st day of captopril administration. A slight but significant increase in urinary PGF2 alpha excretion was also seen in the captopril 100 mg/kg group (105.2 +/- 9.8 vs. control 75.8 +/- 2.1 ng/day). But PG excretion declined during prolonged treatment and these were no significant difference between the control and captopril-treated groups on the 3rd and 6th week. These data suggest that captopril increases renal PG only as an acute phase and that the increase of PG at least partly accounts for natriuretic affects of the agent.

Animals↗
PubMed1981

Relationship between inhibition of pressor response to angiotensin I and blood concentration of captopril following a single oral administration to dogs.

The time courses for the inhibition of the pressor response to AI and for the blood concentration of captopril and its metabolites were determined following a single oral administration of captopril at a dose of 0.8 or 2.5 mg/kg to normal dogs. Captopril was rapidly absorbed from the gastro-intestinal tract attaining a maximum blood concentration 1-1.5h after its administration. The inhibition of the pressor response to AI was closely related with the blood concentration of unchanged captopril but not of total captopril. The blood concentrations of captopril which produced 50 and 100% inhibition were estimated to be 0.1 and 0.4 millimicron/ml respectively. At 2.5 mh/kg the maximum blood concentration attained was 4 times higher than the concentration required to completely inhibit the pressor response to AI, suggesting that a fraction of the absorbed captopril was in excess of the therapeutic requirement.

Administration, Oral↗
PubMed1981

Antihypertensive activity of bucumolol, a beta-adrenergic blocking agent, in spontaneously hypertensive rats.

Effects of bucumolol, a beta-adrenergic blocking agent, on blood pressure and the renin angiotensin system were studied in spontaneously hypertensive rats (SHR). The results were compared with those of propranolol at an equipotent dose in beta-adrenergic blocking activity. Bucumolol lowered blood pressure and decreased plasma renin concentration (PRC) in both acute and long-term experiments. There was a significant correlation between percent changes in blood pressure and PRC following a single administration of bucumolol. Decrease in PRC persisted for the 6-week observation period despite the sustained reduction in blood pressure. On the other hand, propranolol did not lower blood pressure in acute experiment while it decreased renin release. These results suggest that inhibition of renin release is involved in the antihypertensive action of bucumolol.

Adrenergic beta-Antagonists↗
PubMed1981

Effects of bucumolol, a beta-adrenergic blocking agent, and its d-isomer on myocardial infarction produced by coronary artery ligation in rats.

Acute ligation of the left coronary artery of rats produced abnormal Q-wave in the electrocardiogram, tachycardia and frequent ventricular fibrillation. Serum CPK level was elevated, reaching a maximum at 3 to 5 hours after ligation and returning to near the pre-ligation level 24 hours later, when CPK activity in the left ventricle markedly decreased. Pretreatment with bucumolol at 2.5 mg/Kg s.c. and 5 mg/Kg s.c. lessened these changes and increased the survival rate in a dose related manner. d-Bucumolol at 5 mg/Kg, on the other hand, increased survival rate primarily by suppressing ventricular fibrillation without any significant effect on other parameters. These results suggest that the membrane stabilizing action does not contribute to protective actions of bucumolol against myocardial ischemia.

Adrenergic beta-Antagonists↗
PubMed1981

Assessment of beta-blockade and the non-specific effect of bucumolol, a beta-adrenergic blocking agent, on atrioventricular conduction in anesthetized dogs.

The effects of the beta-adrenergic blocking agent bucumolol [dl-5-methyl-8-(2-hydroxy-3-t-butylaminoproxy)coumarin] and its optical isomers were compared with those of propranolol and pindolol on the functional refractory period and the conduction time of atrioventricular (A-V) transmission in dogs. In dogs with intact nerves anesthetized with pentobarbital, bucumolol and propranolol (30 micrograms - 1 mg/kg) prolonged both parameters by blockade of background sympathetic nervous tone to A-V conduction. The optical d- and l-isomers of bucumolol depressed A-V conduction almost in parallel with their beta-blocking actions. In dogs with cardiac sympathectomy and bilateral vagotomy, or pretreated with reserpine, the dromotropic activity was lowered and the beta-blocking dose (30 micrograms - 1 mg/kg) of bucumolol and propranolol had less effect on A-V conduction, while larger doses (3-10 mg/kg) produced additional depression of the conduction. Pindolol, on the other hand, had a positive dromotropic action, reflecting its intrinsic stimulatory action. It is concluded that A-V conduction is affected by the existing tone of sympathetic nervous activity and that bucumolol has no beta-stimulant action and depresses A-V conduction by beta-blockade and by a non-specific action.

Adrenergic beta-Antagonists↗
PubMed1981

Long-term effects of captopril on cellular sodium content and mechanical properties of aortic smooth muscle from spontaneously hypertensive rats.

The long-term effects of captopril on passive Na permeability and Na content in aortic smooth muscles of spontaneously hypertensive rats (SHR) were examined in relation to the mechanical properties of the muscles. Captopril or hydralazine when administered for 6 weeks exhibited antihypertensive action throughout the period. Cellular Na in both freshly excised aortas and incubated aortas from SHR leaked out more rapidly in cold Li-solution than those from normotensive Wistar-Kyoto rats, suggesting increased permeability in SHR aortas. Long-term treatment with captopril decreased the "permeability" of the vascular membrane of SHR, whereas hydralazine failed to decrease it. Incubation of the aortas in K+-free Tyrode's solution produced a slowly developing contraction. The rate of rise of this contraction was faster in SHR aorta that in Wistar-Kyoto aorta. In aortas from captopril-treated SHR, the rate of rise in the contraction was suppressed. The contractile response to K+-free medium was related to the passive permeability to Na and thereby to the increment of cellular Na. It is suggested that, after prolonged administration, captopril alters the abnormal permeability to Na of the vascular smooth muscle membrane in SHR and that the alteration contributes to the antihypertensive effect of the agent.

Animals↗
PubMed1981

Cardiovascular pharmacology of bumepidil, a new synthetic vasoactive compound for coronary circulation.

Intravenously administered 8-tert.-butyl-7,8-dihydro-5-methyl-6H-pyrrolo[3,2-e]triazolo[1,5-alpyrimidine (bumepidil, CS-611) increased the coronary sinus outflow as well as intramyocardial flows in both subendocardial and subepicardial layers in the anesthetized dog and also the increase in the coronary arterial inflow was observed with short onset time, within 10 min when given orally to the conscious dog, and time for maximum effect is also short, i.e., 20 min after the oral administration. In the anesthetized rabbit flow-increase in the brain by CS-611 was next to the coronary, followed by the stomach and small intestines while there was no organ which showed a decreased flow. In the anesthetized open-chest dog cardiac output was increased by CS-611 while myocardial oxygen consumption was little affected. In addition, CS-611 exerted antiarrhythmic action on ventricular ectopics induced by coronary ligation of the conscious dog. A correlation between the increase in myocardial flow by CS-611 in the intact heart and the antiarrhythmic action in the coronary-lighted heart still remains to be studied further.

Animals↗
PubMed1980

Cellular synthesis and axonal transport of gamma-aminobutyric acid in a photoreceptor cell of the barnacle.

1. [3H]glutamate or [3H]gamma-aminobutyric acid (GABA) was injected into the photoreceptor cell of the lateral ocellus of Balanus eburneus, in order to study the transmitter substance of the cell. 2. The photoreceptor cell synthesized [3H]GABA from injected [3H]glutamate. 3. The newly formed [3H]GABA moved inside the photoreceptor axon towards the axon terminal with a velocity of about 0.9 mm/hr. Injected [3H]GABA moved at 0.9 mm/hr and also at 0.4 mm/hr. 4. Axonally transported [3H]GABA reached the axon terminal within several hours following the injection. It did not accumulate at the terminal, but gradually disappeared. 5. Light-microscope and electron-microscope autoradiography following the injection of [3H]GABA revealed that [3H]-reacted silver grains were present in a certain type of axon terminal. The terminal thus identified as that of a photoreceptor cell contains many clear, polymorphic synaptic vesicles about 300-500 A in diameter, some dense-cored vesicles 700-1300 A in diameter, and glycogen granules. The terminal forms many synapses, and each synapse has a synaptic dense body. The terminal always faces two post-synaptic elements at the synapse, forming a triad with a gap distance of about 160-200 A. 6. A GABA analogue, [3H]di-aminobutyric acid, was selectively taken up into the terminals previously identified as those of photoreceptors. 7. These results support the notion that the transmitter substance of the photoreceptor cell of the barnacle is GABA.

Animals↗