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Biomedical subjects

S Takeo

Publications and source records attributed to S Takeo.

At least 181 records · Page 10Linked to original sources
PubMed1985

Modification of cardiac sarcolemmal Na+-Ca2+ exchange by diltiazem and verapamil.

Cardiac sarcolemmal membranes were isolated from the rat heart and their ability for Na+-Ca2+ exchange in the absence or presence of diltiazem and verapamil was examined. Maximal Ca2+ influx activity of membranes due to Na+-dependent reaction occurred within 3 min and was about 5 nmol Ca2+/mg protein. Diltiazem (0.1 to 10 microM) depressed the Ca2+ influx activity significantly whereas verapamil (0.1 to 10 microM) had no effect at initial stages of the reaction (10 to 20 sec). The inhibitory effect of diltiazem on Ca2+ influx was found to be of an uncompetitive nature. Sodium was found to cause a rapid Ca2+ efflux from the calcium loaded membrane vesicles; about 70% of the Ca2+ efflux activity was increased by 0.1 to 10 microM of verapamil and 10 microM of diltiazem significantly. The stimulatory effect of these agents on Ca2+ efflux was associated with a change in Ka value from 16 to 5 mM Na+. Both diltiazem (0.1-3 microM) and verapamil (0.1-10 microM) did not affect the membrane Na+-K+ ATPase activity, but diltiazem in high concentrations (10-30 microM) had an inhibitory action. Specific calcium channel blocking agents, nitrendipine and nifedipine, depressed sodium-dependent Ca2+-efflux activity. A beta-adrenoreceptor antagonist, propranolol, unlike acebutolol, increased sodium-induced Ca2+-influx at high concentrations (10-100 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Acebutolol↗
PubMed1985

Adrenochrome uptake and subcellular distribution in the isolated perfused rat heart.

Adrenochrome uptake and its subcellular distribution were examined using isolated perfused rat heart preparation. The heart was perfused for 30 min with a medium containing 1 to 50 mg/l of 14C-adrenochrome and the subcellular fractions were isolated to measure their radioactivities. A decline in contractile force, a rise in resting tension and an increase in adrenochrome uptake by the heart were seen to depend upon the time of perfusion and the concentration of adrenochrome in the medium. The sarcolemmal fraction had the highest uptake of adrenochrome and this was followed by the microsomal fraction; some accumulation of adrenochrome was also observed in the myofibrillar and mitochondrial fractions. Either 10 or 20 min reperfusion of the heart previously exposed to 25 mg/l of adrenochrome, resulted in approximately 50 or 37% of the radioactivity remaining in the heart; this indicates irreversible binding of adrenochrome to the tissue. Reperfusion of the heart showed restoration of the resting tension but the contractile force did not show any recovery. Propranolol and iproniazid, which have been shown to inhibit the adrenochrome induced cardiotoxicity, reduced adrenochrome uptake by the heart, and prevented adrenochrome-induced depression in contractile force and rise in resting tension. These results indicate that adrenochrome is taken up by the heart and induces cardiac disturbances through its action on different subcellular organelles in the myocardium.

Adrenochrome↗
PubMed1985

Comparison of the effects of nifedipine on ureter and coronary artery isolated from the dog.

The effect of nifedipine (Adalat) on isolated dog ureter was compared with that on isolated coronary artery. Nifedipine at a concentration of 10(-8) mol/l significantly decreased the frequency of ureteral rhythmic contractions evoked by potassium, and suppressed the force of these contractions at a concentration of 3 X 10(-8) mol/l. In potassium-contracted coronary artery strips, nifedipine at concentrations more than 3 X 10(-9) mol/l produced significant relaxations in a concentration-dependent manner. The results indicate that nifedipine is able to act inhibitorily on ureteral contractions, and inhibition of pace making activities in ureteral smooth muscle was suggested as a mode of action of nifedipine.

Animals↗
PubMed1984

Possible alpha-adrenoceptor blocking activity of arotinolol (S-596), a new beta-adrenoceptor blocking agent in isolated dog coronary artery.

Effects of arotinolol on dog coronary arteries were investigated in vitro. In distal portions of left circumflex coronary arteries contracted with 3 X 10(-2)M KCl, norephinephrine relaxed the strips in a concentration-dependent fashion. Propranolol (10(-6)M) converted the norepinephrine-induced relaxations to contractions, and arotinolol (10(-6)-10(-5)M) inhibited the relaxations induced by norepinephrine in a concentration-dependent manner. In proximal portions of the strips after potassium-contracture, norephinephrine produced concentration-dependent contractions which were augmented by propranolol (10(-6)M) and inhibited by arotinolol (10(-6)-10(-5)M). These results suggest that arotinolol has an alpha-adrenoceptor blocking activity in addition to a beta-adrenoceptor blocking action in dog coronary arteries.

Adrenergic alpha-Antagonists↗
PubMed1984

Effects of an antihypertensive agent, nipradilol, on isolated coronary artery of the dog.

Effects of nipradilol on proximal, middle and distal portions of left coronary arteries of the dog were investigated in vitro. Nipradilol (10(-7)-10(-3) M) produced a concentration-dependent relaxation in helical strips of isolated coronary artery under potassium contracture. The relaxation in the middle portions was most pronounced, it was 10% of the equimolar concentrations of nitroglycerin and significantly greater than that of propranolol. In the proximal portions of the coronary arteries, nipradilol (3 X 10(-8)-3 X 10(-7) M) showed a tendency to augment the contractile responses to norepinephrine; in the middle portions it reversed the relaxant responses to norepinephrine into contractile effects in a concentration-dependent manner. In distal portions, nipradilol significantly decreased the relaxant responses of the strips to norepinephrine. The findings demonstrate direct vasodilating and beta-adrenoceptor blocking actions of nipradilol in isolated coronary arteries of the dog.

Adrenergic beta-Antagonists↗
PubMed1984

Changes in cardiac myofibrillar ATPase activity during development of hyperthyroidism in the rabbit.

This study examined changes in cardiac myofibrillar ATPase activity during the development of hyperthyroidism and the relationships between changes in myofibrillar ATPase activity and hemodynamic parameters in rabbits. Calcium-stimulated, magnesium-dependent ATPase (Ca-ATPase) activity of cardiac myofibrils exhibited about a 30% increase after the first week of treatment with excess desiccated thyroid tissue powder (thyroid-treatment) and did not show further increase during thyroid-treatment. Development of cardiac hypertrophy and increases in systolic and diastolic blood pressure were dependent upon prolonged periods of thyroid-treatment lasting from 3 days to 4 weeks, whereas the maximal increase (about 55%) in heart rate was seen after the first week of thyroid-treatment. The elevated level lasted throughout subsequent thyroid-treatment. Lineweaver-Burk plots showed an increase in Km and Vmax values for Ca-ATPase activity of myofibrillar preparation from the thyrotoxic hearts of treated animals. Increased Ca-ATPase activity was correlated with thyroid-induced changes in heart rate. Propranolol partially reduced the thyroid-induced increase in Ca-ATPase activity and heart rate, suggesting participation of beta-adrenoceptors in the thyroid-induced increases of Ca-ATPase activity and heart rate.

Adenosine Triphosphatases↗
PubMed1984

Antitumor activity of macrophages in lung cancer patients with special reference to location of macrophages.

Antitumor activity of macrophages from the peripheral blood, pleural cavity, and alveoli of 35 patients with primary lung cancer was examined. Cytostatic activities of peripheral blood monocytes and alveolar macrophages from either tumor-bearing or non-tumor-bearing segments declined in association with metastasis to regional lymph nodes, an increase in tumor size, and the development of pleural invasion. However, no such correlation could be observed between the cytostatic activity of pleural cavity macrophages and the degree of pleural invasion. The cytostatic activity of pleural cavity macrophages was found to be suppressed when the pleural invasion extended beyond the visceral pleura to the neighboring lobe or chest wall. On the other hand, the cytostatic activity of pleural cavity macrophages was markedly augmented when pleural invasion was limited to within the visceral pleura, although it was low in patients with no visceral pleural invasion. These results suggest that the pleural cavity is isolated from sites of systemic immunological response and that systemic immunological response does not strongly affect pleural cavity macrophages.

Cell Line↗
PubMed1983

Possible mechanisms for reoxygenation-induced recovery of myocardial high-energy phosphates after hypoxia.

Changes in several factors responsible for high-energy phosphate production and metabolism in the heart perfused under hypoxic and subsequent reoxygenated conditions were studied using rabbit heart Langendorff preparation. A marked decline in myocardial ATP and creatine phosphate contents was observed with prolonged periods of hypoxia lasting from 15 to 60 min. Upon reoxygenation after 15 or 30 min hypoxia, creatine phosphate levels were fully recovered, whereas ATP contents were partially restored. Possible mechanisms responsible for reoxygenation-induced differential recovery of high-energy phosphate contents were investigated. Mitochondrial function for generating ATP was depressed upon hypoxia for longer than 15 min hypoxia, and the decreased function was found to be irreversible upon reoxygenation even after 15 min hypoxia. However, mitochondrial ability to generate ATP in the heart receiving 60 min hypoxia was still observed to some extent. Creatine phosphokinase activity of the myocardium exposed to hypoxic solution for 60 min showed only 19% depression. A release of creatine phosphokinase from the perfused heart was observed after more than 30 min of hypoxic perfusion or during reoxygenated perfusion after 60 min hypoxia. Changes in creatine phosphokinase activities of the myocardium and of the perfusate were not associated with those in myocardial high-energy phosphate contents. Hypoxia also induced significant release of adenine nucleotide metabolites from the perfused heart in a biphasic manner. Substrates responsible for the release of the metabolites were found to be mainly inosine and partly hypoxanthine. The metabolite release was also supported by our finding of a decrease in total adenine nucleotide contents of the myocardium upon hypoxia. The present results suggested a crucial role of hypoxia-induced release of adenine nucleotide metabolites in a differential recovery of ATP and creatine phosphate upon reoxygenation.

Adenine Nucleotides↗
PubMed1983

Changes in electrical potential difference and sodium-potassium ATPase of canine mucosa after jejunal-ileal bypass surgery.

Changes in electrical potential difference and sodium-potassium ATPase activity of rectal mucosa in dogs were examined before and after jejunal-ileal bypass surgery. The potential difference in the postoperative period was significantly higher (P less than 0.05) than the preoperative value. The potential difference increased by 160% at the 3rd day after the surgery, and then gradually declined with prolonged recovery periods. Ouabain-sensitive sodium-potassium ATPase activity also increased at the 3rd day (160%) and at the 10th day (86%) after the surgery. Fourteen days after the surgery the sodium-potassium ATPase activity returned almost to the preoperative value. These results indicated a close correlation between changes in transmucosal potential difference and sodium-potassium ATPase activity of rectal mucosa, suggesting a significant participation of sodium-potassium ATPase in changes of potential difference induced by jejunal-ileal bypass surgery.

Animals↗
PubMed1983

Characterization of propranolol-induced relaxation of coronary artery.

Effects of propranolol on coronary artery were investigated in isolated dog coronary arteries and in isolated hearts of rats and guinea-pigs. Cumulative administration of dl-propranolol produced concentration-dependent relaxation of coronary arterial strips under potassium-contracture. There was no difference in relaxant potency between the optical isomers of propranolol. Lidocaine produced less relaxation than dl-propranolol, while atenolol and practolol scarcely affected the contraction. dl-Propranolol-induced relaxation was significantly restored by additional calcium or prevented by prior administration of calcium. In isolated hearts of rats and guinea-pigs which were perfused at a constant coronary inflow and paced at a constant rate, bolus administration of dl-propranolol produced dose-dependent falls in coronary perfusion pressure without significant changes in myocardial contractile force. Results indicate that propranolol may have relaxant activities on coronary arteries through inhibition of calcium influx in the cell membrane of coronary arterial smooth muscle.

Animals↗
PubMed1983

Effects of 2-nicotinamidoethyl nitrate (SG-75, nicorandil) on indomethacin-induced contractions of isolated dog coronary arteries.

Effects of 2-nicotinamidoethyl nitrate (SG-75) on contractile responses of dog coronary arteries to indomethacin were investigated in vitro. Indomethacin (3 X 10(-8) and 3 X 10(-7) Gm/ml) produced contractions of isolated coronary arterial strips, which were reproduced by successive administration of the drug. SG-75 (10(-5) Gm/ml) administered 5 min prior to indomethacin, significantly depressed indomethacin-induced contractions of the strips. In coronary arterial strips under potassium-contracture, SG-75 10(-8)-10(-4) Gm/ml) produced concentration-dependent relaxations, which were not affected by prior administration of indomethacin (3 X 10(-6) Gm/ml). Tranylcypromine (10(-4) Gm/ml) did not influence the relaxant responses of the strips to SG-75 (10(-8)-10(-5) Gm/ml) but significantly depressed them to SG-75 (10(-4) Gm/ml). Results indicate that large doses of SG-75 will induce a relaxant effect on isolated dog coronary arteries through activation of intravascular biosynthesis or release of prostacyclin from vascular tissues.

Animals↗
PubMed1983

Effects of a new beta-adrenoceptor blocking agent, S-596 (arotinolol), on isolated dog coronary arteries.

Effects of S-596 on dog coronary arteries were investigated in vitro. S-596 produced concentration-dependent relaxations of coronary arterial strips under potassium-, prostaglandin (PG) F2 alpha- or PGE2-contracture. S-596-induced relaxations of the strips were not influenced by tetraethylammonium or tranylcypromine, but restored by additional Ca++ or prevented by prior administration of Ca++. In distal portions of coronary arteries, S-596 significantly inhibited concentration-dependent relaxations of the strips induced by norepinephrine and reversed to weak contractions. In proximal portions, S-596 significantly inhibited concentration-dependent contractions induced by norepinephrine. Results indicate that S-596 has a nonspecific relaxant effect on isolated dog coronary arteries maybe through impairment of Ca++ availability and simultaneously has an alpha-adrenoceptor blocking effect, particularly on large coronary arteries.

Adrenergic beta-Antagonists↗
PubMed1982

Effects of 4-aminopyridine and tetraethylammonium on relaxant responses of isolated dog coronary arteries to 2-nicotinamidoethyl nitrate (SG-75).

Effects of 4-aminopyridine (4-AP) and tetraethylammonium (TEA) on vasodilator actions of 2-nicotinamidoethyl nitrate (SG-75) were investigated using isolated dog coronary arteries. SG-75 10(-8)--10(-4) Gm/ml produced concentration-dependent relaxations of coronary arterial strips which were contracted with potassium 30 mM or prostaglandin (PG) F2 alpha 10(-6) Gm/ml. Both 4-AP 5 x 10(-4) Gm/ml and TEA 1.6 x 10(-3) Gm/ml produced further contractions of the strips under potassium or PGF 2 alpha contracture. The potency to constrict the strips was greater in 4-AP than in TEA. 4-AP 5 x 10(-4) Gm/ml and TEA 1.6 x 10(-3) Gm/ml did not affect the SG-75-induced relaxations of the strips under potassium-contracture, but significantly depressed them under PGF2 alpha-contracture. In the strips under a resting state, 4-AP 5 x 10(-4) Gm/ml increased tension and produced oscillations in their contractions, but TEA 1.6 x 10(-3) Gm/ml did not. Results suggest that SG-75 may display its relaxant effect on isolated dog coronary arteries in part through an increase in potassium conductance.

4-Aminopyridine↗
PubMed1982

Relaxant effect of trapidil on isolated dog bronchus.

Relaxant effects of trapidil on dog bronchi were pharmacologically analyzed in vitro. Trapidil concentration-dependently relaxed bronchial strips contracted with methacholine, histamine or potassium. In the strips under methacholine-contracture, theophylline, papaverine, isoproterenol and atropine produced concentration-dependent relaxations. Propranolol significantly decreased isoproterenol-induced relaxations of bronchial strips under methacholine-contracture, but did not trapidil-induced relaxations. Prostaglandin (PG) E1 and PGE2 in high doses slightly relaxed bronchial strips under methacholine-contracture, but PGI2 hardly affected them. Tranylcypromine did not influence relaxant responses of the strips to trapidil. The results indicate that trapidil produces relaxations of bronchial smooth muscle through a non-specific action other than adrenergic beta-receptor activation or endogenous prostaglandin biosynthesis.

Animals↗
PubMed1982

Vitamin D-induced myocardial lesions and the protection by carbocromen.

Effects of high doses of vitamin D on rat hearts were investigated 72 h after the administration of 500 000 U/kg. Histological examination showed disseminated focal necrosis with reactive round cell and granulocytic infiltration in the heart. The calcium content was increased by about 70%. These findings indicate vitamin D-induced myocardial lesions. Heart mitochondrial calcium binding and uptake activities were lower than in control animals. Na+-K+-ATPase activity of heart washed particles was reduced by the treatment with vitamin D whereas neither calcium binding and uptake activities of cardiac sarcoplasmic reticulum nor myofibrillar ATPase activity were affected. Carbocromen (20 and 100 mg/kg/d) treatment reduced vitamin D-induced decreases in mitochondrial calcium accumulating ability and Na+-K+-ATPase activity of heart washed particle, suggesting a beneficial effect of carbocromen against vitamin D-induced cardiac injury.

Animals↗