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Biomedical subjects

M Sakanashi

Publications and source records attributed to M Sakanashi.

At least 109 records · Page 6Linked to original sources
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

Effects of organic Ca2+-antagonists on membrane characteristics of nodose ganglion cells in the rabbit.

The effects of Ca2+-antagonists, diltiazem, verapamil and nifedipine on excised and superfused nodose ganglia of the rabbit were investigated with intracellular recording techniques. In a Na-free solution, somata of nodose ganglion C-cells were capable of eliciting Ca-spikes which were maintained by a Ca-influx when stimulated by passing currents. At a concentration of 10(-5) M, spike amplitude was inhibited to 24% of control by diltiazem, to 16% by verapamil, and to 13% by nifedipine. In a normal physiological solution, diltiazem at 10(-6) M, verapamil at 10(-6) M, and nifedipine at 10(-7) M reduced the maximal rate of rise and at 10(-7) M produced a reduction of the maximal rate of fall of the action potentials accompanied with a prolonged duration, although the resting membrane potential and the amplitude of the action potentials were not altered. The results reveal membrane characteristics of ganglion cells and suggest that Ca2+-antagonists depress not only Ca-influx but also Na-influx and K-efflux.

Action Potentials↗
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

Effects of some prostaglandins on urinary bladder and urethra isolated from the dog.

Effects of prostaglandins (PGs) E1, E2, E2 and F2 alpha on the vesical and urethral smooth muscles of dogs were isometrically investigated in vitro. In vesical smooth muscles, 10(-8)-10(-6) PGE1/ml produced biphasic responses in the dome preparations; relaxation at 10(-8) g/ml and contractions at 10(-7)-10(-6) g/ml. In the trigone preparations, 10(-8)-10(-6) g PGE1/ml caused dose-dependent contractions. 10(-8)-10(-6)M g PGE2/ml and 10(-7)-10(-6) g PGF2 alpha /ml induced dose-dependent contractions of the dome and the trigone preparations. In urethral smooth muscles, 10(-8)-10(-6) g PGE1/ml and 10(-8)-10(-6) g PGE2/ml produced dose-dependent relaxations, while 10(-8)-10(-6) g PGF2 alpha /ml caused dose-dependent contractions. Results indicate that PGE, particularly PGE2, is able to stimulate micturition through vesical contraction and urethral relaxation.

Alprostadil↗
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↗
PubMed1983

Possible antiarrhythmic activities of trapidil.

Possible antiarrhythmic activities of 5-methyl-7-diethylamino-s-triazolo(1,5-a)pyrimidine (trapidil, Rocornal) were investigated in vitro and in vivo. Trapidil significantly increased the amount of aconitine or ouabain needed for production of ventricular arrhythmias in rats and guinea pigs. Trapidil also produced a significant increase in threshold current of electrical stimuli which induced ventricular tachycardia in dogs under acute myocardial ischemia. Electrophysiological examinations on effects of trapidil on isolated rabbit ventricular muscle cells showed shortening of the action potential duration (APD) and prolongation of the effective refractory period (ERP), resulting in an increase in the ratio of ERP/APD. The results indicate that trapidil will have a possible effectiveness in inhibiting ventricular arrhythmias.

Aconitine↗
PubMed1983

A pharmacological investigation on a possible calcium antagonistic action of propranolol.

The present study was designed to investigate the mechanisms of smooth muscle relaxant effects of propranolol. The relaxant effects of the drug on potassium (K+)-contracture or lanthanum (La3+)-contracture were studied using smooth muscle preparations of dog coronary artery and colon in comparison with those of nitroglycerin, nifedipine and papaverine. Nitroglycerin relaxed the coronary artery preparations under K+-contracture as well as La3+-contracture, but did not relax the colon preparations under K+- and La3+-contracture. Papaverine relaxed both types of smooth muscles under K+- and La3+-contracture. Nifedipine relaxed the coronary artery and the colon preparations under K+-contracture, but did not relax them under La3+-contracture. Propranolol produced the same relaxant effects on both preparations as nifedipine. Furthermore, propranolol concentration-dependently inhibited the calcium-induced contractions of the coronary arterial preparations. The results suggest that propranolol, like nifedipine, may have a calcium antagonistic action in the cell membrane of smooth muscles.

Animals↗
PubMed1982

Effects of acetylcholine on the tone and miniature contractions of isolated dog urinary bladder.

Effects of acetylcholine on the tone and miniature contractions of dog urinary bladder were investigated in vitro. In both dome and trigone preparations, cumulative administrations of acetylcholine produced dose-dependent increases in the tone, which were dose-dependently depressed by prior administration of atropine and augmented by neostigmine. The frequency of miniature contractions in the dome and trigone was dose-dependently increased by acetylcholine. The dose-response curves of the frequency for acetylcholine were shifted to the right by atropine and to the left by neostigmine in both preparations. The amplitude of miniature contractions in both preparations was not significantly changed by acetylcholine. A computer analysis showed that changes in the tone of the bladder had the positive correlation to the frequency of miniature contractions. The results indicate that acetylcholine would act on the urinary bladder through activation of muscarinic receptors, and that there is the positive correlation between changes in the tone and the frequency of miniature contractions.

Acetylcholine↗
PubMed1982

Effects of adrenergic drugs on miniature contractions of isolated dog urinary bladder.

Isolated dog urinary bladder showed spontaneous miniature contractions under a steady state. In dome preparations, norepinephrine and isoproterenol decreased the frequency of miniature contractions, while epinephrine produced biphasic responses on it; increase by low concentration and decrease by high concentrations. The height of miniature contractions was decreased by these drugs. In trigone preparations, norepinephrine and epinephrine increased the frequency of miniature contractions, while isoproterenol decreased it. These drugs decreased the height of miniature contractions. In both preparations, phentolamine enhanced the decreases in frequency and height by norepinephrine, epinephrine and isoproterenol, while propranolol depressed or reversed them. A computer analysis showed positive and significant correlations between changes in tension development of bladder and frequency and height of miniature contractions. Results indicate that miniature contractions in both dome and trigone of isolated dog urinary bladder are increased by activation of alpha-adrenoceptors and decreased by activation of beta-adrenoceptors.

Animals↗
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

A possible mechanism involved in generation of automaticity of isolated human renal artery.

A possible mechanism involved in generation of automaticity of isolated human renal arteries was investigated qualitatively. Helical strips of human renal arteries showed rapid contractions followed by marked oscillations in the tension by administrations of vasoconstrictor agents such as norepinephrine, epinephrine, dopamine and 5-HT. Vasodilator agents such as acetylcholine and isoproterenol did not produce any change in these strips, but high doses of acetylcholine and isoproterenol evoked marked oscillations together with increases in the vascular tone. Prostaglandins E1, E2 and F2 alpha increased the vascular tone of the renal arterial strips, and generated marked oscillations in their contractions which were inhibited by aspirin or indomethacin. Two renal arterial strips showed marked oscillations in the tension by passive elevation of the basal tone of the strips. The marked oscillations did not appear when indomethacin was previously administered. The results indicate that mechanical stimulation of renal arterial smooth muscle, such as contractions, may induce enhancement of endogenous prostaglandin biosynthesis, resulting in generation of automaticity of isolated human renal arteries.

Acetylcholine↗
PubMed1981

Relaxation of isolated dog coronary artery induced by propranolol.

The effects of propranolol and atenolol on isolated dog coronary arteries contracted with potassium were investigated in vitro. Propranolol at high concentrations (3 x 10(-5)-10(-4) M) produced relaxations of the coronary arterial strips, which were restored or prevented by exogenous calcium ions. Atenolol (10(-5)-10(-4) M) never changed the tension of the strips. The results suggest that propranolol may inhibit the coronary arteries through its calcium antagonistic action.

Animals↗
PubMed1981

Actions of some autonomic drugs on isolated dog quiescent ureter.

Actions of some autonomic drugs on upper, middle and lower portion of isolated dog ureters under quiescent state were investigated quantitatively. Noradrenaline and adrenaline at lower concentrations evoked contractions in each portion of the ureters and increased the concentration-dependent frequency and tension of these contractions, but attenuated them at higher concentrations. Phentolamine significantly depressed these contractions, while propranolol enhanced them. Phenylephrine increased the concentration-dependent frequency and tension of contractions, which were suppressed by phentolamine. Acetylcholine at higher concentrations produced contractions of the ureters, and phentolamine or hexamethonium suppressed them. The results indicate that ureteral contractions may be stimulated through an activation of alpha-adrenoceptors and be attenuated through an activation of beta-adrenoceptors, and that acetylcholine may release noradrenaline from sympathetic nerve endings through an activation of presynaptic nicotinic receptors, resulting in ureteral contractions.

Animals↗
PubMed1981

Further investigations on potassium-induced automaticity of isolated human renal artery.

Experiments were designed to investigate generation of automaticity of isolated human renal arteries induced by administration of potassium in vitro. Helical strips of human renal arteries showed marked oscillations in the potassium-induced contractions which persisted for 2 hr. Indomethacin and aspirin dose-dependently inhibited these oscillations. Tranylcypromine and mepacrine also had an inhibitory action on the oscillations of the strips induced by potassium. In the strips which reached a steady state 2 hr after administration of potassium, phospholipase A2 and bradykinin produced marked oscillations. Our results indicate that human renal arteries can generate automaticity in the contractions induced by potassium, and that such automaticity may be related to the biosynthesis of prostaglandins.

Adult↗