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Biomedical subjects

S Shibata

Publications and source records attributed to S Shibata.

At least 883 records · Page 49Linked to original sources
PubMed1980

Mechanism of the excitatory action of palytoxin and N-acetylpalytoxin in the isolated guinea-pig vas deferens.

Palytoxin (PTX), one of the most well known potent toxic substances among marine toxins, caused a slow phasic contraction of the isolated guinea-pig vas deferens (second component) followed by the first rapid phasic contraction (first component) at concentrations above 3 x 10(-9) M. N-acetylpalytoxin, one of its derivatives, also produced similar actions but its potency was about 1/100 of that of PTX. The second component of PTX-induced contraction, but not the first component, was markedly inhibited by treatments with phentolamine, reserpine and 6-hydroxydopamine, but remained unaffected by atropine and mecamylamine pretreatment. Tetrodotoxin partially inhibited the second component, whereas the second component was markedly inhibited by solutions low in Na+ (85.2 mM) or containing verapamil (10(-6) M). Both components were completely abolished by high Mg++ or Ca++-free medium. It is concluded that the first component was the result of a direct action of PTX on smooth muscle sites, whereas the second phase was the result of an indirect action mediated through the norephinephrine release from the adrenergic nerve terminals.

Acrylamides↗
PubMed1980

Pressor response to 5-hydroxytryptamine, norepinephrine and KCi in the perfused hindquarter preparation from the spontaneously hypertensive rat.

The pressor response to 5-hydroxytryptamine (5-HT), norepinephrine (NE), and KCI was studied in the blood- and Ringer's- perfused hindquarters of the spontaneously hypertensive rat (SHR) and the Kyoto normotensive Wistar rat in two age groups: 8 to 10 weeks and 6 to 8 months. In both preparations, the response to 5-HT, NE and KCI was greater in the young and old SHRs than in the age-matched normotensive Wistar rats. The enhanced responsiveness to 5-HT in old SHRs was of greater magnitude than that to NE or KCI, whereas in young SHRs the enhanced responsiveness to the three pressor agents was of similar magnitude. This appears to be due in part to a greater reduction in responsiveness to NE and KCI than to 5-HT as the animal becomes older. Enhanced responsiveness to 5-HT also occurs in the renal hypertensive rat. However, there was no difference in responsiveness to low doses of NE or KCI in the renal hypertensive rat. The response to 5-HT in the old SHR was blocked by methysergide but was not affected by phentolamine, isoproterenol or nitroglycerin. In the old SHR made hypotensive by occlusion of the abdominal aorta for a duration of 3 to 5 weeks, the responsiveness to all three pressor agents was reduced but was most marked for 5-HT. These latter results suggest that blood pressure per se contributes to the enhanced responsiveness to NE, KCI and, to a greater extent, 5-HT.

Animals↗
PubMed1980

Possible generation of potent vasocontracting substance from prostaglandin endoperoxide analogs, human platelets mixture.

The mixture of human platelets and prostaglandin (PG) endoperoxide analogs (U46619 and U44069) at threshold concentrations caused a marked enhanced vasocontraction of rabbit aortae and bovine coronary arteries. THe configuration of the mixture-induced contraction was a sustained and tonic form. On the other hand, the thromboxane A2-like substance which was generated during the incubation of arachidonic acid with human platelets caused a transient and phasic contraction, and the amplitude of this contraction was much less than that of the mixture. Even after exposure to high temperature for various time periods, the mixture was still able to cause the enhanced vasocontraction. However, this mixture lost the activity of vasocontraction after an incubation in strong acid (pH 1) or alkali (pH 12) for 10 min. Serotonin and alpha adrenoceptor antagonists had no effect on the mixture-induced contraction. When tissues were incubated in Ca-free medium for a few minutes, the mixture failed to cause vasocontraction, whereas the contractile responses to histamine, norepinephrine and serotonin were not affected. When tissues were pretreated with imidazole (10(-5) M), which is a thromboxane synthetase inhibitor, the vasocontration induced by the mixture was potentiated rather than inhibited, whereas the thromboxane A2-like substance-induced contraction was inhibited. When either the tissue was pretreated with or platelets were incubated with indomethacin, the mixture failed to cause the enhanced vasocontraction. The new synthetic arginine derivatives (T1189 and T1233) nearly abolished the vasocontractile response to the mixture. However, both derivatives failed to inhibit the vasocontractions of PGE2 and PGF2 alpha, arachidonic acid and KCl. These results suggest the possibility that during the incubation of endoperoxides with human platelets a potent vasocontractile substance could be generated and such a substance does not resemble thromboxane A2 or any of the PGs tested.

Adult↗
PubMed1979

Creatine phosphate in rat platelets decreased by ADP or thrombin.

ADP or thrombin caused a transient change in creatine phosphate (CP) content of rat platelets. At 25 degrees C the CP content decreased most 30 sec after the addition of ADP or thrombin and recovered thereafter. ATP or AMP was without effect. The rat platelets aggregated at 25 degrees C by ADP or thrombin, but the changes in CP content by these inducers were also observed in the platelet preparations unable to aggregate by the lack of Ca2+. A persistent chilling made the platelets lose their ability to change CP content. It was suggested that in rat platelets CP is consumed in the early stage of the response to the aggregating agents, presumably donating the energy for shape change.

Adenosine Diphosphate↗
PubMed1979

Effect of cardiotonic polypeptide anthopleurin-A on canine Purkinje and ventricular muscle fibers.

Effects of Anthopleurin-A (AP-A, polypeptide from sea anemone) were studied on electrophysiological properties of isolated canine Purkinje and ventricular muscle fibers. Ap-A (in concentrations above 20 micrograms/l) produced a dose-dependent increase in action potential duration (APD) and the refractory period (RFP) in electrically driven Purkinje fibers, but had no effect on other parameters. Similar but less prominent change in APD and RFP was observed in ventricular muscle fibers. AP-A in high concentrations (200 micrograms/l or higher) did alter the spontaneous firing rate of Purkinje fibers. Since AP-A in low concentrations will increase the refractory period of conducting fibers without affecting a conduction velocity, it may abolish some re-entrant arrhythmias.

Action Potentials↗