S Yokoyama

Publications (2)0 Total impact

• Article: Effects of bradykinin on lymphatic pumping in rat mesentery.

  S Yokoyama, J N Benoit
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  ABSTRACT: The effects of bradykinin on lymphatic pump activity of rat mesenteric collecting duct were studied, and the receptor subtype responsible for the bradykinin response was evaluated. Rats were anesthetized with intraperitoneal alpha-chloralose and urethan, and exteriorized mesenteries were studied using intravital microscopic techniques. The diameter of the collecting lymph vessels (approximately 100 microns) was continuously monitored and lymphatic pump parameters (end diastolic diameter, end systolic diameter, stroke volume index, ejection fraction, contraction frequency, and pump flow index) were calculated. Bradykinin (0.1-1.0 nM) did not affect end diastolic diameter, end systolic diameter, stroke volume index, and ejection fraction. Bradykinin increased lymphatic contraction frequency and pump flow index in a dose-dependent manner. Des-Arg9-[Leu8]bradykinin (B1 antagonist, 0.1 microM) had no effect on baseline lymphatic pumping but completely inhibited the bradykinin-induced increase in contraction frequency. N-acetyl-D-Arg-[Hyp3,Thi5,8,D-Phe7] bradykinin (B2 antagonist, 0.1 microM) significantly depressed lymphatic contraction frequency in baseline conditions but had no effect on bradykinin-induced increases in contraction frequency. These results indicate that bradykinin induces positive chronotropic but not inotropic effects on lymphatic pump activity through the stimulation of B1 receptors.
  The American journal of physiology 06/1996; 270(5 Pt 1):G752-6.
• Article: Hypoxia-reoxygenation impairs endothelium-dependent relaxation in isolated rat aorta.

  S Yokoyama, R J Korthuis, J N Benoit
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  ABSTRACT: The effects of hypoxia followed by reoxygenation on endothelium-dependent relaxation in isolated rat aorta were investigated. Acetylcholine (ACh, 3 nM-10 microM) and calcium ionophore A-23187 (3 nM-300 nM)-induced endothelium-dependent vasorelaxation of isolated rate aortic vessel rings was impaired after 15 min of hypoxia followed by 30 min of reoxygenation. Impairment of ACh-induced relaxation was prevented by pretreatment with the combination of superoxide dismutase (200 U/ml) and catalase (1,000 U/ml). Hypoxia-reoxygenation did not affect sodium nitroprusside (0.1 nM-1 microM)-induced endothelium-independent relaxation nor the dissociation constant of ACh to endothelial M3 muscarinic receptors. Propidium iodide staining of the vascular endothelium revealed a significant increase in the number of dead endothelial cells on the aortic vessel rings following hypoxia-reoxygenation, but not on those pretreated with superoxide dismutase and catalase. These results suggest that hypoxia-reoxygenation impairs endothelium-dependent relaxation of rat aorta by a mechanism that involves oxidant-mediated endothelial cell death.
  The American journal of physiology 06/1996; 270(5 Pt 2):R1126-31.