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Publications (2)4.8 Total impact

  • Risuke Mizuno · Sachiko Watanabe · Toshio Ohhashi ·
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    ABSTRACT: We investigated the effects of NT-702, a selective phosphodiesterase (PDE) 3 inhibitor, on arterioles isolated from rabbit lumbar spinal cords. NT-702 caused a dose-dependent dilation of the isolated spinal arterioles. The disruption of endothelium produced a significant reduction of higher concentrations (10(-7) and 10(-6) M), but not lower concentrations (less than 10(-8) M), of NT-702-induced vasodilation. The NT-702-induced vasodilation of the arterioles with endothelium was not affected by pretreatment with an inhibitor of nitric oxide, cyclooxygenase, or cytochrome P-450 monooxygenase. In contrast, catalase reduced significantly the higher concentrations of NT-702-induced vasodilation only. Tetraethylammonium (TEA) completely reduced the lower concentrations of NT-702-induced vasodilation, but decreased only partially the higher concentrations of NT-702-induced vasodilation of the arterioles with endothelium. Hydrogen peroxide dilated significantly the isolated arterioles with endothelium, the response of which was reduced significantly by TEA. KT5720 (a selective protein kinase inhibitor) significantly decreased both the lower and higher concentrations of NT-702-induced vasodilation of the arterioles with endothelium. The findings suggest that NT-702 dose-dependently dilated the isolated spinal arterioles of rabbits via endothelium-dependent and endothelium-independent mechanisms. Protein kinase A (PKA)- and TEA-sensitive K(+) channels may be involved in the NT-702-induced vasodilation. Moreover, hydrogen peroxide may contribute in part to the endothelium-dependent higher concentrations of NT-702-induced vasodilation.
    The Journal of Physiological Sciences 07/2008; 58(4):229-37. DOI:10.2170/physiolsci.RP003808 · 1.90 Impact Factor
  • Sachiko Watanabe · Yasuaki Yashiro · Risuke Mizuno · Toshio Ohhashi ·
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    ABSTRACT: Flow-induced vasodilation in hamster cremasteric arterioles was investigated with special reference to the roles of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). Arterioles (approximately 60 microm resting diameter) were cannulated, and suffused with MOPS solution at 37 degrees C (mean intraluminal pressure: 80 cm H(2)O). Step increases in the perfusate flow elicited a dose-dependent vasodilation, which was almost proportional to the increases in calculated wall shear stress (WSS). N(omega)-nitro L-arginine methyl ester (L-NAME, 100 microM) reduced the flow-induced vasodilation by approximately 50%, whereas indomethacin (10 microM) produced no significant effect. In the presence of L-NAME, the residual vasodilation was eliminated by treatment with the cytochrome P-450 monooxygenase inhibitor 17-octadecynoic acid (17-ODYA, 50 microM), sulfaphenazol (10 microM), tetraethylammonium (TEA, 3 mM; a nonselective Ca(2+)-activated K(+) channel inhibitor), or charybdotoxin (ChTX, 0.1 microM; intermediate or large conductance Ca(2+)-activated K(+) channel inhibitor). In the absence of L-NAME, the dilation was also reduced by approximately 50% by treatment with 17-ODYA, TEA, or ChTX. The residual vasodilation was eliminated by additional treatment with L-NAME. The inhibitor of ATP-sensitive K(+) channels (K(ATP)), glibenclamide, also caused a significant, but partial, reduction of the flow-induced vasodilation. The residual vasodilation was completely reduced by additional treatment with 17-ODYA, but not L-NAME. These findings suggest that in hamster cremaster, higher flow rate produces NO, K(ATP), and EDHF vasodilation of the arterioles under physiological conditions.
    Journal of Vascular Research 03/2005; 42(2):137-47. DOI:10.1159/000083652 · 2.90 Impact Factor