TY - JOUR
T1 - Increased activity of calcium channels and Rho-associated kinase in the basilar artery during chronic hypertension in vivo
AU - Kitazono, Takanari
AU - Ago, Tetsuro
AU - Kamouchi, Masahiro
AU - Santa, Naohiko
AU - Ooboshi, Hiroaki
AU - Fujishima, Masatoshi
AU - Ibayashi, Setsuro
PY - 2002/5
Y1 - 2002/5
N2 - Objectives. Several factors mediating vascular responses appear to play an important role in the increased resistance of cerebral blood vessels during hypertension. The objective of this study was to elucidate the mechanisms by which hypertension increases the basal tone of the basilar artery in vivo. Methods. Using a cranial window, we examined effects of inhibitors of L-type voltage-dependent calcium channels (nicardipine) and Rho-associated kinase (Y-27632) on the baseline diameter of the basilar artery in spontaneously hypertensive rats (SHR) and compared to the responses in normotensive Wistar-Kyoto (WKY) rats. Results. Topical application of nicardipine (10-8, 10-7 and 10-6 mol/I) produced dilatation of the basilar artery. Nicardipine-induced vasodilatation was enhanced in SHR compared to WKY rats. Nicardipine (10-6 mol/I) dilated the artery in WKY rats and SHR by 9 ± 2 and 24 ± 4%, respectively. Topical application of Y-27632 (10-7, 10-6 and 10-5 mol/I) produced dilatation of the basilar artery in WKY rats in a concentration-related manner. The vasodilatation produced by Y-27632 was markedly enhanced in SHR compared to WKY rats. Y-27632 (10-5 mol/I) dilated the artery in WKY rats and SHR by 14 ± 2 and 45 ± 6%, respectively. We also tested the effects of inhibitors of nitric oxide synthase (NG-nitro-L-arginine methyl ester, L-NAME), ATP-sensitive potassium channels (glibenclamide) and large-conductance calcium-activated potassium channels (tetraetyhlammonium, TEA). L-NAME and, to a lesser extent, glibenclamide produced similar constriction of the basilar artery in both strains. TEA did not affect the baseline diameter of the basilar artery in WKY rats and produced small but significant vasoconstriction in SHR. Conclusions. These results suggest that the activity of L-type calcium channels and Rho-associated kinase is enhanced in the basilar artery during hypertension in vivo. The enhanced contractility may contribute to the increased resistance of the basilar artery during chronic hypertension in vivo.
AB - Objectives. Several factors mediating vascular responses appear to play an important role in the increased resistance of cerebral blood vessels during hypertension. The objective of this study was to elucidate the mechanisms by which hypertension increases the basal tone of the basilar artery in vivo. Methods. Using a cranial window, we examined effects of inhibitors of L-type voltage-dependent calcium channels (nicardipine) and Rho-associated kinase (Y-27632) on the baseline diameter of the basilar artery in spontaneously hypertensive rats (SHR) and compared to the responses in normotensive Wistar-Kyoto (WKY) rats. Results. Topical application of nicardipine (10-8, 10-7 and 10-6 mol/I) produced dilatation of the basilar artery. Nicardipine-induced vasodilatation was enhanced in SHR compared to WKY rats. Nicardipine (10-6 mol/I) dilated the artery in WKY rats and SHR by 9 ± 2 and 24 ± 4%, respectively. Topical application of Y-27632 (10-7, 10-6 and 10-5 mol/I) produced dilatation of the basilar artery in WKY rats in a concentration-related manner. The vasodilatation produced by Y-27632 was markedly enhanced in SHR compared to WKY rats. Y-27632 (10-5 mol/I) dilated the artery in WKY rats and SHR by 14 ± 2 and 45 ± 6%, respectively. We also tested the effects of inhibitors of nitric oxide synthase (NG-nitro-L-arginine methyl ester, L-NAME), ATP-sensitive potassium channels (glibenclamide) and large-conductance calcium-activated potassium channels (tetraetyhlammonium, TEA). L-NAME and, to a lesser extent, glibenclamide produced similar constriction of the basilar artery in both strains. TEA did not affect the baseline diameter of the basilar artery in WKY rats and produced small but significant vasoconstriction in SHR. Conclusions. These results suggest that the activity of L-type calcium channels and Rho-associated kinase is enhanced in the basilar artery during hypertension in vivo. The enhanced contractility may contribute to the increased resistance of the basilar artery during chronic hypertension in vivo.
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U2 - 10.1097/00004872-200205000-00022
DO - 10.1097/00004872-200205000-00022
M3 - Article
C2 - 12011648
AN - SCOPUS:0036563397
SN - 0263-6352
VL - 20
SP - 879
EP - 884
JO - Journal of hypertension
JF - Journal of hypertension
IS - 5
ER -