Increased activity of calcium channels and Rho-associated kinase in the basilar artery during chronic hypertension in vivo

Takanari Kitazono, Tetsuro Ago, Masahiro Kamouchi, Naohiko Santa, Hiroaki Ooboshi, Masatoshi Fujishima, Setsuro Ibayashi

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)879-884
Number of pages6
JournalJournal of Hypertension
Volume20
Issue number5
DOIs
Publication statusPublished - May 1 2002

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rho-Associated Kinases
Basilar Artery
Calcium Channels
Inbred WKY Rats
Inbred SHR Rats
Hypertension
Nicardipine
NG-Nitroarginine Methyl Ester
L-Type Calcium Channels
Glyburide
Vasodilation
Dilatation
Arteries
Large-Conductance Calcium-Activated Potassium Channels
KATP Channels
Vasoconstriction
Constriction
Nitric Oxide Synthase
Blood Vessels
Y 27632

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Increased activity of calcium channels and Rho-associated kinase in the basilar artery during chronic hypertension in vivo. / Kitazono, Takanari; Ago, Tetsuro; Kamouchi, Masahiro; Santa, Naohiko; Ooboshi, Hiroaki; Fujishima, Masatoshi; Ibayashi, Setsuro.

In: Journal of Hypertension, Vol. 20, No. 5, 01.05.2002, p. 879-884.

Research output: Contribution to journalArticle

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abstract = "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.",
author = "Takanari Kitazono and Tetsuro Ago and Masahiro Kamouchi and Naohiko Santa and Hiroaki Ooboshi and Masatoshi Fujishima and Setsuro Ibayashi",
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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 - 2002/5/1

Y1 - 2002/5/1

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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JF - Journal of Hypertension

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