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Research ArticleCARDIOVASCULAR

Activation of Capsaicin-Sensitive Sensory Neurons by Carvedilol, a Nonselective β-Blocker, in Spontaneous Hypertensive Rats

Kenji Okajima, Naoaki Harada, Mitsuhiro Uchiba and Hirotaka Isobe
Journal of Pharmacology and Experimental Therapeutics May 2004, 309 (2) 684-691; DOI: https://doi.org/10.1124/jpet.103.061150
Kenji Okajima
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Naoaki Harada
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Mitsuhiro Uchiba
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Hirotaka Isobe
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Abstract

We performed a study in spontaneous hypertensive rats (SHR) to determine whether carvedilol, a nonselective β-adrenoceptor antagonist, activates capsaicin-sensitive sensory neurons (CSSNs), thereby promoting the release of calcitonin gene-related peptide (CGRP), a neuropeptide with an important role in maintenance of cardiovascular homeostasis. Carvedilol given intravenously at a dose of 0.3 mg/kg transiently decreased the mean arterial blood pressure (MABP) and increased renal tissue blood flow with increases in CGRP levels in plasma and kidney. These effects induced by carvedilol were not seen in animals pretreated with capsazepine, an antagonist of capsaicin. Although 1.0 mg/kg cavedilol markedly decreased MABP, it neither increased renal tissue blood flow nor CGRP levels in plasma and kidney. Prazosin, a selective α1-adrenoceptor antagonist, and bisoprolol, a selective β1-adrenoceptor antagonist, decreased MABP with capsazepine, showing no antagonistic action in either cases, and these agents increased neither renal tissue blood flow nor levels of CGRP in plasma and kidney. Both ICI 118,551 [(±)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol], a selective β2-adrenoceptor antagonist, at a dose of 0.25 mg/kg and capsaicin mimicked effects induced by 0.3 mg/kg carvedilol. Administration of 1.0 mg/kg ICI 118,551 produced effects similar to those induced by 1.0 mg/kg carvedilol. These observations strongly suggested that the low dose of carvedilol might activate CSSNs in SHR to increase the release of CGRP, thereby decreasing blood pressure with an increase in renal tissue blood flow. The effects induced by carvedilol seemed to be mediated by its β2-adrenoceptor blockade activity.

Footnotes

  • This study was supported, in part, by departmental funds from Kumamoto University School of Medicine.

  • Article, publication date, and citation information can be found at http://jpet.aspetjournals.org.

  • DOI: 10.1124/jpet.103.061150.

  • ABBREVIATIONS: CSSN, capsaicin-sensitive sensory neuron(s); CGRP, calcitonin gene-related peptide; CHF, congestive heart failure; SHR; spontaneous hypertensive rats; CPZ, capsazepine; TFA, trifluoroacetic acid; MABP, mean arterial blood pressure; ICI 118,551, (±)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol.

    • Received October 7, 2003.
    • Accepted February 5, 2004.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 309 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 309, Issue 2
1 May 2004
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Research ArticleCARDIOVASCULAR

Activation of Capsaicin-Sensitive Sensory Neurons by Carvedilol, a Nonselective β-Blocker, in Spontaneous Hypertensive Rats

Kenji Okajima, Naoaki Harada, Mitsuhiro Uchiba and Hirotaka Isobe
Journal of Pharmacology and Experimental Therapeutics May 1, 2004, 309 (2) 684-691; DOI: https://doi.org/10.1124/jpet.103.061150

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Research ArticleCARDIOVASCULAR

Activation of Capsaicin-Sensitive Sensory Neurons by Carvedilol, a Nonselective β-Blocker, in Spontaneous Hypertensive Rats

Kenji Okajima, Naoaki Harada, Mitsuhiro Uchiba and Hirotaka Isobe
Journal of Pharmacology and Experimental Therapeutics May 1, 2004, 309 (2) 684-691; DOI: https://doi.org/10.1124/jpet.103.061150
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