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Calcium Antagonistic Properties of the Sesquiterpene T‐Cadinol : A Comparison with Nimodipine in the Isolated Rat Aorta

Claeson, Per ; Zygmunt, Peter LU orcid and Högestätt, Edward D. LU (1991) In Pharmacology and Toxicology 69(3). p.173-177
Abstract

Abstract: (+)‐T‐Cadinol is a sesquiterpene with smooth muscle relaxing properties. In the isolated rat aorta, T‐cadinol relaxed contractions induced by 60 mM K+ in a concentration‐dependent fashion. The dihydropyridine calcium antagonist nimodipine was approximately 4,000 times more potent than T‐cadinol. While both drugs nearly abolished the K+‐induced contractions, they only partially relaxed contractions induced by phenylephrine. The relaxation induced by T‐cadinol and nimodipine in K+‐contracted aortic rings, was completely reversed by the calcium channel activator Bay K8644. In aortic preparations partially depolarized by 20 mM K+, Bay K8644 induced a concentration‐dependent contraction.... (More)

Abstract: (+)‐T‐Cadinol is a sesquiterpene with smooth muscle relaxing properties. In the isolated rat aorta, T‐cadinol relaxed contractions induced by 60 mM K+ in a concentration‐dependent fashion. The dihydropyridine calcium antagonist nimodipine was approximately 4,000 times more potent than T‐cadinol. While both drugs nearly abolished the K+‐induced contractions, they only partially relaxed contractions induced by phenylephrine. The relaxation induced by T‐cadinol and nimodipine in K+‐contracted aortic rings, was completely reversed by the calcium channel activator Bay K8644. In aortic preparations partially depolarized by 20 mM K+, Bay K8644 induced a concentration‐dependent contraction. Nimodipine shifted the Bay K8644 concentration‐response curve to the right in a parallel manner, consistent with a competitive mode of inhibition. T‐cadinol at concentrations less than 10−3.5 M also produced a right‐ward shift of the Bay K8644 concentration‐response curve with a maintained maximum response. However, the highest T‐cadinol concentration used (10−3.5 M) significantly reduced the maximum response. In conclusion, although T‐cadinol and nimodipine display marked structural differences, their pharmacological profiles of action have several features in common, suggesting that T‐cadinol is a calcium antagonist, possibly interacting with the dihydropyridine binding sites on the calcium channels. 1991 Nordic Pharmacological Society

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type
Contribution to journal
publication status
published
subject
in
Pharmacology and Toxicology
volume
69
issue
3
pages
5 pages
publisher
Wiley-Blackwell
external identifiers
  • scopus:0025870588
  • pmid:1724563
ISSN
0901-9928
DOI
10.1111/j.1600-0773.1991.tb01293.x
language
English
LU publication?
yes
id
d6f8b508-8664-4c8e-beee-32c1f978b090
date added to LUP
2019-05-31 21:43:12
date last changed
2024-01-01 09:01:58
@article{d6f8b508-8664-4c8e-beee-32c1f978b090,
  abstract     = {{<p>Abstract:  (+)‐T‐Cadinol is a sesquiterpene with smooth muscle relaxing properties. In the isolated rat aorta, T‐cadinol relaxed contractions induced by 60 mM K<sup>+</sup> in a concentration‐dependent fashion. The dihydropyridine calcium antagonist nimodipine was approximately 4,000 times more potent than T‐cadinol. While both drugs nearly abolished the K<sup>+</sup>‐induced contractions, they only partially relaxed contractions induced by phenylephrine. The relaxation induced by T‐cadinol and nimodipine in K<sup>+</sup>‐contracted aortic rings, was completely reversed by the calcium channel activator Bay K8644. In aortic preparations partially depolarized by 20 mM K<sup>+</sup>, Bay K8644 induced a concentration‐dependent contraction. Nimodipine shifted the Bay K8644 concentration‐response curve to the right in a parallel manner, consistent with a competitive mode of inhibition. T‐cadinol at concentrations less than 10<sup>−3.5</sup> M also produced a right‐ward shift of the Bay K8644 concentration‐response curve with a maintained maximum response. However, the highest T‐cadinol concentration used (10<sup>−3.5</sup> M) significantly reduced the maximum response. In conclusion, although T‐cadinol and nimodipine display marked structural differences, their pharmacological profiles of action have several features in common, suggesting that T‐cadinol is a calcium antagonist, possibly interacting with the dihydropyridine binding sites on the calcium channels. 1991 Nordic Pharmacological Society</p>}},
  author       = {{Claeson, Per and Zygmunt, Peter and Högestätt, Edward D.}},
  issn         = {{0901-9928}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{3}},
  pages        = {{173--177}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Pharmacology and Toxicology}},
  title        = {{Calcium Antagonistic Properties of the Sesquiterpene T‐Cadinol : A Comparison with Nimodipine in the Isolated Rat Aorta}},
  url          = {{http://dx.doi.org/10.1111/j.1600-0773.1991.tb01293.x}},
  doi          = {{10.1111/j.1600-0773.1991.tb01293.x}},
  volume       = {{69}},
  year         = {{1991}},
}