Calcium Antagonistic Properties of the Sesquiterpene T‐Cadinol : A Comparison with Nimodipine in the Isolated Rat Aorta
Claeson, Per ; Zygmunt, Peter LU
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
(Less)
- author
- Claeson, Per
; Zygmunt, Peter
LU
and Högestätt, Edward D.
LU
- organization
- publishing date
- 1991-01-01
- 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
- 2025-10-14 11:05:38
@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}},
}