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Comparative Study
. 1991 Feb;102(2):337-44.
doi: 10.1111/j.1476-5381.1991.tb12175.x.

Differences between the effects of cromakalim and nifedipine on agonist-induced responses in rabbit aorta

Affiliations
Comparative Study

Differences between the effects of cromakalim and nifedipine on agonist-induced responses in rabbit aorta

K M Bray et al. Br J Pharmacol. 1991 Feb.

Abstract

1. The effects of cromakalim on endothelium-denuded rabbit aortic strips were compared with those of the calcium (Ca2+) entry blocking agent, nifedipine. 2. Pre-incubation with cromakalim or nifedipine had no significant effect on the initial phasic component of noradrenaline (NA)-induced responses. 3. Cromakalim (0.3-10 microM), but not nifedipine, inhibited the maintained tonic contractions produced by NA. The effects of cromakalim were antagonized by raising extracellular [K+] or by glibenclamide. 4. Nifedipine inhibited contractions produced by KCl (40 mM) whereas cromakalim had no effect. 5. In Ca2(+)-free physiological salt solution (PSS), cromakalim produced a significant inhibition of both the refilling of and the release of Ca2+ from NA-releasable Ca2+ stores, whereas nifedipine was ineffective. 6. In tissues preloaded with 42K+ cromakalim (0.3-10 microM) produced a concentration-dependent increase in the 42K+ efflux rate coefficient. NA (0.3 microM) also produced an increase in the rate of efflux of 42K+, an effect which was not antagonized by nifedipine (0.3 microM). 7. When microelectrodes were used, cromakalim (1-10 microM) produced a maintained concentration-dependent membrane hyperpolarization. However, low concentrations of cromakalim (less than 1 microM) which relaxed the aorta had no effect on membrane potential. NA had no significant effect on membrane potential. 9. It is concluded that the ability of cromakalim to relax NA-induced contractions in rabbit aorta is not exerted by the indirect closure of nifedipine-sensitive Ca2+ channels. Instead, cromakalim may exert a direct inhibitory action on Ca2+ uptake into and release from Ca2+ stores and additionally inhibit the pathway through which Ca2+ passes from the extracellular fluid to intracellular Ca2+ stores.

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References

    1. Science. 1989 Jul 14;245(4914):177-80 - PubMed
    1. J Pharmacol Exp Ther. 1988 Jun;245(3):751-60 - PubMed
    1. Naunyn Schmiedebergs Arch Pharmacol. 1988 Sep;338(3):319-26 - PubMed
    1. Br J Pharmacol. 1988 Nov;95(3):741-52 - PubMed
    1. J Pharmacol Exp Ther. 1989 Jan;248(1):149-56 - PubMed

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