Abstract
In human bronchial muscle preparations, nifedipine (3 μM) significantly inhibited the histamine, ACh and KCl contractions. However, the dihydropyridine did not modify the contractile responses induced by either leukotriene D4 (LTD4) or anti-human IgE (a-IgE). In human airways, SK&F 96365 (30 μM and 100 μM) markedly reduced the KCl and, at the higher concentration, LTD4 maximal contractions. In addition, when preparations were treated with nifedipine (3 μM), SK&F 96365 (100 μM) significantly blocked responses to both LTD4 and a-IgE. The calcium chelating agent ethylene glycol-bis (β-amino-ethyl ether) N,N,N′,N′-tetraacetic acid (4 mM) also inhibited the a-IgE-induced contractions. These data demonstrate that the nifedipine-resistant component of the LTD4 and a-IgE contractions was inhibited by SK&F 96365 and suggest that the cysteinyl-leukotriene receptor in human airways may be intimately linked with a receptor-operated calcium-entry mechanism.
Footnotes
-
Send reprint requests to: Dr. Charles Brink, CNRS ERS 566, Centre Chirurgical Marie Lannelongue, 133 av de la Résistance, 92350 Le Plessis-Robinson, France.
- Abbreviations:
- LTD4
- leukotriene D4
- a-IgE
- anti-human IgE
- EGTA
- ethylene glycol-bis (β-amino-ethyl ether) N,N,N′,N′-tetraacetic acid
- CysLT1
- cysteinyl-leukotriene receptor
- VOC
- voltage-operated channel
- ROC
- receptor-operated channel
- AIC
- (atropine, 1 μM
- indomethacin
- 3 μM and chlorpheniramine, 1 μM)
- Received May 27, 1997.
- Accepted October 17, 1997.
- The American Society for Pharmacology and Experimental Therapeutics
JPET articles become freely available 12 months after publication, and remain freely available for 5 years.Non-open access articles that fall outside this five year window are available only to institutional subscribers and current ASPET members, or through the article purchase feature at the bottom of the page.
|