Role of sodium in antigen-induced contraction of tracheal smooth muscle in dogs

Yu, J.; Guia, A.; Mink, S.; Kepron, W.; Cragoe, E.J.; Sharma, S.; Bose, R.

Respiration Physiology 91(1): 111-124

1993


ISSN/ISBN: 0034-5687
PMID: 8382833
DOI: 10.1016/0034-5687(93)90093-p
Accession: 009370034

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Abstract
We examined the role of Na+ influx in the airway response to antigen (ragweed pollen extract) in sensitized dogs, using amiloride analogs to block Na+-dependent processes. In in vivo studies, respiratory resistance was measured in amiloride treated and untreated groups. The resistance increased by 9.3 cmH-2O cntdot L-1 cntdot sec in response to ragweed aerosol in the untreated group, but increased only by 5.2 cmH-2O cntdot L-1 cntdot sec in the treated group. In in vitro studies, isometric tension was measured in ragweed pollen sensitized tracheal strips. Tissues were treated with amiloride or its derivatives (50 mu-M) for specifically blocking Na+ channels (phenamil), Na+-H+ exchanger (5-(N-methyl-N-guanidinocarbonyl methyl)-amiloride) or Na+-Ca-2+ exchanger (5-(4-chlorobenzyl)-2',4'-dimethylbenzamil). In untreated strips, tension increased in response to ragweed by 1.9 +- 0.5 mN/mg. The increase was reduced by phenamil (95.2 +- 2.5%; P lt 0.01) and amiloride (41.7 +- 13.1%; P lt 0.01), but not by the other two agents. Furthermore, phenamil also inhibited histamine-induced tension response and histamine-induced 22Na+ uptake of the muscle. We conclude that antigen-induced airway response is attenuated by blocking Na+ influx in smooth muscle.