Atropine and hexamethonium-sensitive, Ca/K-modulated, reversible swelling of mast cells in rat mesentery, due to feeding or exposure to carbachol.

Abstract

Transitory swelling of mesenteric mast cells was observed when 24 h-fasted rats were given access to food. Atropine, an anti-muscarinic drug given (1 mg/kg, i.p.) 60 min prior to feeding, prevented this response; carbachol, a cholinomimetic drug caused it to occur when given (2 micrograms/kg, i.v., 10 min) to fasted rats. Mast cells in the mesentery excised from fasted rats, presented swelling in vitro within 1 min following exposure to 10(-7) M carbachol. This response was inhibited by atropine (10(-8) M) or hexamethonium (10(-8) M), indicating that stimulation of a parasympathetic nerve pathway, reported to exist in rat mesentery, could induce mast cell swelling. Exposure to a Ca2+ free medium also led to rapid swelling of mast cells in the mesentery excised from fasted rats. This result, as well as inhibition of the mast cell response to carbachol caused by increasing the Ca2+ (but not by increasing the Mg2+) content of the incubation medium, suggests that swelling was caused by a sudden decrease of Ca at mast cell membrane sites controlling ion/water fluxes. Mast cells swollen by feeding, carbachol or Ca-lack, reverted to their original condition within 20 min when incubated in balanced salt buffer. Such reversal did not occur in a KCl-enriched medium. An equivalent (in terms of ionic strength), increase in NaCl, did not reproduce this effect, indicating that mast cells have K+-dependent means of compensating for endogenously or drug-induced volume changes. Swelling caused by cholinergic stimulation of mast cells was not accompanied by granule exocytosis.2+ carbachol-treated rat blood in vivo or in vitro, is discussed in terms of putative mast cell-controlled, localized homeostasis in the rat mesentery.