Effect of temperature reduction on the vas deferens hyperresponsiveness of sensitized mice

Abstract

1. The present study was designed to investigate the effect of active sensitization on the responsiveness of mouse vas deferens before and after moderate cooling. Contractile responses to noradrenaline (NA) were isometrically recorded in the vas deferens of control and ovalbumen-sensitized mice at 37 degrees C and 22 degrees C. 2. Enhancement of the vas deferens reactivity to NA was observed in the sensitized vs control mice at 37 degrees C and 22 degrees C (P < 0.01). In sensitized mice, maximal contraction was significantly increased compared with controls, and sensitization-induced hyperresponsiveness was greater at 22 degrees C compared with 37 degrees C. At 37 degrees C, contractile responses to barium chloride were significantly enhanced in the sensitized mice compared with controls, whereas the reduction of the temperature to 22 degrees C produced a marked inhibition of vas deferens contractions in both groups. Caffeine-induced contractions of the vas deferens were similar in control and sensitized mice at 37 degrees C. After moderate cooling to 22 degrees C, vas deferens from sensitized mice became hyperresponsive compared with controls. 3. Ouabain (0.1 mM) produced an increase of NA-induced contraction in control and sensitized vas deferens at 37 degrees C (P < 0.01). It had no significant effect in the control at 22 degrees C but produced a marked inhibition of NA-induced contraction in the sensitized vas deferens at 22 degrees C. Contractions to NA in the presence of vanadate (1 mM) were depressed in control and sensitized mice at both temperatures. 4. These results suggest that sensitization-induced hyperresponsiveness of the mouse vas deferens is mediated by an increased mobilization of intracellular calcium. The involvement of an unknown ouabain-sensitive pathway in sensitization-induced alterations is also discussed.

Loss of nitric oxide release in passively sensitized guinea‐pig aorta with purified immunoglobulin Gl

“…Therefore, in addition to tbe commonly accepted hypotheses for smooth muscle hyperreactivity, such as specific changes in the smooth muscle sarcolemma [13][14][15], an increase in intracellular calcium content [6,16,17], the release of mediators from mast cells [18] and/or the alteration of specific receptors [19,20], the loss of NO release from the vascular endotbeiium can also be involved.…”

“…develop an increased contractile response to various pharmacological stimuli [1-3.5.6|. Active sensitization of animals, especially guinea-pig, to ovalbumen and passive relevant experimental models to study smooth muscle hyperreactivity [3][4][5][6]. In aorta and airways, one hypothesis is that pathophysiological disorders are reliable to a loss of relaxant factors released in normal conditions from the endothelium |3[ or the epithelium [7].…”