Electrogenic and electroneutral components of the sympathetic effect on fluid absorption in the rat jejunum

Abstract

The aim of the study was to test the hypothesis that the sympathetic nerves to the jejunum enhance net fluid absorption rate by inhibiting an electrogenic flux of anions into the lumen. The design of the experiments was based on the observation that the effect of catecholamines on electrogenic transport is abolished by yohimbine, an alpha 2 adrenergic antagonist. Net electrogenic transport in jejunal segments of anaesthetized rats was estimated by measurement of the transepithelial potential difference (PD) and short-circuit current (SCC). Net fluid absorption rate was quantified by a gravimetric technique. The sympathetic nerves to the segment were stimulated electrically, both in vitro and in vivo. The effect of sympathetic nerve stimulation on SCC and net fluid transport was determined in the absence and presence of the alpha-adrenergic antagonists phentolamine (a non-selective alpha-adrenergic antagonist), prazosin (a selective alpha 1-antagonist) and yohimbine (a selective alpha 2-antagonist). Sympathetic nerve stimulation decreased PD and SCC and increased net fluid absorption rate. Phentolamine abolished both the electrogenic response and the effect on net fluid absorption rate, without having any significant intrinsic effects on either parameter. Prazosin per se markedly increased net fluid absorption rate, but did not significantly influence the sympathetic effect on SCC or net fluid absorption rate. Yohimbine abolished the electrogenic effect of sympathetic stimulation, and per se increased net fluid absorption rate in innervated but not in denervated segments. In innervated segments, the absorption rate during sympathetic nerve stimulation was similar in controls and yohimbine-treated animals. In denervated segments, yohimbine significantly attenuated the sympathetic response. The results suggest that the sympathetic nerves enhance fluid absorption rate via effects on both electrogenic and electroneutral epithelial transport. These two components of the sympathetic response seem to be mediated by different alpha-receptor mechanisms.