1989Acta Physiologica ScandinavicaRequires access

Evidence for sympathetic regulation of the hydraulic conductance of rat jejunal mucosa in vivo

M. Hemlin, Henrik Sjövall

Open publisher page 7 citations

Abstract

The aim of the study was to test the hypothesis that sympathetic nerve stimulation inhibits jejunal fluid secretion by decreasing the hydraulic conductance (Lp) of the mucosa. Jejunal segments of anaesthetized rats were mounted in a specially constructed chamber which makes it possible to measure net fluid transport together with transmural potential difference or short circuit current in vivo. Lp was estimated by measuring the effects on net fluid transport rate elicited by stepwise changes in luminal pressure. Lp was measured in four groups of animals: (1) under control conditions; (2) after hexamethonium administration, to block intramural secretory neurons; (3) during efferent stimulation of the mesenteric nerves, to activate sympathetic neurons, and (4) during mesenteric nerve stimulation (MNS) after pre-treatment with phentolamine, an alpha-adrenergic antagonist, to block the sympathetic effector mechanism. Lp measured at positive luminal pressures in control animals was approximately 4 microliters min-1 cmH2O-1 100 cm-2 serosal surface area. When measured at negative luminal pressures, this value increased approximately threefold. Hexamethonium did not significantly influence Lp. At positive luminal pressures, MNS decreased Lp to a value not significantly different from zero. This effect was abolished by phentolamine. At negative luminal pressures, MNS decreased Lp by approximately 50% and this effect was partly antagonized by phentolamine. The results suggest that a decrease in mucosal hydraulic conductance may contribute to the antisecretory effect of sympathetic nerve stimulation in vivo.

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What this paper is about

The aim of the study was to test the hypothesis that sympathetic nerve stimulation inhibits jejunal fluid secretion by decreasing the hydraulic conductance (Lp) of the mucosa. Jejunal segments of anaesthetized rats were mounted in a specially constructed chamber which makes it possible to measure net fluid transport together with transmural potential difference or short circuit current in vivo. Lp was estimated by measuring the effects on net fluid transport rate elicited by stepwise changes in luminal pressure. Lp was measured in four groups of animals: (1) under control conditions; (2) after hexamethonium administration, to block intramural secretory neurons; (3) during efferent stimulation of the mesenteric nerves, to activate sympathetic neurons, and (4) during mesenteric nerve stimulation (MNS) after pre-treatment with phentolamine, an alpha-adrenergic antagonist, to block the sympathetic effector mechanism. Lp measured at positive luminal pressures in control animals was approximately 4 microliters min-1 cmH2O-1 100 cm-2 serosal surface area. When measured at negative luminal pressures, this value increased approximately threefold. Hexamethonium did not significantly influence Lp. At positive luminal pressures, MNS decreased Lp to a value not significantly different from zero. This effect was abolished by phentolamine. At negative luminal pressures, MNS decreased Lp by approximately 50% and this effect was partly antagonized by phentolamine. The results suggest that a decrease in mucosal hydraulic conductance may contribute to the antisecretory effect of sympathetic nerve stimulation in vivo.

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Available abstract

The aim of the study was to test the hypothesis that sympathetic nerve stimulation inhibits jejunal fluid secretion by decreasing the hydraulic conductance (Lp) of the mucosa. Jejunal segments of anaesthetized rats were mounted in a specially constructed chamber which makes it possible to measure net fluid transport together with transmural potential difference or short circuit current in vivo. Lp was estimated by measuring the effects on net fluid transport rate elicited by stepwise changes in luminal pressure. Lp was measured in four groups of animals: (1) under control conditions; (2) after hexamethonium administration, to block intramural secretory neurons; (3) during efferent stimulation of the mesenteric nerves, to activate sympathetic neurons, and (4) during mesenteric nerve stimulation (MNS) after pre-treatment with phentolamine, an alpha-adrenergic antagonist, to block the sympathetic effector mechanism. Lp measured at positive luminal pressures in control animals was approximately 4 microliters min-1 cmH2O-1 100 cm-2 serosal surface area. When measured at negative luminal pressures, this value increased approximately threefold. Hexamethonium did not significantly influence Lp. At positive luminal pressures, MNS decreased Lp to a value not significantly different from zero. This effect was abolished by phentolamine. At negative luminal pressures, MNS decreased Lp by approximately 50% and this effect was partly antagonized by phentolamine. The results suggest that a decrease in mucosal hydraulic conductance may contribute to the antisecretory effect of sympathetic nerve stimulation in vivo.

Key concepts: Phentolamine, Hexamethonium, Endocrinology, Stimulation, Internal medicine, Chemistry, Adrenergic antagonist, In vivo

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