Effects of atropine and tetrodotoxin on neurotensin‐induced ileal sodium transport in the dog

Abstract

Neurotensin was infused intravenously, in the presence or absence of intravenous atropine or intraarterial tetrodotoxin, into dogs anaesthetized with sodium pentobarbitone. Net and unidirectional fluxes of sodium and blood flows in the ileum were measured. Arterial and mesenteric venous blood pressures, haematocrits and plasma total solids were also determined. Neurotensin caused a transient increase in net sodium absorption which was not associated with significant changes in unidirectional fluxes. This was followed by prolonged net secretion which was associated with an increase in unidirectional sodium secretion and a smaller decrease in sodium absorption. Potassium secretion was also increased when net sodium secretion increased. Neurotensin increased haematocrit and total solids and decreased arterial pressure at the same time that secretion occurred. Atropine blocked all the cardiovascular effects of neurotensin and reduced its early effects on both absorption and secretion but not the later effects on secretion. Tetrodotoxin only blocked the increase in absorption but not the secretion or the cardiovascular effects. It was concluded that there is a cholinergic step in the cardiovascular effects of neurotensin and that the early effects of neurotensin on secretion are due to active secretion supported by fluid leakage from the plasma. The later effects of neurotensin on secretion do not have a cholinergic step and are due primarily to an active secretion. The increased absorption is mediated partly through intrinsic nerves of the gut.