Cyclic nucleotide-mediated effects of ANF and VIP on flounder intestinal ion transport

The observation that two classes of neuronal depolarizing agents cause TTX-sensitive inhibition of basal ion transport establishes that NaCl absorption in flounder intestine is subject to regulation by enteric nerves located in the submucosa.

Abstract

The purpose of this study was to compare the effects of atriopeptin III (AP-III), vasoactive intestinal peptide (VIP), and ionomycin on Na and Cl influx and to correlate changes in transport with effects on intracellular adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 5'-cyclic monophosphate (cGMP) content of the tissue. In addition, the question of whether AP-III inhibits ion transport directly by acting on enterocyte receptors for AP-III or indirectly by stimulation of enteric nerves in the submucosa was also addressed. The results showed that AP-III, ionomycin, and bumetanide all inhibited the initial rate of Na and Cl influx, suggesting that they directly block Na-K-2Cl cotransport activity. VIP had no effect on unidirectional influx of Na and Cl. AP-III caused a fourfold increase in intracellular [cGMP] without any significant effect on [cAMP]. VIP stimulated [cAMP] by fourfold but had no effect on [cAMP]. Ionomycin had no effect on either [cAMP] or [cGMP]. Inhibition of transport by AP-III could not be blocked by tetrodotoxin (TTX), indicating that enteric nerves in the submucosa are not directly involved in mediating the effects of AP-III on epithelial ion transport. The observation that two classes of neuronal depolarizing agents (veratrine and scorpion venom) cause TTX-sensitive inhibition of basal ion transport establishes that NaCl absorption in flounder intestine is subject to regulation by enteric nerves located in the submucosa.