Atrial natriuretic factor (ANF) does not affect ion transport in human intestine but does in porcine intestine

Abstract

The aim of this study was to test whether atrial natriuretic factor (ANF) exerts any effect on human intestinal ion transport, and the porcine intestine was used as a positive control of ANF's effects. Tissues from human proximal (n = 6) and distal (n = 6) colons, and from distal ileum (n = 6) were mounted in Ussing chambers, and short circuit current (Isc) was measured subsequent to serosal application of ANF (10(-6) M), 8-Br-cyclic guanosine monophosphate (8-Br-cGMP) (10(-4) M), and theophylline (10(-2) M). ANF did not affect Isc whereas 8-Br-cGMP increased Isc by 28 (8-53), 16 (3-36), and 16 (5-41) microA cm-2 in the distal colon (DC), proximal colon (PC) and distal ileum (DI), respectively. Likewise, transepithelial potential difference (PD) became more negative by 5.0 (0.6-8.9), 2.5 (0.4-4.0) and 0.9 (0.3-2.3) mV in DC, PC, and DI, respectively, subsequent to addition of 8-Br-cGMP. Isc and PD were further increased by theophylline. Additional radio-isotope flux studies in human colon revealed that ANF did not affect electroneutral sodium and chloride transport either. For comparison, ANF (10(-6) M) was administered to large intestinal tissues from young pigs in which ANF induced a significant increase in Isc which was comparable to the 8-Br-cGMP response in humans. The porcine Isc response was partly inhibited by chloride-free solution on the serosal side, by serosal application of bumetanide (10(-4) M) and BaCl2 (10(-3) M), and mucosal application of the chloride-channel blocker diphenylamine-2-carboxylate (DPC) (10(-3) M). Mucosal amiloride (10(-5) M) pre-treatment reduced baseline Isc but did not affect the porcine intestinal Isc response to ANF. In vitro radio-autography demonstrated specific binding sites for ANF in porcine distal colon, whereas no apparent labelling was observed in human distal colon. These findings suggest that the lack of effect of ANF on sodium and chloride transport in human distal ileum and colon is probably due to lack of ANF receptors. In the porcine intestine, however, the Isc response induced by ANF seems to involve stimulation of electrogenic chloride secretion, whereas electrogenic sodium absorption seems unaffected.

Segmental differences in the effects of guanylin and Escherichia coli heat‐stable enterotoxin on Cl‐ secretion in human gut.

“…Ussing chamber experiments reveal that ha-ANP has no effect on electrogenic electrolyte transport, either in jejunal or in colonic mucosa. Our observations agree with previous studies suggesting that ha-ANP stimulates intestinal ion transport in other mammalian species but not in the human (Grotmol, Rodnes, Buanes, Christensen & Landsverk, 1993). Recently, in situ hybridization demonstrated expression of GC-A, the ha-ANP receptor, in the lamina propria, i.e.…”

The Interaction of Dietary Fibres with the Colon

“…Studies using porcine colonic tissues have suggested that atrial and brain natriuretic factor (ANF and BNF) lead to a secretion of K + and Cl -, and a reduction in electroneutral NaCl uptake pathways [134][135][136], as might be expected by a hormone that functions to reduce plasma sodium levels. However, ANF did not alter ion absorption or secretion in human colonic tissues, suggesting a lack of ANF receptor in the human colon [134].…”

“…However, ANF did not alter ion absorption or secretion in human colonic tissues, suggesting a lack of ANF receptor in the human colon [134].…”

Intestinal Secretory Response to Atrial Natriuretic Peptide during Postnatal Development in the Rabbit

“…In adult animals, ANP has been shown to induce small intestinal electrolyte secretion [8,9], In the neonate, the role of ANP in fluid regulation and electrolyte homeostasis is un clear [10], Newborn animals appear to have a decreased ability to excrete sodium leaving them susceptible to hypernatremia [11], Of the two distinct manifestations of hyperna tremia, the most common is caused when water loss is greatly out of proportion to sodi um loss, and the second type occurs when an excess sodium load has occurred [11,12], Studies have indicated that newborn infants have increased plasma levels of ANP [ 13,14], but are unable to excrete sodium, suggesting end organ resistance to ANP.…”