Atrial natriuretic factor activates membrane-bound guanylate cyclase of chief cells

Cherner, Jay A.; Singh, Garima; Naik, Latika

doi:10.1016/0024-3205(90)90579-g

Cited by 13 publications

(7 citation statements)

References 10 publications

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“…cGMP has been established as ANF's second messenger in gastrointestinal epithelia (Waldman et al 1984, Ito et al 1988, O'Grady & Wolters 1989, Barsony & Marx 1990, Chemer et al 1990 as well as in other cells (Brenner et al 1990). Of particular interest therefore, was the observation that the human enterocytes were able to respond to an intracellular accumulation of cGMP inasmuch as both electrogenic and electroneutral ion transport were affected.…”

Section: Discussionmentioning

confidence: 99%

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

Grotmol

RøDNES

Buanes

et al. 1993

Acta Physiologica Scandinavica

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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.

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Section: Discussionmentioning

confidence: 99%

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

Grotmol

RøDNES

Buanes

et al. 1993

Acta Physiologica Scandinavica

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“…The participation of ANF in the regulation of gastrointestinal physiology is strongly supported by the finding that ANF gene expression changes along with the digestive state (18). Different biological effects evoked by ANF have been reported in the gastrointestinal tract as well as in exocrine glands (4)(5)(6)12,16,33). We have previously shown that peripherally as well as centrally applied ANF modifies spontaneous and bile salt-evoked bile secretion in the rat (16,7).…”

Section: Introductionmentioning

confidence: 86%

Atrial natriuretic factor stimulates exocrine pancreatic secretion in the rat through NPR-C receptors

Sabbatini¹,

Villagra²,

Davio³

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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Increasing evidence supports the role of atrial natriuretic factor (ANF) in the modulation of gastrointestinal physiology. The effect of ANF on exocrine pancreatic secretion and the possible receptors and pathways involved were studied in vivo. Anesthetized rats were prepared with pancreatic duct cannulation, pyloric ligation, and bile diversion into the duodenum. ANF dose-dependently increased pancreatic secretion of fluid and proteins and enhanced secretin and CCK-evoked response. ANF decreased chloride secretion and increased the pH of the pancreatic juice. Neither cholinergic nor adrenergic blockade affected ANF-stimulated pancreatic secretion. Furthermore, ANF response was not mediated by the release of nitric oxide. ANF-evoked protein secretion was not inhibited by truncal vagotomy, atropine, or Nomega-nitro-l-arginine methyl ester administration. The selective natriuretic peptide receptor-C (NPR-C) receptor agonist cANP-(4-23) mimicked ANF response in a dose-dependent fashion. When the intracellular signaling coupled to NPR-C receptors was investigated in isolated pancreatic acini, results showed that ANF did not modify basal or forskolin-evoked cAMP formation, but it dose-dependently enhanced phosphoinositide hydrolysis, which was blocked by the selective PLC inhibitor U-73122. ANF stimulated exocrine pancreatic secretion in the rat, and its effect was not mediated by nitric oxide or parasympathetic or sympathetic activity. Furthermore, CCK and secretin appear not to be involved in ANF response. Present findings support that ANF exerts a stimulatory effect on pancreatic exocrine secretion mediated by NPR-C receptors coupled to the phosphoinositide pathway.

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“…The preparation procedure was usually completed within 45 minutes. After 30 Effect ofatrial natriuretic peptide onjejunal transport (0net) in the rat (Mean (SD)) plh ' cm-2 nol-h-l'cm-2 (Fig 2). Colonic potential difference was not affected by atrial natriuretic peptide (Fig 2).…”

Section: Methodsmentioning

confidence: 99%

Only pharmacological doses of atrial natriuretic peptide affect intestinal ion transport in non-volume expanded rats.

Lübcke

Brunner

Hutcheson

et al. 1991

Gut

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Pharmacological doses of atrial natriuretic peptide were infused into rats to study its effect on intestinal transport. Saline control or two concentrations ofrat a atrial natriuretic peptide (0.06 or 1-0 nmollminlkg) were administered intravenously (1 ml) over one hour. Jejunal net transport of water and electrolytes was measured with a plasma-like luminal electrolyte solution using a 'closed loop' technique. Distal colonic potential difference and arterial blood pressure were monitored continuously. Blood samples for analysis of plasma atrial natriuretic peptide concentrations were taken at the end of the experiments. Plasma concentrations were increased (mean (SD) (2.1 (0.5) and 24.0 (1.1) nmol/l respectively) compared with the controls (0.023 (0.016) nmol/l). Blood pressure dropped by 30% (p<005) in both groups of rats receiving atrial natriuretic peptide but remained unchanged when control saline was infused. Jejunal net absorption was reduced (p<0.01) only in animals receiving the higher concentration ofpeptide (H20 from 173 (33) to 64 (69) ,ul.h-lhcm-, Na from 25.7 (5.3) to 10.9 (8.9) ,umol.h-1.cm-2). Distal colonic potential difference was not affected by atrial natriuretic peptide. In conclusion massive doses of atrial natriuretic peptide are required to produce any change in intestinal salt and water transport in normal, non-volume expanded rats; these effects could be a nonspecific or 'toxic' response.

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Atrial natriuretic factor activates membrane-bound guanylate cyclase of chief cells

Cited by 13 publications

References 10 publications

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

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

Atrial natriuretic factor stimulates exocrine pancreatic secretion in the rat through NPR-C receptors

Only pharmacological doses of atrial natriuretic peptide affect intestinal ion transport in non-volume expanded rats.

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