Acute exercise inhibits gastric emptying of liquids in rats: influence of the NO-cGMP pathway

Abstract

We previously found that acute exercise inhibited the gastric emptying of liquid in awake rats by causing an acid-base imbalance. In the present study, we investigated the involvement of the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway, vasoactive intestinal peptide (VIP), and corticotropin-releasing factor (CRF) peptide in this phenomenon. Male rats were divided into exercise or sedentary group and were subjected to a 15-min swim session against a load (2.5 or 5% b.w.). The rate of gastric emptying was evaluated after 5, 10, or 20 min postprandially. Separate groups of rats were treated with vehicle (0.9% NaCl, 0.1 mL/100 g, ip) or one of the following agents: atropine (1.0 mg/kg, ip), the NO non-selective inhibitor Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME; 10.0 mg/kg, ip), or the selective cGMP inhibitor 1H-(1,2,4)oxadiazole[4,3-a]quinoxalin-1-one (ODQ; 5.0 mg/kg, ip), the i-NOS non-specific inhibitor (aminoguanidine; 10.0 mg/kg, ip), the corticotropin-releasing factor receptor antagonist (astressin; 100 µg/kg, ip), or the vasoactive intestinal peptide (VIP) receptor antagonist Lys1, Pro2,5, Arg3,4, Tyr6 (100 µg/kg, ip). Compared to sedentary rats, both the 2.5 and 5% exercise groups exhibited higher (P<0.05) values of blood lactate and fractional gastric dye recovery. Corticosterone and NO levels increased (P<0.05) in the 5% exercised rats. Pretreatment with astressin, VIP antagonist, atropine, L-NAME, and ODQ prevented the increase in gastric retention caused by exercise in rats. Acute exercise increased gastric retention, a phenomenon that appears to be mediated by the NO-cGMP pathway, CRF, and VIP receptors.

Alanyl-glutamine protects the intestinal barrier function in trained rats against the impact of acute exhaustive exercise

“…In this sense, we recently reported that acute exercise delays the gastric emptying rate in rats, a phenomenon prevented by bicarbonate treatment. In addition, extracellular acidosis in vitro inhibits cholinergic neurotransmission in the rat gastric fundus by selectively influencing the Gq/11 protein-signaling pathway (22,23). Now, we report for the first time the morphofunctional modifications in the intestinal barrier, such as increased intestinal permeability associated with changes in the transcription of a tight junction (claudin-2) in a physically exhaustive test, which was prevented by AG treatment.…”

P2X7 receptor antagonist improves gastrointestinal disorders in spontaneously hypertensive rats

“…Upon increasing tissue concentrations of ANG II, activation of AT1 and AT2 receptors in the gastric mucosa may contribute to changes in stomach motor activity ( 24 ). Activation of AT1 receptors induces gastric vasoconstriction, thus resulting in deficits in NO production and activity with a direct impact on the GE rate ( 25 ).…”

Knockdown of miR‐19a suppresses gastrointestinal dysmotility diarrhea after TBI by regulating VIP expression

“…Therefore, it is important to study the causes of the abnormal structure, function, quantity, and distribution of ICCs to understand GID diarrhea after TBI. Studies have shown that the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway is associated with gastric emptying in rats (Akm et al, 2018) and that it plays an inhibitory role in the pacing potential of mouse small intestinal ICCs (Kim et al, 2018). In contrast, VIP inhibits the pacemaker activity of ICCs via the NO-cGMP-PKG pathway (Kim et al, 2006).…”