Regulation of Guinea pig intestinal peristalsis by endogenous endothelin acting at ETB receptors

Shahbazian, Anaid; Holzer, Peter

doi:10.1053/gast.2000.8549

Cited by 17 publications

(20 citation statements)

References 40 publications

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“…There were a small number of strips that showed an induction in their spontaneous activity. Although we do not have any explanation for this finding, it has been reported that ET regulates the peristalsis in the guinea pig intestine 19 …”

Section: Discussioncontrasting

confidence: 53%

Endothelin‐3 induces both human and opossum gallbladder contraction mediated mainly by endothelin‐B receptor subtype in vitro

Al-Jiffry¹,

Toouli²,

Saccone³

2002

J of Gastro and Hepatol

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Section: Discussioncontrasting

confidence: 53%

Endothelin‐3 induces both human and opossum gallbladder contraction mediated mainly by endothelin‐B receptor subtype in vitro

Al-Jiffry¹,

Toouli²,

Saccone³

2002

J of Gastro and Hepatol

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“…It is not known why ET‐1 is produced in the biliary tree and its role in physiological and pathologic states is unclear. Recent studies have suggested that ET‐1 may play a role in intestinal motility 12 . Its role in the pathophysiological process of various motility disorder such as ilieus has not been clearly defined 36 .…”

Section: Discussionmentioning

confidence: 99%

Endothelin‐1 stimulates sphincter of Oddi motility and decreases trans‐sphincteric flow: a possible mechanism contributes to cholestasis in disease states

Chen

Schloithe

Toouli

et al. 2003

Neurogastroenterology Motil

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Endothelin-1 (ET-1) is a potent stimulator of gallbladder contractility. Its role in modulation of sphincter of Oddi (SO) motility and trans-sphincteric flow (TSF) has not been evaluated. To characterize the effects of ET-1 on SO motility and TSF, 10 anaesthetized Australian possums (in vivo, n = 6) were given graded doses of ET-1 (5-200 pmol kg-1) via closed intra-arterial injection. Blood pressure, TSF and SO motility (basal pressure, phasic amplitude, contraction frequency) were analysed. For in vitro studies, eight SO rings were subjected to 10-12-10-7 mol L-1 cumulative concentrations of ET-1 in organ bath and SO motility was measured. Data are expressed as mean +/- SEM. Statistical analysis used anova. ET-1 induced a dose-related increase in blood pressure with a maximal increase of 37.5 +/- 2.5 mmHg at 200 pmol kg-1, (P < 0.001). ET-1 also increases SO basal pressure (P < 0.001) and contraction frequency (P < 0.0001). However, the contraction amplitude was not significantly affected. ET-1 decreased TSF in a dose-related manner (P < 0.001) with cessation of TSF at the highest dose (P < 0.001). In vitro studies showed a significant increase in mean SO motility index, and frequency of contractions at higher ET-1 concentrations (10-9-10-7 mol L-1). ET-1 is a potent stimulator of SO motility resulting in a reduction in TSF.

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“…The aborally moving wave of peristaltic contraction resulted in a spike-like increase in the intraluminal pressure and caused emptying of the segment. Drug effects on peristalsis were quantified via changes of the peristaltic pressure threshold [11, 15]. For this reason, the intraluminal pressure recordings were analyzed with the software Peristal 1.0 [11, 15]in order to determine the peristaltic pressure threshold in an objective manner and with a precision of 1 Pa. Inhibition of peristalsis was reflected by an increase in peristaltic pressure threshold, and abolition of peristalsis manifested itself in a lack of propulsive motility in spite of an intraluminal pressure of 400 Pa as set by the position of the outlet tubing [11, 15].…”

Section: Methodsmentioning

confidence: 99%

Inhibition by Female Sex Steroids of Peristalsis in the Guinea Pig Small Intestine

Heinemann

Pieber²,

Holzer³

2002

Digestion

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Aims: The effects of steroid hormones on propulsive peristalsis in the intestine were investigated in order to compare their adverse effect profile on this clinically most important motor pattern. Methods: Peristalsis in isolated segments of the guinea pig small intestine was triggered by luminal distension and recorded via the peristalsis-associated changes of the intraluminal pressure. Drug effects on muscular activity were investigated in a circular muscle preparation of the ileum. Results: Estradiol and progesterone, but not testosterone, hydrocortisone or cholesterol (each at 3–30 µM), caused a prompt and concentration-related increase in the peristaltic pressure threshold at which propulsive muscle contractions were elicited. Mifepristone (RU-486; 30 µM) did not prevent the inhibitory effect of progesterone, but blocked peristalsis per se. Pharmacological blockade of inhibitory neural pathways with N^G-nitro-L-arginine methyl ester (nitric oxide synthase inhibitor), naloxone (opioid receptor antagonist), apamin or suramin plus pyridoxal phosphate-6-azophenyl-2′,4′-disulphonic acid (P2 purinoceptor blockers) counteracted the inhibitory effect of submaximally (10 µM), but not maximally (30 µM), effective concentrations of progesterone. Estradiol and progesterone depressed circular muscle contractions evoked by cholecystokinin octapeptide to a larger degree than responses to the tachykinin NK₁ receptor agonist GR-73,632. Conclusion: The peristaltic motor inhibition caused by sex steroids at micromolar concentrations arises primarily from a depressant action on intestinal muscle activity and may be particularly relevant for high-dose regimens of mifepristone.

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Regulation of Guinea pig intestinal peristalsis by endogenous endothelin acting at ETB receptors

Cited by 17 publications

References 40 publications

Endothelin‐3 induces both human and opossum gallbladder contraction mediated mainly by endothelin‐B receptor subtype in vitro

Endothelin‐3 induces both human and opossum gallbladder contraction mediated mainly by endothelin‐B receptor subtype in vitro

Endothelin‐1 stimulates sphincter of Oddi motility and decreases trans‐sphincteric flow: a possible mechanism contributes to cholestasis in disease states

Inhibition by Female Sex Steroids of Peristalsis in the Guinea Pig Small Intestine

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