Development of an organ bath technique to assess intestinal motility in isolated mouse ileum and colon.

We investigated the mechanisms involved in the nitric oxide (NO)-induced inhibitory effects on longitudinal smooth muscle of mouse ileum, using organ bath technique. Exogenously applied NO, delivered as sodium nitroprusside (SNP; 0.1–100 µmol/L) induced a concentration-dependent reduction of the ileal spontaneous contractions. 1H-[1,2,4]oxadiazolol[4,3,a]quinoxalin-1-one (ODQ; 1 µmol/L), a guanilyl cyclase inhibitor, reduced the SNP-induced effects. Tetraethylammonium chloride (20 mmol/L), a non-selective K+ channel blocker, and charybdotoxin (0.1 µmol/L), blocker of large conductance Ca2+-dependent K+ channels, significantly reduced SNP-induced inhibitory effects. In contrast, apamin (0.1 µmol/L), blocker of small conductance Ca2+-dependent K+ channels, was not able to affect the response to SNP. Ciclopiazonic acid (10 µmol/L) or thapsigargin (0.1 µmol/L), sarcoplasmatic reticulum Ca2+-ATPase inhibitors, decreased the SNP-inhibitory effects. Ryanodine (10 µmol/L), inhibitor of Ca2+ release from ryanodine-sensitive intracellular stores, significantly reduced the SNP inhibitory effects. The membrane permeable analogue of cGMP, 8-bromoguanosine 3′,5′-cyclic monophosphate (100 µmol/L), also reduced spontaneous mechanical activity, and its effect was antagonized by ryanodine. The present study suggests that NO causes inhibitory effects on longitudinal smooth muscle of mouse ileum through cGMP which in turn would activate the large conductance Ca2+-dependent K+ channels, via localized ryanodine-sensitive Ca2+ release.Key words: nitric oxide, mouse ileum, potassium channels, calcium stores.

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Corticotropin releasing hormone (CRH) is a proinflammatory peptide in mouse ileum

Gastroenterology ◽

10.1016/s0016-5085(01)80188-8 ◽

2001 ◽

Vol 120 (5) ◽

pp. A38-A39

Author(s):

M WLK ◽

C WANG ◽

M VENICHAKI ◽

S KUHNTMOORE ◽

D ZHAO ◽

...

Keyword(s):

Corticotropin Releasing Hormone ◽

Releasing Hormone ◽

Mouse Ileum

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GABAb receptor-mediated inhibition of cholinergic function in mouse ileum requires the GABAb1 subunit

Gastroenterology ◽

10.1016/s0016-5085(01)80979-3 ◽

2001 ◽

Vol 120 (5) ◽

pp. A198-A198

Author(s):

G SANGER ◽

M MUNONYARA ◽

H PROSSER ◽

M PANGALOS ◽

A HUNTER ◽

...

Keyword(s):

Gabab Receptor ◽

Cholinergic Function ◽

Mouse Ileum

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Anticholinergic effect of Carum copticum on intestinal motility of rats

Planta Medica ◽

10.1055/s-2007-987333 ◽

2007 ◽

Vol 73 (09) ◽

Author(s):

SH Hejazian ◽

M Mahdavi ◽

MH Dashti

Keyword(s):

Intestinal Motility ◽

Anticholinergic Effect ◽

Carum Copticum

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Faculty of 1000 evaluation for Randomized clinical trial on the influence of anaesthesia protocol on intestinal motility during laparoscopic surgery requiring small bowel anastomosis.

F1000 - Post-publication peer review of the biomedical literature ◽

10.3410/f.717958961.793466621 ◽

2012 ◽

Author(s):

David Alpers

Keyword(s):

Clinical Trial ◽

Laparoscopic Surgery ◽

Small Bowel ◽

Randomized Clinical Trial ◽

Intestinal Motility ◽

Bowel Anastomosis

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The Effect on Health of Some Cardiovascular Risk Factors

Revista de Chimie ◽

10.37358/rc.17.10.5863 ◽

2017 ◽

Vol 68 (10) ◽

pp. 2237-2242

Author(s):

Germaine Savoiu Balint ◽

Mihaiela Andoni ◽

Ramona Amina Popovici ◽

Laura Cristina Rusu ◽

Ioana Citu ◽

...

Keyword(s):

Nitric Oxide ◽

Vascular Reactivity ◽

Vascular Wall ◽

Dose Effect ◽

Organ Bath ◽

Before And After ◽

Specific Receptors ◽

Oxide Synthase ◽

Endothelial Nitric Oxide ◽

Relaxing Response

Arterial endothelium produces a large ramge of active factors which are indispensable for modulation of vasomotor tone and maintenance of vascular wall integrity. From these factors, nitric oxide (NO), wich is released by the endothelial cells as a response to acetylcholine or adenosine action on specific receptors, plays an important role.NO is the result of oxidation process of L-arginine into L-citrulline, under the action of endothelial nitric oxide synthase (NOSe), wich is activated by intracelluar Ca2+ - calmodulin complex . Our study, performed in isolated organ bath, analyzed vascular reactivity of 12 guinea pigs� thoracic aorta rings. After phenylephrine -PHE 10-5 mol/L precontraction, the dose-effect curves for acetylcoline � ACH, adenosine 5� phosphate - 5�ADP and sodium nitroprusside � SNP were determined, before and after incubation of preparation, for 1 hour, with 5% hydrosoluble cigarettes smoke extract (CSE). Statistic analysis, performed with the use of t pair test and ANOVA parametric test, showed that incubation of vascular preparation with 5% CSE has increased the contractile response to PHE 10-5 mol/L (p[0.05), has reduced the endothelium-dependent relaxing response to ATP 10-5 mol/L (p[0.001) and 5�ADP 10-5 molo/L (p[0.001), but has not significantly modified the endothelium-independent relaxing response to SNP 10-5 mol/L (p=0.05). As a conclusion, vascular rings incubation with 5% CSE induced a decrease of endothelium NO synthesis under the action of AXH and 5�ADP, but did not change the smooth muscle fiber respomse in the presence of NO released by SNP.

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Effects of electroacupuncture on disorder of intestinal motility in a rat model of irritable bowel syndrome

Journal of Chinese Integrative Medicine ◽

10.3736/jcim20100913 ◽

2010 ◽

pp. 883-887 ◽

Cited By ~ 4

Author(s):

ZJ Wang

Keyword(s):

Irritable Bowel Syndrome ◽

Rat Model ◽

Intestinal Motility ◽

Irritable Bowel

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Selective estrogen receptor-α and estrogen receptor-β agonists rapidly decrease pulmonary artery vasoconstriction by a nitric oxide-dependent mechanism

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.90667.2008 ◽

2008 ◽

Vol 295 (5) ◽

pp. R1486-R1493 ◽

Cited By ~ 40

Author(s):

Tim Lahm ◽

Paul R. Crisostomo ◽

Troy A. Markel ◽

Meijing Wang ◽

Yue Wang ◽

...

Keyword(s):

Nitric Oxide ◽

Estrogen Receptor ◽

Pulmonary Artery ◽

Hypoxic Pulmonary Vasoconstriction ◽

Organ Bath ◽

Sprague Dawley ◽

Response Curves ◽

Vascular Effects ◽

M 10 ◽

Dependent Mechanism

Both endogenous and exogenous estrogen decrease pulmonary artery (PA) vasoconstriction. Whether these effects are mediated via estrogen receptor (ER)-α or ER-β, and whether the contribution of ERs is stimulus-dependent, remains unknown. We hypothesized that administration of the selective ER-α agonist propylpyrazole triol (PPT) and/or the selective ER-β agonist diarylpropiolnitrile (DPN) rapidly decreases PA vasoconstriction induced by pharmacologic and hypoxic stimuli via a nitric oxide (NO)-dependent mechanism. PA rings ( n = 3–10/group) from adult male Sprague-Dawley rats were suspended in physiologic organ baths. Force displacement was measured. Vasoconstrictor responses to phenylephrine (10−8M − 10−5M) and hypoxia (Po2 35–45 mmHg) were determined. Endothelium-dependent and -independent vasorelaxation were measured by generating dose-response curves to acetylcholine (10−8M − 10−4M) and sodium nitroprusside (10−9M − 10−5M). PPT or DPN (10−9M − 5 × 10−5M) were added to the organ bath in the presence and absence of the NO-synthase inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) (10−4M). Selective ER-α activation (PPT, 5 × 10−5M) rapidly (<20 min) decreased phenylephrine-induced vasoconstriction. This effect, as well as PPT's effects on endothelium-dependent vasorelaxation, were neutralized by l-NAME. In contrast, selective ER-β activation (DPN, 5 × 10−5M) rapidly decreased phase II of hypoxic pulmonary vasoconstriction (HPV). l-NAME eliminated this phenomenon. Lower PPT or DPN concentrations were less effective. We conclude that both ER-α and ER-β decrease PA vasoconstriction. The immediate onset of effect suggests a nongenomic mechanism. The contribution of specific ERs appears to be stimulus specific, with ER-α primarily modulating phenylephrine-induced vasoconstriction, and ER-β inhibiting HPV. NO inhibition eliminates these effects, suggesting a central role for NO in mediating the pulmonary vascular effects of both ER-α and ER-β.

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Aging Additively Influences Insulin- and Insulin-Like Growth Factor-1-Mediated Endothelial Dysfunction and Antioxidant Deficiency in Spontaneously Hypertensive Rats

Biomedicines ◽

10.3390/biomedicines9060676 ◽

2021 ◽

Vol 9 (6) ◽

pp. 676

Author(s):

Kunanya Masodsai ◽

Yi-Yuan Lin ◽

Sih-Yin Lin ◽

Chia-Ting Su ◽

Shin-Da Lee ◽

...

Keyword(s):

Growth Factor ◽

Endothelial Dysfunction ◽

Spontaneously Hypertensive Rats ◽

No Production ◽

Organ Bath ◽

Insulin Like Growth Factor ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Nos Inhibitors ◽

Wistar Kyoto

This study aimed to investigate the aging-related endothelial dysfunction mediated by insulin and insulin-like growth factor-1 (IGF-1) and antioxidant deficiency in hypertension. Male spontaneously hypertensive rats (SHRs) and age-matched normotensive Wistar–Kyoto rats (WKYs) were randomly divided into 24-week-old (younger) and 48-week-old (older) groups, respectively. The endothelial function was evaluated by the insulin- and IGF-1-mediated vasorelaxation of aortic rings via the organ bath system. Serum levels of nitric oxide (NO), malondialdehyde (MDA), catalase, and total antioxidant capacity (TAC) were examined. The insulin- and IGF-1-mediated vasorelaxation was significantly impaired in both 24- and 48-week-old SHRs compared with age-matched WKYs and was significantly worse in the 48-week-old SHR than the 24-week-old SHR. After pretreatments of phosphoinositide 3-kinase (PI3K) or NO synthase (NOS) inhibitors, the insulin- and IGF-1-mediated vasorelaxation became similar among four groups. The serum level of MDA was significantly increased, while the NO, catalase, and TAC were significantly reduced in the 48-week-old SHR compared with the 24-week-old SHR. This study demonstrated that the process of aging additively affected insulin- and IGF-1-mediated endothelial dysfunction in SHRs, which could be partly attributed to the reduced NO production and antioxidant deficiency.

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