Bladder smooth muscle dysfunction in patients with irritable bowel syndrome.

We tested the hypothesis that spontaneous release of vasoactive intestinal peptide (VIP) from enteric neurons maintains homeostasis in smooth muscle function in mild inflammatory insults and that infusion of exogenous VIP has therapeutic effects on colonic smooth muscle dysfunction in inflammation. In vitro experiments were performed on human colonic circular smooth muscle tissues and in vivo on rats. The incubation of human colonic circular smooth muscle strips with TNF-α suppressed their contractile response to ACh and the expression of the pore-forming α1C subunit of Cav1.2 channels. VIP reversed both effects by blocking the translocation of NF-κB to the nucleus and its binding to the κB recognition sites on hα1C1b promoter. The translocation of NF-κB was inhibited by blocking the degradation of IκBβ. Induction of inflammation by a subthreshold dose of 17 mg/kg trinitrobenzene sulfonic acid (TNBS) in rats moderately decreased muscularis externa concentration of VIP, and it had little effect on the contractile response of circular smooth muscle strips to ACh. The blockade of VIP and pituitary adenylate cyclase-activating peptide receptors 1/2 during mild inflammatory insult significantly worsened the suppression of contractility and the inflammatory response. The induction of more severe inflammation by 68 mg/kg TNBS induced marked suppression of colonic circular muscle contractility and decrease in serum VIP. Exogenous infusion of VIP by an osmotic pump reversed these effects. We conclude that the spontaneous release of VIP from the enteric motor neurons maintains homeostasis in smooth muscle function in mild inflammation by blocking the activation of NF-κB. The infusion of exogenous VIP mitigates colonic inflammatory response and smooth muscle dysfunction.

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Smooth muscle dysfunction occurs independently of impaired endothelium-dependent dilation in adults at risk of atherosclerosis

Journal of the American College of Cardiology ◽

10.1016/s0735-1097(98)00206-x ◽

1998 ◽

Vol 32 (1) ◽

pp. 123-127 ◽

Cited By ~ 224

Author(s):

Mark R Adams ◽

Jacqui Robinson ◽

Robyn McCredie ◽

J.Paul Seale ◽

Keld E Sorensen ◽

...

Keyword(s):

At Risk ◽

Smooth Muscle ◽

Muscle Dysfunction ◽

Smooth Muscle Dysfunction

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Su2050 Supernatants of Mucosal Biopsies From Irritable Bowel Syndrome Patients Impair Human Colonic Smooth Muscle Contractility

Gastroenterology ◽

10.1016/s0016-5085(15)31979-x ◽

2015 ◽

Vol 148 (4) ◽

pp. S-585

Author(s):

Michele Pier Luca Guarino ◽

Giovanni Barbara ◽

Alessia Cicenia ◽

Annamaria Altomare ◽

M. Raffaella Barbaro ◽

...

Keyword(s):

Irritable Bowel Syndrome ◽

Smooth Muscle ◽

Muscle Contractility ◽

Smooth Muscle Contractility ◽

Irritable Bowel

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Airway Smooth Muscle Dysfunction in Asthma

Reference Module in Biomedical Sciences ◽

10.1016/b978-0-08-102723-3.00109-8 ◽

2021 ◽

Author(s):

Cynthia J. Koziol-White ◽

Reynold A. Panettieri

Keyword(s):

Smooth Muscle ◽

Airway Smooth Muscle ◽

Muscle Dysfunction ◽

Smooth Muscle Dysfunction

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High-resolution iris and retinal imaging in multisystemic smooth muscle dysfunction syndrome due to a novel Asn117Lys substitution in ACTA2: a case report

BMC Ophthalmology ◽

10.1186/s12886-020-01344-w ◽

2020 ◽

Vol 20 (1) ◽

Cited By ~ 1

Author(s):

Aisling B. Mc Glacken-Byrne ◽

David Prentice ◽

Danial Roshandel ◽

Michael R. Brown ◽

Philip Tuch ◽

...

Keyword(s):

Smooth Muscle ◽

Case Report ◽

High Resolution ◽

Retinal Imaging ◽

Muscle Dysfunction ◽

Smooth Muscle Dysfunction

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MR Imaging Diagnosis of ACTA2

Neurographics ◽

10.3174/ng.1900013 ◽

2019 ◽

Vol 9 (6) ◽

pp. 409-413

Author(s):

R. Farias-Moeller ◽

S.M. Lew ◽

R. Sacho ◽

T.G. Kelly

Keyword(s):

Smooth Muscle ◽

Clinical Manifestations ◽

Muscle Dysfunction ◽

Imaging Features ◽

Imaging Diagnosis ◽

Childhood Stroke ◽

Intestinal Dysmotility ◽

Prognostic Implications ◽

Smooth Muscle Dysfunction ◽

Large Vessel Disease

Smooth muscle alpha-2 actin (ACTA2) mutations are associated with diffuse smooth-muscle dysfunction syndrome and produce distinct imaging features. Clinical manifestations include intrathoracic large-vessel disease, nonreactive mydriasis, bladder hypotonia, and intestinal dysmotility. ACTA2 mutations are associated with childhood stroke due to diffuse cerebral arteriopathy distinct from moyamoya disease. Recognition of this syndrome has important clinical and prognostic implications. The purpose of this article is to review the unique imaging phenotypes associated with ACTA2 mutations, including vascular and nonvascular abnormalities.

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