Angiotensin II type II receptors and colonic dysmotility in 2,4-dinitrofluorobenzenesulfonic acid-induced colitis in rats

Gaetano Felice Caldara, Antonella Amato, Rosa Maria Serio, Michelangelo Auteri, Maria Grazia Zizzo, Domenico Nuzzo, Marta Di Carlo, Domenico Nuzzo, Marta Di Carlo

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2 Citazioni (Scopus)

Abstract

Background: Angiotensin II (Ang II), the main peptide of the renin-angiotensin system (RAS), has been suggested to be involved in inflammatory bowel diseases. Since RAS has emerged as gut motility regulator, and dysmotility is associated with intestinal inflammation, our objective was to investigate in rat 2,4-dinitrobenzenesulfonic acid (DNBS)-induced colitis the functionality of RAS and its contribution to colonic motor alterations. Methods: The effects of Ang II on the longitudinal colonic muscular contractility of control and DNBS-treated rats were characterized in vitro. Transcripts encoding for Ang II receptors were investigated by RT-PCR. Key Results: Inflamed preparations showed a longitudinal muscle marked hypocontractility. Angiotensin II caused contractile effects in both preparations, but the responses in DNBS preparations were reduced compared to controls. In both preparations, Losartan, AT1 receptor antagonist, reduced Ang II effects. PD123319, AT2 receptor antagonist, enhanced Ang II responses only in DNBS rats, as well as Nω-Nitro-L-arginine (L-NNA), nitric oxide (NO) synthase inhibitor, or tetrodotoxin (TTX), neural toxin. The co-administration of PD123319 and TTX or L-NNA produced no additive effects. PD123319 per se improved colonic contractility in inflamed tissues. The effect was reduced in the presence of L-NNA or TTX. All Ang II receptor subtypes were expressed in both preparations. Conclusions & Inferences: AT1 receptors mediate Ang II contractile responses in rat colon. During inflammation a recruitment of Ang II AT2 receptors would counteract AT1-contractile activity. A tonic activation of AT2 receptors would contribute to the general reduction in muscle contractility during experimental inflammation. A role for enteric neurons and NO is also suggested.
Lingua originaleEnglish
pagine (da-a)e13019-
Numero di pagine11
RivistaDefault journal
Stato di pubblicazionePublished - 2017

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Angiotensin Receptors
Colitis
Angiotensin II
Tetrodotoxin
Renin-Angiotensin System
Acids
Angiotensin Receptor Antagonists
Inflammation
Angiotensin Type 2 Receptor
Muscles
Angiotensin Type 1 Receptor
Losartan
Inflammatory Bowel Diseases
Nitric Oxide Synthase
Arginine
Nitric Oxide
Colon
Neurons
Polymerase Chain Reaction
Peptides

All Science Journal Classification (ASJC) codes

  • Physiology
  • Endocrine and Autonomic Systems
  • Gastroenterology

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title = "Angiotensin II type II receptors and colonic dysmotility in 2,4-dinitrofluorobenzenesulfonic acid-induced colitis in rats",
abstract = "Background: Angiotensin II (Ang II), the main peptide of the renin-angiotensin system (RAS), has been suggested to be involved in inflammatory bowel diseases. Since RAS has emerged as gut motility regulator, and dysmotility is associated with intestinal inflammation, our objective was to investigate in rat 2,4-dinitrobenzenesulfonic acid (DNBS)-induced colitis the functionality of RAS and its contribution to colonic motor alterations. Methods: The effects of Ang II on the longitudinal colonic muscular contractility of control and DNBS-treated rats were characterized in vitro. Transcripts encoding for Ang II receptors were investigated by RT-PCR. Key Results: Inflamed preparations showed a longitudinal muscle marked hypocontractility. Angiotensin II caused contractile effects in both preparations, but the responses in DNBS preparations were reduced compared to controls. In both preparations, Losartan, AT1 receptor antagonist, reduced Ang II effects. PD123319, AT2 receptor antagonist, enhanced Ang II responses only in DNBS rats, as well as Nω-Nitro-L-arginine (L-NNA), nitric oxide (NO) synthase inhibitor, or tetrodotoxin (TTX), neural toxin. The co-administration of PD123319 and TTX or L-NNA produced no additive effects. PD123319 per se improved colonic contractility in inflamed tissues. The effect was reduced in the presence of L-NNA or TTX. All Ang II receptor subtypes were expressed in both preparations. Conclusions & Inferences: AT1 receptors mediate Ang II contractile responses in rat colon. During inflammation a recruitment of Ang II AT2 receptors would counteract AT1-contractile activity. A tonic activation of AT2 receptors would contribute to the general reduction in muscle contractility during experimental inflammation. A role for enteric neurons and NO is also suggested.",
author = "Caldara, {Gaetano Felice} and Antonella Amato and Serio, {Rosa Maria} and Michelangelo Auteri and Zizzo, {Maria Grazia} and Domenico Nuzzo and {Di Carlo}, Marta and Domenico Nuzzo and {Di Carlo}, Marta",
year = "2017",
language = "English",
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TY - JOUR

T1 - Angiotensin II type II receptors and colonic dysmotility in 2,4-dinitrofluorobenzenesulfonic acid-induced colitis in rats

AU - Caldara, Gaetano Felice

AU - Amato, Antonella

AU - Serio, Rosa Maria

AU - Auteri, Michelangelo

AU - Zizzo, Maria Grazia

AU - Nuzzo, Domenico

AU - Di Carlo, Marta

AU - Nuzzo, Domenico

AU - Di Carlo, Marta

PY - 2017

Y1 - 2017

N2 - Background: Angiotensin II (Ang II), the main peptide of the renin-angiotensin system (RAS), has been suggested to be involved in inflammatory bowel diseases. Since RAS has emerged as gut motility regulator, and dysmotility is associated with intestinal inflammation, our objective was to investigate in rat 2,4-dinitrobenzenesulfonic acid (DNBS)-induced colitis the functionality of RAS and its contribution to colonic motor alterations. Methods: The effects of Ang II on the longitudinal colonic muscular contractility of control and DNBS-treated rats were characterized in vitro. Transcripts encoding for Ang II receptors were investigated by RT-PCR. Key Results: Inflamed preparations showed a longitudinal muscle marked hypocontractility. Angiotensin II caused contractile effects in both preparations, but the responses in DNBS preparations were reduced compared to controls. In both preparations, Losartan, AT1 receptor antagonist, reduced Ang II effects. PD123319, AT2 receptor antagonist, enhanced Ang II responses only in DNBS rats, as well as Nω-Nitro-L-arginine (L-NNA), nitric oxide (NO) synthase inhibitor, or tetrodotoxin (TTX), neural toxin. The co-administration of PD123319 and TTX or L-NNA produced no additive effects. PD123319 per se improved colonic contractility in inflamed tissues. The effect was reduced in the presence of L-NNA or TTX. All Ang II receptor subtypes were expressed in both preparations. Conclusions & Inferences: AT1 receptors mediate Ang II contractile responses in rat colon. During inflammation a recruitment of Ang II AT2 receptors would counteract AT1-contractile activity. A tonic activation of AT2 receptors would contribute to the general reduction in muscle contractility during experimental inflammation. A role for enteric neurons and NO is also suggested.

AB - Background: Angiotensin II (Ang II), the main peptide of the renin-angiotensin system (RAS), has been suggested to be involved in inflammatory bowel diseases. Since RAS has emerged as gut motility regulator, and dysmotility is associated with intestinal inflammation, our objective was to investigate in rat 2,4-dinitrobenzenesulfonic acid (DNBS)-induced colitis the functionality of RAS and its contribution to colonic motor alterations. Methods: The effects of Ang II on the longitudinal colonic muscular contractility of control and DNBS-treated rats were characterized in vitro. Transcripts encoding for Ang II receptors were investigated by RT-PCR. Key Results: Inflamed preparations showed a longitudinal muscle marked hypocontractility. Angiotensin II caused contractile effects in both preparations, but the responses in DNBS preparations were reduced compared to controls. In both preparations, Losartan, AT1 receptor antagonist, reduced Ang II effects. PD123319, AT2 receptor antagonist, enhanced Ang II responses only in DNBS rats, as well as Nω-Nitro-L-arginine (L-NNA), nitric oxide (NO) synthase inhibitor, or tetrodotoxin (TTX), neural toxin. The co-administration of PD123319 and TTX or L-NNA produced no additive effects. PD123319 per se improved colonic contractility in inflamed tissues. The effect was reduced in the presence of L-NNA or TTX. All Ang II receptor subtypes were expressed in both preparations. Conclusions & Inferences: AT1 receptors mediate Ang II contractile responses in rat colon. During inflammation a recruitment of Ang II AT2 receptors would counteract AT1-contractile activity. A tonic activation of AT2 receptors would contribute to the general reduction in muscle contractility during experimental inflammation. A role for enteric neurons and NO is also suggested.

UR - http://hdl.handle.net/10447/225704

UR - http://www.wiley.com/bw/journal.asp?ref=1350-1925&site=1

M3 - Article

SP - e13019-

JO - Default journal

JF - Default journal

ER -