Angiotensin IV induced contractions in human jejunal wall musculature in vitro

Malinauskas, Mangirdas; Stankevičius, Edgaras; Casselbrant, Anna

doi:10.1016/j.peptides.2014.07.008

Peptides

2014

DOI: 10.1016/j.peptides.2014.07.008

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Angiotensin IV induced contractions in human jejunal wall musculature in vitro

Mangirdas Malinauskas

Edgaras Stankevičius

Anna Casselbrant

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2015

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“…In different systems, these three substances are known to activate RhoA/ ROCK via the G protein-coupled receptors (GPCRs) AT 1 -R, TXA2 receptor (TPR), and PGF 2␣ receptor (FPR), respectively (1,50). Recent studies from different laboratories have demonstrated the role of RAS (8,21,33,48) and AA pathways in the contractility of the human gastrointestinal smooth muscle (5,11,13,24). However, to our knowledge, there have been no published data demonstrating the role of RAS and AA pathway on basal muscular tone in human IAS.…”

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confidence: 99%

Nature of extracellular signal that triggers RhoA/ROCK activation for the basal internal anal sphincter tone in humans

Rattan

Singh

Kumar

et al. 2015

American Journal of Physiology-Gastrointestinal and Liver Physi

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The extracellular signal that triggers activation of rho-associated kinase (RhoA/ROCK), the major molecular determinant of basal internal anal sphincter (IAS) smooth muscle tone, is not known. Using human IAS tissues, we identified the presence of the biosynthetic machineries for angiotensin II (ANG II), thromboxane A2 (TXA2), and prostaglandin F2α (PGF2α). These end products of the renin-angiotensin system (RAS) (ANG II) and arachidonic acid (TXA2 and PGF2α) pathways and their effects in human IAS vs. rectal smooth muscle (RSM) were studied. A multipronged approach utilizing immunocytochemistry, Western blot analyses, and force measurements was implemented. Additionally, in a systematic analysis of the effects of respective inhibitors along different steps of biosynthesis and those of antagonists, their end products were evaluated either individually or in combination. To further describe the molecular mechanism for the IAS tone via these pathways, we monitored RhoA/ROCK activation and its signal transduction cascade. Data showed characteristically higher expression of biosynthetic machineries of RAS and AA pathways in the IAS compared with the RSM. Additionally, specific inhibition of the arachidonic acid (AA) pathway caused ~80% decrease in the IAS tone, whereas that of RAS lead to ~20% decrease. Signal transduction studies revealed that the end products of both AA and RAS pathways cause increase in the IAS tone via activation of RhoA/ROCK. Both AA and RAS (via the release of their end products TXA2, PGF2α, and ANG II, respectively), provide extracellular signals which activate RhoA/ROCK for the maintenance of the basal tone in human IAS.

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confidence: 99%

Nature of extracellular signal that triggers RhoA/ROCK activation for the basal internal anal sphincter tone in humans

Rattan

Singh

Kumar

et al. 2015

American Journal of Physiology-Gastrointestinal and Liver Physi

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Angiotensin IV induced contractions in human jejunal wall musculature in vitro

Cited by 1 publication

References 32 publications

Nature of extracellular signal that triggers RhoA/ROCK activation for the basal internal anal sphincter tone in humans

Nature of extracellular signal that triggers RhoA/ROCK activation for the basal internal anal sphincter tone in humans

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