Role of VIP and Substance P in NANC Innervation in the Longitudinal Smooth Muscle of the Rat Jejunum—Influence of Extrinsic Denervation

2007 ◽  
Vol 141 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Michael S. Kasparek ◽  
Javairiah Fatima ◽  
Corey W. Iqbal ◽  
Judith A. Duenes ◽  
Michael G. Sarr
Keyword(s):  
Smooth Muscle ◽  
Substance P ◽  
Rat Jejunum ◽  
Extrinsic Denervation ◽  
Longitudinal Smooth Muscle ◽  
Nanc Innervation

Mechanism of galanin-induced contraction of longitudinal smooth muscle of the rat jejunum

1998 ◽  
Vol 274 (2) ◽  
pp. G306-G313 ◽  
Author(s):  
Simon A. Ahtaridis ◽  
Surender S. Katoch ◽  
Robert S. Moreland
Keyword(s):  
Smooth Muscle ◽  
Pertussis Toxin ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Effective Concentration ◽  
Rat Jejunum ◽  
Myosin Light Chain Phosphorylation ◽  
Half Maximum ◽  
Longitudinal Smooth Muscle ◽  
Intracellular Ca

Intact and α-toxin-permeabilized longitudinal smooth muscle were mounted for measurement of force and myosin light chain phosphorylation. Galanin contracted intact jejunum with a half-maximum effective concentration of 9.2 ± 0.1 nM. Neither atropine, hexamethonium, guanethidine, nor tetrodotoxin affected the contraction. The contraction was also unaffected by depletion of intracellular Ca2+ or by addition of thapsigargin; removal of extracellular Ca2+ or addition of nifedipine abolished the contraction. Galanin increased myosin light chain phosphorylation levels concomitantly with force. During continued tissue stimulation, force fell to suprabasal values, whereas myosin light chain phosphorylation levels remained elevated. Galanin increased Ca2+ sensitivity of contraction in α-toxin-permeabilized tissues, and this was reversed by either guanosine 5′- O-(2-thiodiphosphate) or pertussis toxin. These results suggest that galanin-induced contraction of longitudinal jejunal smooth muscle is dependent on a pertussis toxin-sensitive G protein that is apparently not coupled to the release of intracellular Ca2+but to the influx of extracellular Ca2+ and involves an initial myofilament Ca2+ sensitization followed by Ca2+ desensitization.

A structured review on the female urethral anatomy and innervation with an emphasis on the role of the urethral longitudinal smooth muscle

2019 ◽  
Vol 31 (1) ◽  
pp. 63-71 ◽  
Author(s):  
Michelle Alexandra Mistry ◽  
Niels Klarskov ◽  
John O. DeLancey ◽  
Gunnar Lose
Keyword(s):  
Smooth Muscle ◽  
Longitudinal Smooth Muscle

scholarly journals Relationship between stimulated phosphatidic acid production and inositol lipid hydrolysis in intestinal longitudinal smooth muscle from guinea pig

1987 ◽  
Vol 244 (3) ◽  
pp. 763-768 ◽  
Author(s):  
R S E Mallows ◽  
T B Bolton
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Substance P ◽  
Guinea Pig ◽  
Phosphatidic Acid ◽  
Inositol Phosphates ◽  
Muscle Layer ◽  
Phospholipid Hydrolysis ◽  
Longitudinal Smooth Muscle ◽  
Inositol Phospholipid

Accumulation of [32P]phosphatidic acid (PA) and total [3H]inositol phosphates (IPs) was measured in the longitudinal smooth-muscle layer from guinea-pig small intestine. Stimulation with carbachol, histamine and substance P produced increases in accumulation of both [3H]IPs and [32P]PA over the same concentration range. The increase in [32P]PA accumulation in response to carbachol (1 microM-0.1 mM) was inhibited in the presence of atropine (0.5 microM). Buffering the external free [Ca2+] to 10 nM did not prevent the carbachol-stimulated increase in [32P]PA accumulation. Carbachol and Ca2+ appear to act synergistically to increase accumulation of [32P]PA. In contrast, although incubation with noradrenaline also increased accumulation of [3H]IPs, no increase in accumulation of [32P]PA could be detected. These results suggest that an increase in formation of IPs is not necessarily accompanied by an increase in PA formation, and imply the existence of receptor-modulated pathways regulating PA concentrations other than by phospholipase-C-catalysed inositol phospholipid hydrolysis.

Neutral endopeptidase inhibitors potentiate substance P-induced contraction in gut smooth muscle

1989 ◽  
Vol 256 (1) ◽  
pp. G39-G43 ◽  
Author(s):  
T. D. Djokic ◽  
K. Sekizawa ◽  
D. B. Borson ◽  
J. A. Nadel
Keyword(s):  
Smooth Muscle ◽  
Substance P ◽  
Neutral Endopeptidase ◽  
Serine Proteinases ◽  
Response Curves ◽  
Contractile Responses ◽  
Rat Ileum ◽  
Kininase Ii ◽  
Carboxypeptidase N

To determine the role of endogenous neutral endopeptidase (NEP), also called enkephalinase (EC 3.4.24.11), in regulating tachykinin-induced contraction of gut smooth muscle, we studied the effects of NEP inhibitors on the contractile responses to substance P (SP) in isolated longitudinal strips of ileum or duodenum in rats and ferrets. Leucine-thiorphan and phosphoramidon shifted the concentration-response curves of SP to lower concentrations in all tissues studied, but the sensitivity to SP was greater and the effect of leucine-thiorphan was less in the ferret, a finding that correlated with the observation that the ferret ileum contained substantially less NEP activity than rat ileum. Captopril, bestatin, MGTA, leupeptin, and physostigmine did not alter contractile responses to SP, suggesting that kininase II, aminopeptidases, carboxypeptidase N, serine proteinases, and acetylcholinesterase do not modulate the SP-induced effects. These studies suggest that, in the ileum and duodenum, NEP modulates the actions of SP and, furthermore, that the sensitivity of tissues may be determined, at least in part, by the amount of enzymatically active NEP present.

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