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.

Proteolytic Inactivation of Substance P and Neurokinin A in the Longitudinal Muscle Layer of Guinea Pig Small Intestine

2006 ◽  
Vol 47 (3) ◽  
pp. 856-864 ◽  
Author(s):  
R. Nau ◽  
G. Schäfer ◽  
C. F. Deacon ◽  
T. Cole ◽  
D. V. Agoston ◽  
...  
Keyword(s):  
Small Intestine ◽  
Substance P ◽  
Guinea Pig ◽  
Longitudinal Muscle ◽  
Muscle Layer ◽  
Neurokinin A ◽  
Longitudinal Muscle Layer

scholarly journals The effects of elevated cyclic AMP levels on histamine-H1-receptor-stimulated inositol phospholipid hydrolysis and calcium mobilization in the smooth-muscle cell line DDT1MF-2

1993 ◽  
Vol 292 (2) ◽  
pp. 409-417 ◽  
Author(s):  
J M Dickenson ◽  
T E White ◽  
S J Hill
Keyword(s):  
Smooth Muscle ◽  
Cyclic Amp ◽  
Smooth Muscle Cell ◽  
Cell Line ◽  
Muscle Cell ◽  
Inositol Phosphates ◽  
Cyclic Amp Phosphodiesterase ◽  
Phospholipid Hydrolysis ◽  
Inositol Phospholipid ◽  
Muscle Cell Line

The effects of raising cyclic AMP levels, by forskolin stimulation, beta-adrenoceptor activation or cyclic AMP phosphodiesterase inhibition, on inositol phospholipid hydrolysis and increases in intracellular free [Ca2+] ([Ca2+]i) elicited by a range of agonists have been investigated in the hamster vas deferens smooth-muscle cell line DDT1MF-2. Isoprenaline (log [EC50 (M)] = -7.7 +/- 0.2), forskolin and the type IV cyclic AMP phosphodiesterase inhibitor rolipram elicited significant increases in the accumulation of cyclic [3H]AMP. Pretreatment with forskolin (10 microM) attenuated histamine (100 microM)- and N6-cyclopentyladenosine (CPA; 300 nM)-induced release of intracellular Ca2+, observed when cells are stimulated in Ca(2+)-free buffer containing 0.1 mM EGTA. Forskolin had no effect on ATP (100 microM)- or bradykinin (1 microM)-stimulated release of intracellular Ca2+. Histamine-induced intracellular Ca2+ release was also inhibited by pretreatment with rolipram (100 microM) or the membrane-permeant cyclic AMP analogue (Sp)-adenosine 3′,5′-monophosphothioate (100 microM). Isoprenaline (1 microM) pretreatment (in the presence of 10 microM rolipram, a concentration which on its own did not decrease the histamine response) attenuated histamine-induced intracellular Ca2+ release. Forskolin inhibited histamine (100 microM)- and CPA (100 nM) stimulated accumulation of [3H]-inositol phosphates, but was without effect on ATP or bradykinin responses. Addition of forskolin (in the presence of 100 microM rolipram) after the cells had been stimulated with histamine (in experiments initiated in Ca(2+)-free buffer) inhibited the rise in [Ca2+]i observed when extracellular Ca2+ (2 mM) was re-applied (owing to receptor-mediated Ca2+ influx). Finally, the refilling of intracellular Ca2+ stores (after receptor-mediated Ca2+ influx is blocked by mepyramine) can be demonstrated in the presence of raised cyclic AMP levels.

The longitudinal smooth muscle layer of the pig small intestine is innervated by both myenteric and submucous neurons

2002 ◽  
Vol 117 (6) ◽  
pp. 481-492 ◽  
Author(s):  
Jurgen Hens ◽  
Mariusz Gajda ◽  
Dietrich W. Scheuermann ◽  
Dirk Adriaensen ◽  
J.-P. Timmermans
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Muscle Layer ◽  
Smooth Muscle Layer ◽  
Longitudinal Smooth Muscle

EndothelinB receptor on guinea pig small intestinal smooth muscle cells

1992 ◽  
Vol 262 (2) ◽  
pp. G308-G311 ◽  
Author(s):  
M. Yoshinaga ◽  
Y. Chijiiwa ◽  
T. Misawa ◽  
N. Harada ◽  
H. Nawata
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Binding Characteristics ◽  
Longitudinal Smooth Muscle ◽  
Etb Receptor ◽  
Small Intestinal ◽  
Functional Receptor

We investigated the binding characteristics of the endothelin (ET) receptor and the mechanism by which ET induces contraction of longitudinal smooth muscle cells of the guinea pig small intestine by using vasoactive intestinal contractor (VIC), a mouse variant of ET-2. A functional receptor for VIC was found to exist on longitudinal smooth muscle cells. These cells showed a similar binding of and contractile response to ET-1, ET-2, and ET-3. Inhibitors of both intracellular and extracellular Ca2+ movement attenuated the VIC-induced contraction of longitudinal smooth muscle cells. These results suggest that smooth muscle cells of the guinea pig small intestine express the ETB receptor that primarily mediates the contractile effect on smooth muscle cells. In addition, ET-induced contraction depends on intracellular as well as extracellular Ca2+.

K transport and mechanical responses of isolated longitudinal smooth muscle from guinea pig ileum

1961 ◽  
Vol 200 (4) ◽  
pp. 789-793 ◽  
Author(s):  
George B. Weiss ◽  
Robert E. Coalson ◽  
Leon Hurwitz
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Contractile Response ◽  
Muscle Tone ◽  
Muscle Layer ◽  
Smooth Muscle Contraction ◽  
Potassium Ion ◽  
Guinea Pig Ileum ◽  
Potassium Efflux ◽  
Longitudinal Smooth Muscle

The longitudinal smooth muscle layer of the guinea pig ileum was isolated in order to investigate its contractile responses and unidirectional K42 fluxes. Pilocarpine (7.5 x 10–6 m), acetylcholine (6.6 x 10–6 m), and a modified Tyrode's solution in which potassium ion was substituted for almost all the sodium ion were employed as excitatory agents. Cocaine (8.5 x 10–4 m) and a calcium-free Tyrode's solution served as inhibitory agents. Smooth muscle tone and potassium efflux of this relatively pure tissue were both increased by all three excitatory substances. Moreover, acetylcholine and pilocarpine produced a decrease in the influx of potassium ion. Bathing the tissue in a calcium-free medium for 1 hour before introducing pilocarpine to the muscle bath eliminated the contractile response that this drug ordinarily produces, but did not diminish appreciably the increase in K42 efflux. These observations are qualitatively similar to results previously obtained in analogous experiments on isolated whole ileum. In addition, cocaine (8.5 x 10–4 m) was found to block the contractile response and about three-quarters of the enhanced K42 efflux elicited by the isotonic potassium solution. It is presumed that cocaine acting at the membrane impedes ion fluxes important for smooth muscle contraction.

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