The effects of calcium and magnesium on inhibitory junctional transmission in smooth muscle of guinea pig small intestine

1975 ◽  
Vol 360 (2) ◽  
pp. 109-119 ◽  
Author(s):  
Mollie E. Holman ◽  
John P. Weinrich
1987 ◽  
Vol 244 (3) ◽  
pp. 763-768 ◽  
Author(s):  
R S E Mallows ◽  
T B Bolton

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.


1974 ◽  
Vol 52 (2) ◽  
pp. 298-303 ◽  
Author(s):  
W. M. Yau ◽  
G. M. Makhlouf ◽  
L. E. Edwards ◽  
J. T. Farrar

The mode of action of cholecystokinin (CCK), an octapeptide fragment of CCK, caerulein, and pentagastrin on isolated guinea pig ileal muscle was investigated and their relative potencies determined. On a molar basis, octapeptide-CCK and caerulein were about twice as potent as CCK, whereas pentagastrin and Urecholine were respectively 23 and 46 times less potent. Scopolamine (6.84 × 10−4 M) inhibited the response to all four peptides relatively less than the response to Urecholine. Tetrodotoxin (0.1 μg/ml) inhibited the response to all peptides by 91%. It was concluded that the effect of these peptides on ileal muscle was largely mediated by cholinergic mechanisms. It could not be ascertained, however, whether the effect resulted solely from release of acetylcholine by nerve endings or from the participation of acetylcholine mainly as a synergist of the peptides' action on smooth muscle fibers.


2001 ◽  
Vol 120 (5) ◽  
pp. A225-A225
Author(s):  
M COSTA ◽  
S YUAN ◽  
T RAINSFORD ◽  
S BROOKES ◽  
G HENNIG

1992 ◽  
Vol 262 (2) ◽  
pp. G308-G311 ◽  
Author(s):  
M. Yoshinaga ◽  
Y. Chijiiwa ◽  
T. Misawa ◽  
N. Harada ◽  
H. Nawata

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+.


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