The Action of Cholecystokinin and Related Peptides on Guinea Pig Small Intestine

1974 ◽  
Vol 52 (2) ◽  
pp. 298-303 ◽  
Author(s):  
W. M. Yau ◽  
G. M. Makhlouf ◽  
L. E. Edwards ◽  
J. T. Farrar
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Guinea Pig ◽  
Mode Of Action ◽  
Muscle Fibers ◽  
Nerve Endings ◽  
Cholinergic Mechanisms ◽  
Molar Basis ◽  
Release Of Acetylcholine ◽  
Relative Potencies

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.

Relative potencies of histamine H1-agonists on guinea-pig tracheal smooth muscle

1984 ◽  
Vol 106 (2) ◽  
pp. 405-409 ◽  
Author(s):  
Richard W.S. Harrison ◽  
Heather Carswell ◽  
J.Michael Young
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Tracheal Smooth Muscle ◽  
Relative Potencies

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.

Interaction of enkephalin and caerulein on guinea pig small intestine

1983 ◽  
Vol 244 (1) ◽  
pp. G65-G70
Author(s):  
W. M. Yau ◽  
P. F. Lingle ◽  
M. L. Youther
Keyword(s):  
Small Intestine ◽  
Guinea Pig ◽  
Muscarinic Receptors ◽  
Dose Response ◽  
Response Curve ◽  
Acetylcholine Release ◽  
Control Level ◽  
Release Studies ◽  
Release Of Acetylcholine

This is a report on the effect of caerulein and methionine-enkephalin interaction on mechanical contraction and acetylcholine release in vitro. The ability of enkephalin to relax caerulein-induced contractions and the manner in which the caerulein dose-response curve was shifted in the presence of enkephalin strongly suggest that enkephalin and caerulein are functional antagonists in this system. The failure of enkephalin to alter the action of exogenous acetylcholine implies that such an antagonism is not mediated through a competition with postsynaptic muscarinic receptors on the muscle. Data from acetylcholine-release studies indicate that caerulein stimulation was dose related. As with the mechanical contractions, the release of acetylcholine in response to caerulein was inhibited by enkephalin. However, naloxone was capable of blocking this inhibition and restoring the release to its control level without interfering with caerulein stimulation. These data provide evidence for the modulatory roles of neuronal peptides in the cholinergic control of gut motility.

Exogenous opiates: their local mechanisms of action in the canine small intestine and stomach

1987 ◽  
Vol 253 (2) ◽  
pp. G179-G188 ◽  
Author(s):  
J. E. Fox ◽  
E. E. Daniel
Keyword(s):  
Small Intestine ◽  
Mechanisms Of Action ◽  
Low Doses ◽  
Field Stimulation ◽  
Direct Stimulation ◽  
Distal Stomach ◽  
Phasic Activity ◽  
Release Of Acetylcholine ◽  
Relative Potencies ◽  
Stimulation Of

Methionine-enkephalin (Met-Enk) and dynorphin were injected intra-arterially into the distal stomach and small intestine of the anesthetized dog during quiescence and phasic activity initiated by field stimulation or intra-arterially administered motilin. The effects of morphine, [D-Ala2, N-Me-Phe4, Met(O)5-ol]enkephalin (Met-ol), and [D-Ala2, D-Leu5]enkephalin (DADLE) were also examined. Opiates had no effect on the quiescent stomach but produced inhibition of phasic contractions (potencies: dynorphin greater than Met-Enk greater than Met-ol greater than DADLE greater than morphine). In the quiescent small intestine, low doses of each opiate, except dynorphin, produced excitation (potencies: Met-Enk congruent to Met-ol congruent to DADLE greater than morphine). Excitation apparently occurred via release of acetylcholine and a partially naloxone-sensitive direct stimulation of smooth muscle. During phasic activity all opiates produced inhibition of phasic muscular contractions (relative potencies as in the stomach). Inhibition by dynorphin in both the stomach and small intestine was shown to occur via naloxone-sensitive inhibition of release of acetylcholine from nerves. Thus inhibition by opiates appears common to the stomach and small intestine, and excitation is a function of opiate action only in the small intestine. Dynorphin may be a natural neuropeptide causing inhibition, and Met-Enk may be a natural neuropeptide causing excitation.

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