Efffect of vasoactive intestinal polypeptide on gallbladder smooth muscle in vitro.

1978 ◽  
Vol 234 (1) ◽  
pp. E44 ◽  
Author(s):  
J P Ryan ◽  
S Ryave
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Motor Activity ◽  
Vasoactive Intestinal Polypeptide ◽  
Muscle Tone ◽  
Contractile Activity ◽  
Gastrointestinal Hormones ◽  
Resting Tension ◽  
Intestinal Polypeptide

The effect of vasoactive intestinal polypeptide (VIP) on basal and octapeptide of cholecystokinin (OP-CCK) induced tension was examined with guinea pig gallbladder smooth muscle strips in vitro. VIP alone produced dose-related decreases in resting tension and antagonized spontaneous contractile activity where present. In combination with OP-CCK, VIP decreased the expected contractile respone. The degree of antagonism depended upon the concentrations of OP-CCK and VIP. VIP had no effect on acetylcholine-induced contractions. From these observations, we propose that VIP can affect gallbladder motor activity by decreaseing smooth muscle tone and by antagonizing cholecystokinin. These findings lend further support to our proposal that gallbladder motor function may depend upon the action and interaction of the gastrointestinal hormones.

Nuclear Fos immunoreactivity in guinea pig myenteric neurons following activation of motor activity

1997 ◽  
Vol 273 (2) ◽  
pp. G498-G507 ◽  
Author(s):  
R. C. Ritter ◽  
M. Costa ◽  
S. H. Brookes
Keyword(s):  
Electrical Stimulation ◽  
Guinea Pig ◽  
Motor Activity ◽  
Muscle Tone ◽  
Smooth Muscle Contraction ◽  
Early Gene ◽  
Enteric Neurons ◽  
Experimental Conditions ◽  
Fos Expression

To identify enteric neurons activated during intestinal motor activity, we examined myenteric plexus of guinea pig small intestinal segments for expression of the immediate early gene product, Fos. Fos immunoreactivity was detected immunohistochemically following in vitro manipulations, which included distension, electrical stimulation, exposure to forskolin, and peristalsis. All of these manipulations induced neuronal Fos expression, which was prevented by tetrodotoxin, indicating that expression depended on nerve activity. Distension-induced Fos expression was blocked by omega-conotoxin and significantly reduced by hexamethonium, indicating that neurons expressing Fos immunoreactivity were activated synaptically. Blocking smooth muscle contraction with nicardipine reduced expression of neuronal Fos, suggesting that muscle tone influences neuronal activity. Calbindin-immunoreactive putative sensory neurons did not express Fos during distension, peristalsis, or exposure to forskolin and expressed Fos only weakly after strong electrical stimulation. Conversely, calretinin-immunoreactive ascending excitatory interneurons and longitudinal muscle motoneurons exhibited Fos immunoreactivity after all experimental manipulations. These results indicate that Fos expression can, with some caution, be used to identify classes of enteric neurons activated by different stimuli under various experimental conditions.

Role of nitric oxide-related inhibition in intestinal function: relation to vasoactive intestinal polypeptide

1994 ◽  
Vol 266 (1) ◽  
pp. G31-G39 ◽  
Author(s):  
E. E. Daniel ◽  
C. Haugh ◽  
Z. Woskowska ◽  
S. Cipris ◽  
J. Jury ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Motor Activity ◽  
Vasoactive Intestinal Polypeptide ◽  
Contractile Activity ◽  
Low Frequency ◽  
Circular Muscle ◽  
Arginine Infusion ◽  
Intestinal Segments ◽  
Intestinal Polypeptide

This study examined the role of nitric oxide (NO) in tonic inhibition of motor activity in isolated, perfused canine ileal segments. Brief addition of N omega-nitro-L-arginine methyl ester (L-NAME) to the perfusate caused, after a delay, a concentration-dependent persistent increase in tonic and phasic activity of circular muscle. This increased motor activity was prevented or reversed by addition of L- but not D-arginine to the perfusate. Removal of Ca2+ or addition of 10(-7) M omega-conotoxin (GVIA) to the perfusate markedly reduced this response. The motor activity induced by L-NAME was accompanied by loss of distal inhibition and enhanced excitation to low-frequency field stimulation. L-NAME infusion significantly reduced tonic vasoactive intestinal polypeptide (VIP) output, sodium nitroprusside increased VIP output, but L-arginine infusion did not restore VIP output. Atropine (10(-7) M) and/or hexamethonium (10(-4) M) reduced the motor response to L-NAME by 75%. Atropine reduced and hexamethonium nearly abolished VIP output. We conclude that there is tonic Ca(2+)-dependent NO output from perfused intestinal segments dependent on nerves with N-Ca channels, that NO acts to inhibit muscle directly and by inhibiting release of excitatory mediators, and that this output is the primary inhibitory determinant of contractile activity.

Interaction of gastrin I, secretin, and cholecystokinin on gallbladder smooth muscle

1976 ◽  
Vol 230 (3) ◽  
pp. 553-556 ◽  
Author(s):  
J Ryan ◽  
S Cohen
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Motor Function ◽  
Muscle Tone ◽  
Dose Range ◽  
Maximum Response ◽  
Maximal Response ◽  
Gallbladder Contraction ◽  
Gallbladder Contractility

The effect of cholecystokinin (CCK), the octapeptide of cholecystokinin (CCK-OP), gastrin I, and secretin was studied on guinea pig gallbladder smooth muscle in vitro. Both CCK and CCK-OP stimulated gallbladder contraction, with CCK-OP being more potent. Gastrin I, over a wide dose range, had no effect on gallbladder contractility. Secretin alone also showed no effect on gallbladder smooth muscle but in combination with CCK-OP it produced a noncompetitive type of inhibition. Michaelis-Menten kinetics showed the calculated maximum response of the secretin plus CCK-OP interaction to be less than with CCK-OP alone. There was no change in the dose required to achieve half-maximal response, D50. These studies indicate that: a) CCK-OP has a greater effect on gallbladder contractility than CCK, b) gastrin I has no effect on gallbladder muscle tone, and c) secretin acts as a noncompetitive antagonist of CCK-OP. These findings suggest that gallbladder motor function may be determined in part by the interaction of secretin and CCK rather than solely in response to CCK.

The effect of vasoactive intestinal polypeptide on the urinary bladder and taenia coli of the guinea pig

1979 ◽  
Vol 57 (1) ◽  
pp. 106-108 ◽  
Author(s):  
A. Johns
Keyword(s):  
Urinary Bladder ◽  
Guinea Pig ◽  
Vasoactive Intestinal Polypeptide ◽  
Contractile Activity ◽  
Taenia Coli ◽  
Weak Contraction ◽  
Intestinal Polypeptide

The effect of vasoactive intestinal polypeptide (VIP) on the contractile activity of the urinary bladder and taenia coli of the guinea pig has been investigated. In the urinary bladder VIP caused a weak contraction and a small potentiation of the nerve-induced contraction. In the taenia coli VIP caused a small relaxation and had no effect on the nerve-induced relaxation of the preparation. The present experiments provide no evidence that VIP fulfills a role as a neurotransmitter in the urinary bladder or taenia coli, but it could be a modulator of transmitter action in the urinary bladder.

Effects of immunological sensitization on the responses and sensitivity of guinea pig airways to bronchoconstrictors. Modulation by selective inhibition of arachidonic acid metabolism

1983 ◽  
Vol 61 (8) ◽  
pp. 876-887 ◽  
Author(s):  
Maan H. Saad ◽  
John F. Burka
Keyword(s):  
Guinea Pig ◽  
Contractile Activity ◽  
Nordihydroguaiaretic Acid ◽  
Selective Inhibition ◽  
Arachidonic Acid Metabolism ◽  
Resting Tension ◽  
Low Concentrations ◽  
High Concentrations ◽  
Inhibitor Treatment

The force generated by tracheal spirals and lung parenchymal strips from normal and ovalbumin-sensitized guinea pigs was measured in vitro, after challenge with histamine, carbachol, leukotriene (LT) C4, LTD4, or a prostaglandin endoperoxide analog (U-44069). The responses and sensitivity of airway tissues to the above agonists were identical in normal and sensitized animals. Treatment of tracheal spirals with indomethacin (8.5 μM), phenidone (185 μM), and nordihydroguaiaretic acid (NDGA: 30 μM) reduced resting tension (tone) equally in both normal and sensitized trachea, but did not affect lung parenchymal strips from either group. The responses of tracheal spirals from normal and sensitized animals to low concentrations of histamine, carbachol, LTC4, and LTD4 were reduced or abolished by treatment with the above inhibitors. Responses to higher concentrations of the same agonists were significantly enhanced. In contrast, treatment of normal and sensitized trachea with indomethacin (2.8 and 8.5 μM) did not abolish or reduce the effects of low concentrations of U-44069. However, an enhancement of the effect of high concentrations occurred only on normal tracheal spirals, even though the control tissues from each group responded identically with U-44069 in the absence of any inhibitor. Parenchymal strips increased in sensitivity to histamine, but not carbachol, as a result of time, vehicle, or prior exposure to the drug. Inhibitor treatment did not affect sensitivity or responsiveness of parenchyma to histamine, carbachol, and U-44069, but the contractile activity of LTD4 on both normal and sensitized lung parenchymal strips was reduced by indomethacin, NDGA, and phenidone. We conclude that ovalbumin sensitization does not induce hyperreactivity of guinea pig airways.

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