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PubMed1976

Inhibition of gastric secretion in the dog by 16,16-dimethyl prostaglandin E2.

The synthetic prostaglandin 16,16-dimethyl E2 (PGE2) given by intravenous infusion at 0.4 mug/kg-h inhibited gastric secretion of H+, K+, Cl-, and pepsin in four fistula dogs stimulated by histamine (H), pentagastrin (P), urecholine (U), and 2-deoxy-D-glucose (2-DG). When given for 90 min during steady infusions of near-maximal doses of H, P, and U, PG-E2 caused 75% inhibition of H+ maximally at 90 min and over 85% inhibition of pepsin secretion maximally at 45 min. Recovery of secretion took 1-2 h after infusion of PGE2 was stopped. Injection of KCl, 1 meq/kg, during inhibition of histamine by PGE2 gave only a 15-min transient reversal in inhibition. When PGE2 was given as background to 45-min step-dose responses, 0.1 mug/kg competitively inhibited histamine stimulation and 0.4 mug/kg-h gave 100% inhibition. Against pentagastrin, 0.1 mug PGE2/kg-h had no effect and 0.4 mug caused uncompetitive inhibition; against urecholine, 0.4 mug PGE2/kg-h caused competitive inhibition of H+ secretion. Pepsin was more markedly inhibited in each case. There were no side effects at either dose of PGE2, which is a potent inhibitor of gastric secretion with all forms of stimuli.

Animals↗
PubMed1976

Lower esophageal sphincter pressures and serum gastrin levels after cholinergic stimulation.

To define the role of gastrin, if any, in the response of the lower esophageal sphincter (LES) to bethanechol, serum gastrin determinations and LES pressure measurements were made in controls, patients with vagotomy and antrectomy (V&A), and patients with vagotomy and pyloroplasty (V&P). Despite significant differences in mean basal serum gastrin levels no differences were found in mean resting LES pressures among these groups. In controls significant increases in LES pressure occurred after subcutaneous bethanechol, but serum gastrin levels did not change from basal values. Subcutaneous injections of bethanechol produced significantly greater increases in LES pressures in V&P patients than in V&A patients. Serum gastrin levels did not change in either group; however, background serum gastrin concentrations were significantly greater for V&P patients than V&A patients throughout the study. Intravenous infusion of human gastrin I heptadecapeptide in controls significantly increased sphincter responses to bethanechol. Thus, these studies provide evidence to suggest that the LES response to bethanechol is affected by background serum gastrin levels.

Adult↗
PubMed1976

Series elasticity of urinary bladder smooth muscle.

Loops of rat bladder were stretched between pins in vitro, supported by a clamp that could be suddenly shortened by activation of a solenoid to achieve a quick release of tension. The series elasticity measured in this fashion was found to follow an exponential course and to be modified by the rate of release, indicating a minor viscous component. Tissue length decreased and series elastic stiffness appeared to increase with muscle contraction, but no alteration in series elasticity was evident when the data were related to the tension existing in the tissue at the moment of quick release. Inactivation of the contractile system by removing calcium ion with ethylene glycol-bis-(beta-aminoethylether)-N,N'-tetraacetate (EGTA) similarly did not alter series elasticity when it was related to the tension existing in the tissue. Series elasticity during the stress relaxation following a stretch, and during the contracting and relaxing phases of rhythmic contractions, was also determined by tissue tension. The conclusion drawn is that contractile cross bridges do not contribute to the series elasticity measured in bladder tissue.

Animals↗
PubMed1976

Effects of ions on amylase release by dissociated pancreatic acinar cells.

Dissociated acinar cells prepared from guinea pig and mouse pancreas were intact on the basis of structure, ion content, and their ability to increase release of amylase in response to bethanechol and the calcium ionophore A23187. Guinea pig but not mouse acinar cells increased amylase release in response to caerulein. An increase in the concentration of K+ in the medium, which increases amylase release from whole pancreas, did not increase release. The effect of varying the ionic content of the medium on basal and stimulated amylase release was studied. Bethanechol and caerulein were still able to stimulate amylase release when Ca2+ was omitted from the medium, whereas stimulation induced by A23187 was abolished. Elevation of the concentration of Mg2+ did not affect basal or stimulated amylase release. Removal of Na+ from the medium initially had no effect on amylase release although bethanechol-stimulated release by mouse cells was inion of the HCO3- or Cl- content of the medium did not affect cholinergic stimulation of secretion. It is concluded that stimulated amylase release by isolated acinar cells is relatively independent of the ionic constituency of the bathing medium.

Amylases↗
PubMed1990

Pre- and postjunctional muscarinic receptors in canine bronchi.

Cholinergic receptors on canine bronchial smooth muscle (mediating excitation) or on the cholinergic nerve endings (modulating acetylcholine release) have not yet been characterized. In this study, the effects of agents selective for the various muscarinic receptors on mechanical and electrical responses in isolated segments of canine bronchial smooth muscle (3rd-6th order) were investigated. Carbachol (Cch), bethanechol (Bch), oxotremorine (Oxo), and McNeil A343 (McN) produced membrane depolarization and contractions with a ranked potency order of Oxo approximately Cch greater than Bch greater than McN. Oxo-induced contractions were antagonized by pirenzepine (Pir), AF-DX 116 (AF-DX), or hexahydrosiladifenidol (Hexa); Schild analysis yielded pA2 values of 6.61, 6.81, and 7.40, respectively. Contractions induced by field stimulation (FS) were antagonized by Pir, AF-DX, or Hexa with a potency order of Hexa greater than AF-DX approximately Pir. FS responses were potentiated by lower (i.e., M1-selective) concentrations of Pir, and antagonized by McN. The non-M1 agonists and antagonists had no such effects. These findings indicate that the postjunctional receptors are of the M3 subtype, and that the inhibitory receptors on the cholinergic nerve endings are of the M1 subtype.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1986

Water drinking induced by gastric secretagogues in pigs.

Eleven young pigs, feeding and drinking operantly, were tested for drinking responses to three gastric secretagogues. First, feed was removed for 1 h before the test period, then a continuous intravenous infusion of saline or a secretagogue was begun at a priming rate of 0.6 ml/min for the first 10 min, then at 0.3 ml/min for 50 min. Dose rates were the smallest that would still cause a vigorous gastric secretion. When 0.9% NaCl was infused, the pigs drank a mean of 54 +/- 11 (SE) ml. The comparable volumes for the secretagogues were histamine 174 +/- 41 ml (1 microgram . kg-1 . min-1); pentagastrin 231 +/- 38 ml (0.5 microgram . kg-1 . min-1); and bethanechol 231 +/- 35 ml (1.0-1.5 microgram . kg-1 . min-1). Pretreatment with cimetidine (300 mg iv) depressed the drinking response to histamine to 30 +/- 10 ml and to pentagastrin to 58 +/- 24 ml. Atropine (2 mg iv) depressed the response to bethanechol to 28 +/- 16 ml. Differences between responses to the secretagogues and either control drinking or antagonist-blocked responses were all significant (P less than 0.001). The results indicate that gastric secretion could play a role in stimulation of preprandial water drinking.

Analysis of Variance↗
PubMed1991

Cholinergic reticular mechanisms influence state-dependent ventilatory response to hypercapnia.

Breathing is impaired by the loss of wakefulness that accompanies sleep, certain comatose states, and anesthesia. Although state-dependent decrements in breathing and the ability to respond to hypercapnic stimuli are characteristic of most mammals, the neural mechanisms that cause state-dependent changes in respiratory control remain poorly understood. The present study examined the hypothesis that cholinergic mechanisms in the medial pontine reticular formation (mPRF) can cause state-dependent changes in breathing and in the hypercapnic ventilatory response (HCVR). Six cats were anesthetized with halothane and chronically instrumented for subsequent studies of breathing during wakefulness, non-rapid-eye-movement (NREM) sleep, rapid-eye-movement (REM) sleep, and during the REM sleep-like state caused by mPRF microinjections of carbachol or bethanechol. Minute ventilation was significantly decreased during the carbachol-induced REM sleep-like state (DCarb) compared with wakefulness. The HCVR in NREM, REM, DCarb, and after bethanechol was less than the waking HCVR. These results show for the first time that cholinoceptive regions in the mPRF can cause state-dependent reductions in normocapnic minute ventilation and in the ventilatory response to hypercapnia.

Animals↗
PubMed1991

Defining origin of positive slope in hypercapnic ventilatory response curve.

The sensitivity to CO2 as a respiratory stimulant has traditionally been studied by exposing organisms to progressively increasing levels of inspired CO2 while measuring the corresponding increase in minute ventilation (V). Plots of V as a function of end-tidal CO2 concentration reveal a complex function with a "dogleg" shape. Only the positive slope of the V function is taken as an index of chemosensitivity, but the starting points for such analyses are often chosen arbitrarily. This paper examined the hypotheses that the range of CO2 concentrations over which V slopes are compared may be mathematically defined and that arbitrary choices of this analytic range may influence conclusions about the hypercapnic ventilatory response (HCVR). Three mathematical models attempted to define the origin of the positive slope for the HCVR curve using empirically derived data. The results revealed good agreement that the origin of the positive HCVR slope may be reliably defined by a point that joins the horizontal and positive slope of the HCVR curve. In addition to identifying the "joint-point" statistic, the results suggest that arbitrarily defining the range of CO2 values over which V is analyzed can be replaced by quantitative approaches for identifying the origin of the ventilatory response to hypercapnia.

Animals↗
PubMed1993

Meal initiation occurs after experimental induction of transient declines in blood glucose.

Previous studies have shown that a brief rise in plasma insulin followed by a transient fall and rise in blood glucose precede the initiation of feeding in nondeprived rats. In this study, a cholinergic agonist, bethanechol chloride, which is known to induce a brief spike in plasma insulin, was infused intravenously in an attempt to induce transient declines in blood glucose and meal initiation in free-feeding rats. When the blood glucose response to bethanechol chloride administration met the criteria for a transient decline in blood glucose, meal initiation occurred within 20 min in nine out of ten trials. However, if the blood glucose response to bethanechol chloride administration failed to meet the criteria for a transient decline in blood glucose, meal initiation did not occur. The frequency of successful induction of feeding was higher in the late light cycle (80%) compared with the early light cycle (14%) of the photoperiod. These results suggest that cholinergic stimulation can induce feeding only after a brief fall and rise in blood glucose. The blood glucose and behavioral responses to the cholinergic stimulus appear to be strongly dependent on the metabolic state of the animal. These results further strengthen the evidence for a causal relationship between transient declines in blood glucose and meal initiation in free-feeding rats.

Animals↗
PubMed1985

Active transport of chloride by lateral ventricle choroid plexus of the rat.

The nature of Cl transport and its relation to Na and K transport were analyzed in adult rat lateral ventricle choroid plexus incubated in cerebrospinal fluid (CSF) medium at 37 degrees C and PCO2 = 30 mmHg. In synthetic CSF (extracellular Cl [( Cl]o) = 130 mM), the intracellular Cl [( Cl]i) was three times that estimated for passive distribution. Choroid plexus [Cl]i was not determined by Donnan distribution because [Cl]i remained constant at approximately 50 mM while the [K]i/[K]o ratio was varied 10-fold by drugs and cation substitutions. A [Cl]i/[Cl]o ratio of approximately 0.38 was found when [Cl]o was varied from 15 to 130 mM by isosmotic replacement of Cl with methyl sulfate or isethionate. However, the [Cl]i/[Cl]o ratio increased to greater than 1.0 when [Cl]o was lowered below 5 mM. Reduction in bath temperature to 15 degrees C (CSF PCO2 = 50 mmHg) increased both [Cl]i/[Cl]o and [HCO3]i/[HCO3]o to approximately 0.6. SITS, an inhibitor of Cl-HCO3 transport, reduced [Cl]i by 18 mM, decreasing the [Cl]i/[Cl]o ratio close to the equilibrium value. In contrast, neither furosemide (10(-3) M) nor low CSF [Na]o (3 mM) reduced Cl accumulation. It is concluded that uphill movement of Cl into choroid plexus epithelium occurs primarily by Cl-HCO3 antiport and not by Na-Cl symport.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1978

Exocrine secretion of canine pancreas perfused extracorporeally.

A canine gastroduodenopancreatic block was isolated and perfused extracorporeally with homologous blood. This preparation was used for studying stimulated exocrine secretion of the pancreas. Stimulants were infused intra-arterially. Both vagi were stimulated electrically. Hydrochloric acid or L-phenylalanine were instilled intragastrically. Pancreatic secretion induced by secretin and during HCl instillation was rich in bicarbonate and poor in total protein. Pancreatic secretion obtained during the infusion of normal saline, cholecystokinin, bethanechol chloride or acetylcholine chloride and during instillation of amino acid as well as during electrical stimulation of vagi, contained less bicarbonate and more protein than secretin-induced secretion.

Acetylcholine↗
PubMed1980

Cholinergic pathway of gastric acid secretion in the isolated whole stomach of the mouse.

The isolated whole stomach of the mouse has been used to study the effect of atropine on gastic acid secretion stimulated by acetylcholine, bethanechol and histamine. Atropine inhibited acid secretory response to acetylcholine and bethanechol in a competitive manner. The following pA2 values for atropine were calculated: 6.72, and 7.75, respectively. Slopes of log (DR-1) against log (B) were not significantly different from unity. Histamine-induced acid secretion was not inhibited by atropine. Acid secretory response to acetylcholine was not reduced by concentrations of cimetidine up to 10(-3) mol/l. Acetylcholine-induced acid secretion was not influenced by hexamethonium. In the mouse isolated stomach, acetylcholine stimulates acid secretion through a direct cholinergic pathway.

Acetylcholine↗