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At least 811 records · Page 45Linked to original sources
PubMed1991

Airway generation-dependent induction of muscarinic hyperresponsiveness by thromboxane mimetic in vitro.

We compared the potentiating effect of U46619, a stable thromboxane analogue, on muscarinic contractile responses of rat trachealis and large and small intrapulmonary bronchi. Cylindrical proximal and distal bronchi and midtracheal strips were excised and mounted on an isometric force transducer in a physiologic tissue bath. Dose-response curves to the muscarinic agonist bethanechol (BCh) alone were compared with responses to BCh plus U46619. Airways were incubated for 2 h prior to and during second BCh curves with a noncontractile dose of U46619. U46619 induced a left shift of the dose-response curve in all airways. This was significant only at the ED10 level in trachealis, and at the ED10, ED20, and ED50 levels in large and small bronchi. Muscarinic hyperresponsiveness induced by U46619 was significantly greater in small airways than in large bronchi or trachealis. Stabilization of endogenously released acetylcholine (ACh) with physostigmine did not alter the responses to BCh plus U46619; therefore, this mechanism does not fully explain the induction of hyperresponsiveness by U46619. Our findings demonstrate the induction of a graded increase in muscarinic responsiveness in isolated airways, and they suggest that results of studies of trachealis or proximal bronchi may not necessarily be generalized to the distal resistance airways.

Animals↗
PubMed1987

Modulation of rabbit airway smooth muscle responsiveness by respiratory epithelium. Involvement of an inhibitory metabolite of arachidonic acid.

The integrity of the respiratory epithelium may be important in development of bronchial hyperreactivity; however, the mechanisms involved remain unknown. This study was undertaken to determine if epithelium of rabbit intrapulmonary bronchi is capable of modulating the responsiveness of airway smooth muscle to a pharmacologic stimulus, and whether epithelial-derived prostaglandins play a role in this modulatory function. Mechanical removal of the epithelium from bronchial segments, or incubation of intact bronchi with indomethacin (an inhibitor of prostaglandin synthesis) increased the sensitivity of bronchial smooth muscle to bethanechol. Cyclooxygenase was localized within mucosal epithelial cells of intact airways by avidin-biotin immunoperoxidase staining using a monoclonal antibody to the enzyme. Removal of the epithelium significantly reduced the levels of PGE2 and 6-keto-PGF1 alpha accumulated in the media surrounding bronchial explants. In epithelium-intact bronchi precontracted with bethanechol, arachidonic acid evoked an indomethacin-sensitive relaxation response comparable to relaxation induced by exogenous addition of PGE2. Although PGE2 evoked similar responses in epithelium-denuded bronchi, arachidonic acid-induced relaxation responses were negligible. The results suggest epithelial cells of rabbit bronchi modulate the responsiveness to pharmacologic stimuli by production and release of an inhibitory cyclooxygenase metabolite of arachidonic acid.

Animals↗
PubMed1972

Effects of fasting and feeding on protein synthesis by the rat pancreas.

These experiments were designed to determine whether fasting and feeding were associated with differing rates of protein synthesis in the rat pancreas. It has been established that feeding, acetylcholine, or cholecystokinin-pancreozymin administration was associated with enhanced rates of digestive enzyme secretion; however, the literature is unclear as to effects of such stimulation on enzyme synthesis. Rats fed ad lib. or fasted 24, 48, or 72 hr were used for this study. Pancreases were removed and incubated in tissue culture medium with l-phenylalanine-(14)C, and incorporation into TCA-insoluble material as well as purified amylase was measured. Compared with fed controls, fasting 24, 48, and 72 hr was associated with 29%, 39%, and 35% decreases in incorporation of l-phenylalanine-(14)C into protein. Decreases of similar magnitudes were apparent whether the data were expressed in terms of protein or DNA. Pancreatic amylase isolated from rats fasted 48 hr contained 57% fewer counts of l-phenylalanine-(14)C than amylase isolated from fed rats. Moreover, rats fasted for 24 hr and given bethanechol chloride incorporated greater amounts of l-phenylalanine-(14)C into protein than fasted controls. Studies were performed to exclude changes in pool size of precursor (l-phenylalanine-(14)C) or product (amylase) in accounting for decreases associated with fasting. These studies demonstrate that fasting was associated with decreased rates of pancreatic amylase and protein synthesis in rats.

Amylases↗
PubMed1973

Hormonal control of pancreatic growth.

Investigations have outlined pancreatic secretory and synthetic responses to gastrointestinal hormones. However, there is little information concerning hormonal influences on pancreatic growth. These studies were designed to examine effects of chronic administration of bethanechol and cholecystokinin-pancreozymin (CCK-PZ) on the pancreas. Male albino rats were given saline, bethanechol, 6 mg/kg, or CCK-PZ, 20 U/kg, intraperitoneally twice daily and killed after 5 days. The following changes were studied; pancreatic weight; RNA, DNA, and protein content; and [(14)C]thymidine incorporation into DNA. Bethanechol administration was associated with a 20% increase in pancreatic weight and a 33% increase in mg protein/100 mug DNA. In bethanechol-treated groups, amounts of DNA/gram body weight and incorporation of [(14)C]thymidine into DNA were similar to controls. CCK-PZ administration was associated with a 71% increase in pancreatic weight and a 38% increase in mg protein/100 mug DNA. In CCK-PZ-treated groups, amounts of DNA/gram body weight were increased by 42% and [(14)C]thymidine incorporation into DNA was increased by 185%. These studies indicate that bethanechol administration was associated with increases in pancreatic cell mass (hypertrophy). CCK-PZ administration was associated with increases in cell mass and cell numbers (hypertrophy and hyperplasia). This information suggests the importance of CCK-PZ in maintaining pancreatic functional integrity. Although bethanechol and CCK-PZ elicit similar secretory responses, their mode of action on the cell, at least as far as growth influences are concerned, appears to be different.

Animals↗
PubMed1983

Gastric bicarbonate secretion in humans. Effect of pentagastrin, bethanechol, and 11,16,16-trimethyl prostaglandin E2.

Although the stomach is mainly known for its ability to secrete hydrochloric acid, there is increasing evidence that the gastric mucosa also secretes bicarbonate. A simple method for simultaneous measurement of gastric HCO-3 secretion and H+ secretion was developed from a two-component model of gastric secretion. The method, which is based upon gastric juice volume, H+ concentration, and osmolality, was validated both in vitro and in vivo. In 14 healthy human beings, basal gastric HCO-3 secretion averaged 2.6 mmol/h (range, 0.7-8.7 mmol/h). Basal HCO-3 secretion was approximately 50% of basal H+ secretion and there was a significant correlation between basal HCO-3 and H+ secretion in individual subjects (r = 0.79). HCO-3 was secreted in basal nonparietal secretion at a concentration of approximately 90 mmol/liter. Intravenous pentagastrin infusion markedly stimulated H+ secretion but did not increase HCO-3 secretion. During pentagastrin infusion, the cholinergic agonist, bethanechol, significantly augmented H+ secretion (from 20.2 to 24.7 mmol/h) and increased HCO-3 secretion (from 2.2 to 4.2 mmol/h). A prostaglandin E2 analogue significantly reduced H+ secretion and increased HCO-3 secretion during pentagastrin infusion. The reduction in net gastric juice H+ output following prostaglandin E2 was due more to H+ secretory inhibition than to HCO-3 secretory stimulation. We conclude that the healthy human stomach actively secretes HCO-3 and that gastric HCO-3 secretion can be influenced by cholinergic stimulation and by prostaglandin E2.

Adult↗
PubMed1986

Enterogastrone-like effect of peptide YY is vagally mediated in the dog.

Intraluminal fat inhibits gastric secretion through as yet undetermined mechanisms which involve release of one or more hormonal enterogastrones. As intraluminal fat releases Peptide YY (PYY) in amounts sufficient to inhibit meal-stimulated acid secretion, this ileo-colonic peptide exhibits the characteristics required of an enterogastrone. The present study seeks to determine the mechanism by which PYY inhibits acid secretion by examining the effects of PYY on gastric acid stimulated by pentagastrin, histamine, and bethanechol. In addition, effects of PYY on the acid response to sham feeding and distention of a denervated gastric pouch were examined. A dose of PYY (400 pmol X kg-1 X h-1) was employed that reproduced blood levels observed after intestinal perfusion with oleic acid and inhibited the acid secretory response to an intragastric meal by 35 +/- 6%. This same dose of PYY maximally inhibited histamine- and pentagastrin-stimulated acid secretion by 28 +/- 7% (P less than 0.05), and 17 +/- 4% (P less than 0.05), respectively. Although PYY had no effect on bethanechol-stimulated secretion it markedly inhibited the secretory response to sham feeding, maximally reducing secretion by 90 +/- 4% (P less than 0.01). We speculate that PYY acts by inhibiting acetylcholine release from vagal nerve fibers rather than by inhibiting acetylcholine's action on the parietal cell. The demonstration that PYY virtually abolishes cephalic phase acid secretion while having little if any effect on the response to exogenous secretogogues gives PYY unique characteristics among the known hormonal inhibitors of gastric secretion.

Animals↗
PubMed1988

Direct muscarinic cholinergic inhibition of hepatic glucose production in humans.

To explore the potential role of the parasympathetic nervous system in human glucoregulatory physiology, responses to the muscarinic cholinergic agonist bethanechol (5.0 mg s.c.) and antagonist atropine (1.0 mg i.v.) were measured in normal humans. There were no changes in the plasma glucose concentration or rates of glucose production or utilization following atropine administration. After bethanechol administration there were no changes in the plasma glucose concentration or fluxes despite increments in plasma glucagon (75 +/- 7 to 103 +/- 10 pg/ml, P less than 0.02). There were no changes in insulin or C-peptide levels. To test the hypothesis that direct muscarinic inhibition of glucose production was offset by an indirect action of the agonist, specifically increased glucagon secretion with consequent stimulation of glucose production, bethanechol was administered while glucagon levels were held constant with the islet clamp technique (somatostatin infusion with insulin, glucagon and growth hormone replacement at fixed rates). Under that condition the muscarinic agonist induced a 25% decrement in the plasma glucose concentration (101 +/- 8 to 75 +/- 8 mg/dl, P less than 0.05). When compared with separate clamp control studies (with placebo rather than bethanechol injection) both the rate of glucose production and the glucose concentration were reduced (P less than 0.05) following bethanechol injection; the rate of glucose utilization was unaltered. Thus, we conclude: Withdrawal of parasympathetic tone does not appear to be an important glucoregulatory process in humans. Direct muscarinic cholinergic inhibition of hepatic glucose production occurs in humans but during generalized muscarinic activation this is offset by an indirect muscarinic action, increased glucagon secretion with consequent stimulation of glucose production. Thus, particularly if regional neuronal firing occurs, the parasympathetic nervous system may play an important role in human glucoregulatory physiology.

Adult↗
PubMed1993

Vagal afferent pathway mediates physiological action of cholecystokinin on pancreatic enzyme secretion.

To establish the mechanism(s) and site(s) of action of cholecystokinin (CCK) on pancreatic secretion under physiological conditions, we used an in vivo model using anesthetized rats with pancreaticobiliary cannulas. Infusion of CCK-8 (10-160 pmol/kg per h) produced a dose-dependent increase in plasma CCK levels. CCK-8 infusion at 40 pmol/kg per h produced a plasma CCK level of 7.9 +/- 1.5 pM and an 80% increase in pancreatic protein output over basal. This level was closely approximated by a postprandial peak plasma CCK level by 6.2 +/- 1.1 pM. Pretreatment with atropine or hexamethonium completely abolished pancreatic protein response to low doses of CCK-8 (10-40 pmol/kg per h) but had only partial effect on doses > 40 pmol/kg per h. Bilateral vagotomy also abolished the pancreatic responses to low doses of CCK-8. Similarly perivagal treatment with a sensory neurotoxin, capsaicin, caused a complete inhibition of pancreatic protein secretion in response to CCK-8 infusion. In contrast, pancreatic protein responses to bethanechol were similar in control and capsaicin-treated rats. In separate studies we demonstrated that gastroduodenal but not jejunal application of capsaicin for 30 min abolished pancreatic protein secretion in response to physiological doses of CCK-8. In conclusion, CCK at physiological levels stimulates pancreatic enzyme secretion via a capsaicin-sensitive afferent vagal pathway originating from the gastroduodenal mucosa.

Afferent Pathways↗
PubMed1975

The use of bethanechol chloride with tricyclic antidepressants.

The author describes the use of bethanechol chloride to relieve side effects, including salivary inactivation, constipation, and bladder inhibition, which result from the anticholinergic action of tricyclic antidepressants. He suggests that the use of cholinergic medication during antidepressant therapy may extend the use of the tricyclics to patients who find anticholinergic side effects especially troublesome.

Adult↗
PubMed1993

Treatment of nortriptyline's side effects in elderly patients: a double-blind study of bethanechol.

A double-blind, placebo-controlled study of bethanechol was conducted in 26 elderly depressed patients being treated with nortriptyline. Patients receiving bethanechol had reduced subjective complaints of anticholinergic side effects and showed a trend toward improvement on an objective measure of salivary flow. The potential use of bethanechol in older patients to reduce morbidity and improve compliance with medication regimens is discussed.

Aged↗