Topic
Bethanechol
About: Bethanechol is a research topic. Over the lifetime, 1055 publications have been published within this topic receiving 25281 citations. The topic is also known as: Duvoid® & Urecholine®.
Papers published on a yearly basis
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Papers
TL;DR: These studies indicate that bethanechol administration was associated with increases in pancreatic cell mass and cell numbers (hypertrophy and hyperplasia) and suggests the importance of CCK-PZ in maintaining pancreatic functional integrity.
Abstract: 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.
279 citations
TL;DR: It is concluded that acute stressors have profound effects on intestinal epithelial physiology, stimulating ion secretion and reducing barrier function.
Abstract: Wistar-Kyoto rats were subjected to 4 h restraint stress (RS) or cold restraint stress (CRS), and jejunal tissues were examined in Ussing chambers for alterations in transport functions compared with tissues from unstressed control rats. The baseline short-circuit current (Isc) was significantly elevated in tissues from RS (approximately 50%) and CRS (100%). Substitution of Cl- eliminated the abnormality, suggesting that stress stimulates Cl- secretion. Electrical transmural stimulation of enteric nerves caused a transient increase in Isc in all tissues. The magnitude of this response was significantly less in tissues from CRS than from control rats; however, the ability of the epithelium to secrete in response to exogenous stimulation with bethanechol or vasoactive intestinal polypeptide was unimpaired, implicating a neural change. Tissue conductance was higher in jejunum from RS and CRS rats than from controls. Increased intestinal epithelial permeability in stressed rats was confirmed by significantly greater fluxes of the inert radiolabeled probes, [3H]mannitol and 51Cr-labeled EDTA. No structural changes were observed. We conclude that acute stressors have profound effects on intestinal epithelial physiology, stimulating ion secretion and reducing barrier function.
231 citations
TL;DR: It is found that subdiaphragmatic vagotomy in LSL-Kras +/G12D;Pdx1-Cre mice accelerated PDAC development, whereas treatment with the systemic muscarinic agonist bethanechol restored the normal KC phenotype, thereby suppressing the accelerated tumorigenesis caused by vagotomy, suggesting that cholinergic signaling directly and indirectly suppresses growth of PDAC cells.
Abstract: In many solid tumors, parasympathetic input is provided by the vagus nerve, which has been shown to modulate tumor growth. However, whether cholinergic signaling directly regulates progression of pancreatic cancer (PDAC) has not been defined. Here, we found that subdiaphragmatic vagotomy in LSL-Kras+/G12D;Pdx1-Cre (KC) mice accelerated PDAC development, whereas treatment with the systemic muscarinic agonist bethanechol restored the normal KC phenotype, thereby suppressing the accelerated tumorigenesis caused by vagotomy. In LSL-Kras+/G12D;LSL-Trp53+/R172H;Pdx1-Cre (KPC) mice with established PDAC, bethanechol significantly extended survival. These effects were mediated in part through the CHRM1, which inhibited downstream MAPK/EGFR and PI3K/AKT pathways in PDAC cells. Enhanced cholinergic signaling led to a suppression of the CSC compartment, CD11b+ myeloid cells, TNF-α levels, and metastatic growth in the liver. Therefore, these data suggest that cholinergic signaling directly and indirectly suppresses growth of PDAC cells, and therapies that stimulate muscarinic receptors may be useful in the treatment of PDAC.
226 citations
TL;DR: The results suggest that the excessive stimulation of cholinergic muscarinic receptors can lead to limbic seizures and brain damage in rats, and it is postulated that mus carinic cholinerential mechanisms are linked to the etiology of temporal lobe epilepsy and epileptic brain damage.
Abstract: Microinjections of the cholinergic agonists, carbachol and bethanechol, either into the amygdala or into the dorsal hippocampus produced sustained limbic seizures and brain damage in rats. Systemic administration of pilocarpine in rats resulted in a sequence of convulsive disorders and widespread brain damage as well. Scopolamine prevented the development of convulsive activity and brain damage produced by cholinomimetics. These results suggest that the excessive stimulation of cholinergic muscarinic receptors can lead to limbic seizures and brain damage. It is postulated that muscarinic cholinergic mechanisms are linked to the etiology of temporal lobe epilepsy and epileptic brain damage.
218 citations
TL;DR: It is demonstrated that an abnormality in chloride transport is present in the small intestinal and colonic epithelia of CF patients, which does not respond to either cAMP- or Ca-mediated secretagogues, and may play a role in the pathogenesis of meconium impactions in CF patients.
Abstract: Sodium ion and chloride transport was studied in vitro in small intestinal and colonic tissue from patients with cystic fibrosis (CF) and from non-CF control subjects matched as to age and sex Normal histological appearance and substantial response to mucosal glucose (5 mM, ileum) or mucosal amiloride (10(-5) M, colon) indicated normal tissue viability in both control and CF tissues Electroneutral NaCl absorption was demonstrated in the small intestine of control subjects and CF patients Small intestinal and colonic tissues of control subjects responded to four secretagogues (theophylline, 5 mM; prostaglandin E2, 10(-6) M; calcium ionophore (A23187), 10(-5) M; bethanechol, 5 x 10(-5) M), with electrogenic chloride secretion The tissues of CF patients, however, did not respond to any of the test secretagogues These studies demonstrate that an abnormality in chloride transport is present in the small intestinal and colonic epithelia of CF patients Unlike airway epithelia, which secrete chloride in response to Ca ionophore, the intestinal epithelia of CF patients do not respond to either cAMP- or Ca-mediated secretagogues This abnormality in intestinal electrolyte transport may play a role in the pathogenesis of meconium impactions in CF patients
206 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2025 | 1 |
| 2024 | 1 |
| 2023 | 2 |
| 2022 | 8 |
| 2021 | 1 |
| 2020 | 6 |