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At least 19 recordsLinked to original sources
PubMed1988

Exocrine secretion of epidermal growth factor by the rat prostate: effect of adrenergic agents, cholinergic agents, and vasoactive intestinal peptide.

Perfusion of the rat prostatic urethra in vivo provided a means of collecting the rat prostatic secretory product. The secretion of the protein epidermal growth factor (EGF) was investigated by radioimmunoassay (RIA). Baseline secretion of EGF into prostatic fluid was less than .03 +/- .004 SEM ng/min. The alpha-adrenergic agonist phenylephrine caused an increase in EGF to 3.6 +/- .4 SEM ng per 30-min period. The stimulation was blocked completely by prazosin and only partially by yohimbine, indicating primarily alpha 1 control. One mg/kg IV phenylephrine produced a maximal response. The beta-adrenergic agonist isoproterenol caused no increased secretion of EGF. The cholinergic agonist pilocarpine stimulated EGF secretion to 3.2 +/- .6 SEM ng per 30-min period. Atropine blocked the cholinergic stimulation. The combination of phenylephrine and pilocarpine did not result in greater stimulation than either agent alone. Vasoactive intestinal peptide (VIP) did not stimulate EGF secretion, nor did it augment either pilocarpine or phenylephrine-stimulated secretion. EGF secretion into rat prostatic fluid is under both alpha 1-adrenergic and cholinergic control.

Animals↗
PubMed1984

[Effects of autonomic blockades, beta-adrenergic agent and cholinergic agent on the FHR variability of "Shiba goats"].

The effects of atropine, propranolol, isoproterenol and acetylcholine on the fetal heart rate variability were studied using chronically prepared fetal goats. When atropine, propranolol and atropine-propranolol were injected the STVs decreased by 45.2%, 43.2% and 57.3%, respectively; LTVs also decreased by 72.3%, 52.2% and 73.3%, respectively. STVs and LTVs increased by 39.5% and 34.5% with the injection of isoproterenol, and decreased by 27.6% and 22.7% with acetylcholine. These results suggest that FHR variability represents a change in the heart rate due to reciprocal innervation of adrenergic and cholinergic systems; moreover, the activity of the heart itself exerts some influence on variability. It is also suggested that LTV more strongly reflects autonomic nervous tone whereas STV more strongly reflects heart activity.

Acetylcholine↗
PubMed1986

Adrenergic agents stimulate and cholinergic agents inhibit H+ secretion by amphibian jejunum.

In vitro segments of Amphiuma jejunum secrete H+ spontaneously. This study explored the effect of cholinergic and adrenergic agents on H+ secretion. Segments of mucosa were short-circuited and exposed on their mucosal surface to HCO3- -buffered medium while the pH of the unbuffered serosal medium was held by the pH-stat technique. Methacholine added to the serosal medium nearly abolished the spontaneous short-circuit current (Isc) and serosal alkalinization (JHCO3-) with an EC50 of 3.7 X 10(-7) M. Subsequent addition of norepinephrine (NE) to the serosal medium caused a dose-dependent increase in Isc and JHCO3. For three catecholamines the order of potency was epinephrine greater than NE greater than isoproterenol. The spontaneous Isc was significantly reduced (P less than 0.05) by the gastric H+-K+-ATPase inhibitor omeprazole, while the NE-induced Isc was unaltered by the inhibitor. Replacement of medium Na+ with choline abolished the response to NE. The NE-induced Isc was also reduced by methacholine. Acetazolamide inhibited the spontaneous and NE-induced Isc and JHCO3. In summary, cholinergic and adrenergic agents have opposing effects on intestinal H+-HCO3- transport. Jejunal acid secretion may be controlled in part by these antagonistic influences. Adrenergically activated acid secretion occurs by a different mechanism than spontaneous acid secretion.

Acetazolamide↗
PubMed1998

Central cholinergic nervous system and cholinergic agents.

Central cholinergic nervous system play important role in many physiological and behavioral functions in humans. The activity of the cholinergic nervous system depends upon the production and fate of acetylcholine and all compounds influenced its biosynthesis, storage, release, hydrolysis, interaction with different subtypes of cholinergic receptors, etc., there are very important drugs and therapeutics. This paper summarizes current views on many compounds which can interact with different parts of central cholinergic nervous system.

Acetylcholine↗
PubMed1984

The opiate quasiwithdrawal syndrome in rhesus monkeys: comparison of naloxone-precipitated withdrawal to effects of cholinergic agents.

The effects of the cholinergic agents UM-1046 (3-cyclopropyl-methyl-1,2,3,4,5,6-hexahydro-8-hydroxy-6-methyl-3-benz azo cine hydrochloride) and physostigmine in normal rhesus monkeys were compared to naloxone-precipitated withdrawal in morphine-dependent subjects. The two cholinergic drugs produced effects that resembled one another, as well as some of the effects of naloxone in morphine-dependent subjects. The constellation of signs produced by the cholinergic drugs, while overlapping, was not identical to that produced by naloxone in opiate-dependent subjects. Although cholinergic agents produce many of the signs of opiate withdrawal syndrome in its complete manifestation involves many different neurotransmitter systems.

Animals↗
PubMed1984

Hypoglossal and phrenic responses to cholinergic agents applied to ventral medullary surface.

Application of cholinergic agents on the ventrolateral surface of the medulla in areas in which the "central chemoreceptors" are believed to be located stimulates breathing. It is also known that cranial nerves, such as the hypoglossal, have respiratory modulated activity (greater in inspiration than expiration) that responds to many of the same stimuli which affect breathing. In the present study we compared effects of cholinergic agents (acetylcholine, carbachol, methacholine, eserine) directly applied to chemoreceptive areas on the ventral medullary surface on phrenic and hypoglossal nerve activity. Studies were performed in paralyzed, anesthetized, and artificially ventilated cats after vagotomy. All cholinergic agents increased hypoglossal activity significantly more than phrenic activity in animals ventilated with O2 or 7% CO2 in O2 whether or not the carotid sinus nerves were intact. Atropine applied topically to the same medullary area blocked the respiratory effects of locally administered acetylcholine. The results suggest that cholinergic agents applied centrally can increase both phrenic and hypoglossal activity. Moreover the effects of the drugs are relatively greater on XII nerve activity than on phrenic discharge, suggesting that the drive from medullary cholinergic structures is distributed with unequal weight to different respiratory motoneurons.

Acetylcholine↗
PubMed1987

Modulation of dopamine release from neuron-enriched tissue cultures by cholinergic agents.

Modulation of [3H]dopamine release by cholinergic agents (acetylcholine, atropine, d-tubocurarine, oxotremorine, and nicotine) was studied in primary cell cultures derived from whole brains of foetal rats (17 days of gestation). Monolayer and aggregated neuron-enriched cultures were maintained for 17 days in vitro [3H]Dopamine basal outflow was enhanced by acetylcholine, nicotine, and atropine and was unaffected by oxotremorine, hexamethonium, and d-tubocurarine. The action of nicotine was antagonized by d-tubocurarine, and that of atropine was partially blocked by oxotremorine. A similar picture was seen when the influence of cholinergic agents was studied under depolarizing conditions. The action of oxotremorine was dependent on nerve activity. The presence of both muscarinic and nicotinic antagonists was necessary for abolishing the effect of acetylcholine on the dopamine outflow. These results show that dopamine release in both types of neuron-enriched cultures can be influenced by cholinergic agents and that both muscarinic and nicotinic receptors are involved in regulation of the amine's outflow.

Acetylcholine↗
PubMed1978

Plasma cyclic GMP: response to cholinergic agents.

S.c. injections of cholinergic agents, carbachol, methacholine and bethanechol, into fasted rats caused rapid increases in the plasma concentration of cyclic GMP, with a sharp peak at 5--10 min after the injection. Acetylcholine gave rise to a rapid accumulation of cyclic GMP in plasma only when administered together with physostigmine which produced only a slight, if any, potentiation of the action of the cholinesterase-resistant choline esters. Cyclic AMP also increased after these drugs, but only subsequently to the rise of cyclic GMP; the primary action of the cholinergic drugs appeared to be the increase in cyclic GMP. Atropine was effective not only in abolishing the increase in plasma cyclic GMP induced by cholinergic drugs but also in lowering the baseline level of cyclic GMP. It was concluded that the plasma concentration of cyclic GMP could serve as a good parameter of cholinergic activity in rats.

Acetylcholine↗
PubMed2002

In vivo modulation of a cortical functional sensory representation shortly after topical cholinergic agent application.

The aim of the present study was to determine whether cholinergic increase in the size of a functional representation (collective evoked response from a large population of neurons) can be observed shortly (within an hour) after treatment onset and whether nicotinic receptors can participate in this type of modulation. Cholinergic agonist application has been found previously to increase the response of a single cortical neuron to a stimulus. Also, pairing cholinergic basal forebrain stimulation with delivery of a tone has been reported to increase the size of that tone's functional representation. Whereas the increase in a single cortical neuron response can occur within seconds after cholinergic agonist application, to date the increase in the size of a functional representation has only been investigated within one to several weeks after the onset of pairing basal forebrain stimulation with tone delivery. Furthermore, primarily muscarinic receptors have been implicated in these types of changes in cortical activity. By using optical imaging of intrinsic signals in vivo, we found that the size of a whisker's functional representation in the primary somatosensory cortex of the rat increases substantially within 69 or 46 minutes after topical application of either a muscarinic or nicotinic agonist to the exposed cortex, respectively, and decreases within 23 minutes after topical application of a muscarinic antagonist. For each cholinergic agent, we verified that delivery of a cholinergic agent by means of topical application can lead to the agent's successful penetration through the cortical layers in the time allotted to complete an imaging experiment. Furthermore, the time course of penetration for each agent was characterized. Based on the combined imaging/penetration results, we speculate on potential sites of cholinergic action in the cortex. Irrespective of the exact mechanism of action, we demonstrate here that an increase in the size of a functional sensory representation can occur shortly by means of activation of either nicotinic or muscarinic receptors.

Animals↗
PubMed1982

Hyperuricemic effects of cholinergic agents in rats.

The hyperuricemic effect of cholinergic agents was studied in rats given potassium oxonate which inhibits urate oxidase and in functionally hepatectomized rats. Acetylcholine slightly increased plasma uric acid in the oxonate-treated animals, and the effect was markedly enhanced by pretreatment with physostigmine. Carbachol alone showed the hyperuricemic effect at a smaller dose than acetylcholine. The hyperuricemic effects of physostigmine plus acetylcholine and carbachol alone were also observed in eviscerated rats with nonfunctioning livers. Nephrectomy markedly potentiated cholinergic agent-induced hyperuricemia, and methylatropine but not hexamethonium apparently abolished the induction of hyperuricemia both in potassium oxonate-treated rats and in eviscerated rats with nonfunctioning livers and without kidneys. However, carbachol-induced hyperuricemia was not found in rats given allopurinol whose plasma levels of uric acid were maintained by exogenously administered uric acid. These results supported the ideas that the hyperuricemic effect of cholinergic agents is due to the stimulated production of uric acid and that uric acid production in tissues other than the liver and the gastrointestinal viscera is closely related to the induction mechanisms of hyperuricemia.

Acetylcholine↗
PubMed1984

The effects of adrenergic and cholinergic agents on progesterone production by human corpus luteum in vitro.

We investigated the effects of adrenergic and cholinergic agents on human corpus luteum production of progesterone in vitro. Luteinizing hormone (LH) (50 ng/ml), dibutyryl cyclic adenosine monophosphate (Bu2cAMP) (10(-3)M), and prostaglandin E2 (PGE2) (1 microgram/ml) significantly stimulated the production of progesterone in short-term (4-hour) cell suspensions of five early and middle luteal phase corpora lutea. The adrenergic agents isoproterenol, norepinephrine, and epinephrine, and the cholinergic agents acetylcholine and carbachol at concentrations up to 10(-4)M did not alter basal or stimulated production of progesterone. Similarly, in long-term (10-day) monolayer cultures of cells from four corpora lutea, human chorionic gonadotropin (hCG) (50 ng/ml) and PGE2 stimulated, but none of the adrenergic or cholinergic agents altered, the production of progesterone significantly, except for an inhibitory effect of norepinephrine and carbachol in the presence of 17 beta-estradiol (10(-7)M) added to the culture medium. These results differ strikingly from the consistent stimulatory effect of beta-adrenergic agents on the luteal production of progesterone in several animal species.

Animals↗
PubMed2003

Spinal GABAB receptors mediate antinociceptive actions of cholinergic agents in normal and diabetic rats.

Spinally administered muscarinic receptor agonists or acetylcholinesterase inhibitors can produce antinociception. However, the mechanisms of the action of cholinergic agents in the spinal cord are not fully understood. Activation of spinal muscarinic receptors evokes gamma-aminobutyric acid (GABA) release, which reduces the glutamatergic synaptic input to dorsal horn neurons through GABA(B) receptors. In this study, we determined the functional role of spinal GABA(B) receptors in the antinociceptive action of intrathecal cholinergic agents in normal rats and in a rat model of diabetic neuropathic pain. Diabetes was induced by intraperitoneal streptozotocin in rats. The intrathecal catheter was inserted with its tip positioned at the lumbar spinal level. Nociceptive threshold was measured by the paw withdrawal latency in response to a radiant heat stimulus in normal rats. Mechanical allodynia in diabetic rats was determined by von Frey filaments applied to the hindpaw. The effect of intrathecal muscarine or neostigmine was examined through pretreatment with the specific GABA(B) receptor antagonist, CGP55845, or its vehicle. Intrathecal injection of muscarine or neostigmine significantly increased the withdrawal latency in response to a heat stimulus in normal rats and the withdrawal threshold in response to application of von Frey filaments in diabetic rats. Intrathecal pretreatment with CGP55845 significantly attenuated the effect of both muscarine or neostigmine in normal rats. Furthermore, the antiallodynic effect of intrathecal neostigmine and muscarine was largely eliminated by CGP55845 in diabetic rats. These data suggest that the GABA(B) receptors in the spinal cord mediate both the antinociceptive and antiallodynic actions of intrathecal muscarine or neostigmine in normal rats and in a rat model of diabetic neuropathic pain. This study provides new functional evidence that activation of spinal GABA(B) receptors is one of the important mechanisms underlying the antinociceptive action of intrathecal cholinergic agents.

Analgesics↗
PubMed1991

Cholinergic modulation of excitability in the rat olfactory bulb: effect of local application of cholinergic agents on evoked field potentials.

The effect of exogenously applied cholinergic agents upon mitral-granule cell complex activity of the olfactory bulb was studied in anesthetized rats. Output neurons were activated by electrical paired-pulse stimulation (40-80 ms time interval) applied either to the olfactory nerve (orthodromic stimulation) or to the lateral olfactory tract (antidromic stimulation). Evoked field potentials were recorded in the granule cell layer. Cholinergic agents were introduced close to the mitral cell body layer through a push-pull cannula. With both orthodromic and antidromic stimulations, acetylcholine in the presence of eserine (an acetylcholinesterase blocker), did not alter the conditioning volley, while it induced a significant increase in the amplitude of the test volley. This effect could be replicated using the cholinergic agonist carbachol. This attenuation of the paired-pulse inhibition is due to a reduction of the dendrodendritic inhibitory action of granule cells upon relay cells. Muscarinic and nicotinic transmission were studied using antidromic and orthodromic stimulations, respectively. The selective effect of acetylcholine on the test volley was totally abolished by the blockade of the muscarinic transmission (by atropine). The blockade of the GABAergic transmission (by picrotoxin), could also prevent the acetylcholine-induced effect. The results lead us to propose that in deep bulbar layers, acetylcholine may activate muscarinic receptors situated on second-order GABAergic interneurons. These interneurons could in turn inhibit granule cells (first-order interneurons). The nicotinic antagonist d-tubocurarine selectively enhanced the duration of the late component and did not appear to modify early components when stimulation was applied to the olfactory nerve. This effect related to both the conditioning and the test volleys and the enhancement in the duration of depolarization of granule cell dendrites suggests that normal activation of nicotinic receptors contributes to a faster repolarization of granule cells. Since nicotinic receptors belong to the outer glomerular layer, this result points to the existence of interneurons belonging to the periglomerular region where they receive nicotinic input and project to deep layers where they modulate granule cell activity. Taken together, our results suggest the presence of a phasic muscarinic and a tonic nicotinic modulation of bulbar interneuronal activity. Since both could finally reduce the inhibitory action of granule cells, the action of cholinergic afferents would facilitate transmission of bulbar output neurons to central structures.

Acetylcholine↗
PubMed1993

Rapid response of striatal muscarinic M1-receptor mRNA to muscarinic cholinergic agents in rat brain.

The effects of a single administration of muscarinic cholinergic agents on the level of muscarinic M1-receptor messenger RNA (M1-R mRNA) in the rat striatum were studied. Carbachol increased the M1-R mRNA expression rapidly and transiently, while trihexyphenidyl decreased it. These results suggest that muscarinic cholinergic agents participate in the positive regulation of muscarinic receptor mRNA in the early stage after treatment, contrary to the negative regulation in the chronic stage.

Animals↗
PubMed1976

Enhancement of "one-way" human mixed lymphocyte reaction by cholinergic agents.

"One-way" mixed lymphocyte reaction was not enhanced when the cells were allowed to be exposed to acetylcholine or carbamylcholine at a concentration of 0.01-1.0mumole/ml during the entire period of culture. It was thought to be due to cytotoxicity effect of these agents on responding cells. When the responding cells were incubated with cholinergic agents for 1 hr prior to washing the cells and setting up the mixed cell culture, "one-way" mixed lymphocyte reaction was enhanced. However, when the stimulating cells were similarly treated with either agent, no enhancement of "one-way" mixed lymphocyte reaction was observed. These observations indicate that cholinergic agent induces enhancement of mixed lymphocyte reaction by affecting only the responding cells and not the stimulating cells.

Acetylcholine↗
PubMed1976

The effects of cholinergic agents on ovarian contractility in the rabbit.

Cholinergic nerves have been recognized in the ovaries of several species. Smooth muscle fibers have also been demonstrated within the ovary, and it has been suggested that these elements are involved in the ovulatory process. Ovarian contractility was investigated in 49 ovaries from 25 rabbits in in vivo and in vitro systems and correlated with the time of hCG-induced ovulation. Effects of 6 cholinergic drugs on ovarian contractility were recorded at various intervals from 6 to 20 hours after administration of hCG. Cholinergic agents were administered via the abdominal aorta in the in vivo preparations and added to the bath for in vitro studies. In general, acetylcholine, bethanechol and pilocarpine exerted variable effects. Atropine depressed ovarian contractile activity. No definitive pattern of altered sensitivity to cholinergic drugs could be identified as the time of ovulation was approached; however, a relationship was observed between the amount of cholinergic drug administered and effects on ovarian contractions.

Acetylcholine↗
PubMed2005

The influence of central administration of dopaminergic and cholinergic agents on morphine-induced amnesia in morphine-sensitized mice.

In the present study, effects of intracerebroventricular (i.c.v.) injections of dopaminergic and cholinergic agents on morphine-induced amnesia in morphine-sensitized mice were investigated by using a one-trial passive avoidance task. Amnesia induced by pre-training morphine was significantly reversed in morphine-sensitized mice, which had previously received once daily injections of morphine (20 and 30 mg/kg, s.c.) for 3 days. Three daily injections of SKF 38393 (1, 2 and 4 g/mouse, i.c.v.) or SCH 23390 (0.25, 0.5, 0.75 and 1 g/mouse, i.c.v.) before morphine, and during morphine-sensitization, decreased and increased the amnesia induced by pre-training morphine respectively. Three daily injections of quinpirole (0.3, 1 and 3 g/mouse, i.c.v.) or sulpiride (0.03, 0.1, 0.3 and 1 g/mouse, i.c.v.) before morphine, also decreased and increased the amnesia induced by pre-training morphine respectively. Morphine-sensitized mice received similar injections of cholinergic agents. Three daily injections of physostigmine (1, 3 and 5 g/mouse, i.c.v.) or atropine (1, 4 and 7 g/mouse, i.c.v.) before morphine, and during morphine-sensitization, decreased and increased the amnesia induced by pre-training morphine respectively. Three daily injections of nicotine (0.75, 1 and 2 g/mouse, i.c.v.) or mecamylamine (1, 3 and 6 g/mouse, i.c.v.) before morphine, also decreased and increased the amnesia induced by pre-training morphine respectively. The results suggest that morphine sensitization affects the impairment of memory formation and thus it is postulated that central dopaminergic and cholinergic systems may play an important role in this effect.

Amnesia↗