Drugs online research references
J Neurochem. 1990 Nov;55(5):1546-55.
Evidence that somatostatin enhances endogenous acetylcholine release in the rat hippocampus.
Araujo DM, Lapchak PA, Collier B, Quirion R.
Douglas Hospital Research Center, McGill University, Montreal, Quebec, Canada.
The present experiments show that somatostatin (SS)-like immunoreactive material is present in the hippocampus and that its release can be increased by K+ stimulation of rat hippocampal slices, suggesting that SS-like peptides may be of significance to neurotransmission in the hippocampus. Exogenous SS-28 and SS-14 enhanced the K(+)-evoked release of endogenous acetylcholine (ACh) from rat hippocampal slices, whereas amino-terminal fragments of SS-28 did not. The increased ACh release in the presence of either peptide appeared to be mediated by an interaction with SS receptors because cyclo-SS, a putative SS antagonist, abolished the effects of both SS-28 and SS-14. In addition, the increase in ACh release induced by SS-14 or SS-28 was antagonized by the calcium channel antagonists omega-conotoxin GVIA, nifedipine, and cinnarizine, implicating voltage-sensitive calcium channels in this effect. Moreover, the effect was sensitive to tetrodotoxin, suggesting an indirect action of the peptides at a site distal to cholinergic nerve terminals. Cysteamine, which has been reported to deplete SS content and to increase SS release in brain, augmented the basal and evoked release of ACh from hippocampal slices, without affecting SS-like content and release. Finally, neuropeptide Y, which is colocalized with SS in many neurons of the hippocampal formation, did not alter ACh release, nor did it facilitate the SS-induced increase. The results suggest that in the rat hippocampus, both SS-28 and SS-14 interact with SS receptors to regulate ACh release indirectly by a mechanism that involves alterations of calcium influx during depolarization.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1976754&dopt=Abstract
Jpn J Physiol. 1985;35(5):871-4.
Dihydropyridine BAY K 8644 enables reduction of Ca concentration to induce catecholamine secretion from the perfused cat adrenal.
Sorimachi M, Nishimura S, Yano K.
Dihydropyridine derivative BAY K 8644 increased the rate of catecholamine secretion from the perfused cat adrenal. The magnitude of the response was inversely proportional to the extracellular concentration of Ca, i.e. the lower the Ca concentration, the larger the response. The response was markedly inhibited by Mg or nifedipine.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2416976&dopt=Abstract
J Pharmacol Exp Ther. 1986 Apr;237(1):99-106.
Effects of calcium channel entry blockers, nifedipine and nilvadipine, on colonic motor activity.
Barone FC, White RF, Ormsbee HS 3rd, Wasserman MA.
The effects of the dihydropyridine calcium channel entry blockers nifedipine and nilvadipine on colonic contractions were determined in vitro and in vivo. In circular muscle strips prepared from the canine proximal colon, cumulative concentration-response curves were generated to potassium chloride (KCl), acetylcholine (ACh) and substance P, and the effects of electrical field stimulation were determined. Responses to KCl and ACh were examined in circular muscle strips prepared from the monkey proximal and distal colon. Nifedipine (10(-8) - 10(-6) M) significantly decreased KCl-induced contractions, whereas equimolar concentrations of nilvadipine were less effective at modifying these responses. Both calcium channel entry blockers produced similar significant decreases in ACh, substance P and electrical field stimulation contractions. In anesthetized dogs, strain gauge force transducers were oriented to record proximal colonic circular muscle contractions. Colonic contractions to i.a. infusions of ACh, cholecystokinin-(26-33) and substance P were produced in a small segment of the proximal colon. Nifedipine and nilvadipine (200 micrograms/kg i.v.) significantly decreased maximal ACh contractions. Nilvadipine also decreased maximum cholecystokinin-(26-33) and substance P contractions. Both calcium channel entry blockers decreased systolic and diastolic blood pressure significantly at 100 micrograms/kg i.v. These results indicate that nifedipine and nilvadipine are equieffective at reducing colonic contractile activity to a variety of colonic stimulants and illustrate the importance of extracellular calcium in the mediation of colonic motility
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2420971&dopt=Abstract
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