Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ganglionic Stimulants”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 955 records · Page 53Linked to original sources
PubMed1991

Effects of nicotinic agonists on the NMDA receptor.

The cholinergic nicotinic agonists (-)nicotine and lobeline were observed to partially inhibit whole-cell N-methyl-D-aspartate (NMDA)-induced responses in rat cortical neurons in culture. In addition we found that (-)nicotine, (+)nicotine, and lobeline, but not the nicotine metabolite (-)cotinine nor acetylcholine, were able to displace [3H]dizocilpine ([3H]MK 801) binding in well-washed membranes obtained from rat brain. These results show that certain nicotinic agonists can interact with the NMDA receptor and block its function.

Animals↗
PubMed1992

The interaction of kappa-bungarotoxin with the nicotinic receptor of bovine chromaffin cells.

Whole-cell recording techniques were used to examine acetylcholine-induced nicotinic currents in isolated bovine chromaffin cells. The effects on these currents of kappa-bungarotoxin, a snake venom kappa-neurotoxin, were tested. Exposure of cells to kappa-bungarotoxin (600 nM for 40 min) produced a prolonged blockade of nicotinic currents. The mechanism of this blockade was examined in several ways. Firstly, the pre-exposure of cells to trimetaphan, a competitive nicotinic antagonist, protected against the action of subsequent additions of kappa-bungarotoxin. Secondly, voltage-clamp measurements indicated that the degree of blockade produced by kappa-bungarotoxin was independent of cell membrane potential. Unlike (+)-tubocurarine, kappa-bungarotoxin had no direct agonist effects on nicotinic receptors. It is concluded from the present functional studies and from previously reported binding studies that kappa-bungarotoxin blocks nicotinic responses in bovine chromaffin cells by binding to regions overlying acetylcholine sites on nicotinic receptors.

Acetylcholine↗
PubMed1992

Capsaicin-sensitive nonadrenergic and noncholinergic depressor response to spinal cord stimulation in the pithed rat.

The effects of capsaicin on nonadrenergic, noncholinergic depressor responses to spinal cord stimulation were studied in pithed rats. Mean blood pressure (MBP was maintained at a level of 100 mmHg by continuous infusion of methoxamine and hexamethonium to block autonomic outflow. Electrical stimulation of the lower thoracic region (T9-12) via a pithing rod produced a frequency (1-8 Hz)-dependent fall in elevated MBP. The depressor response was abolished by tetrodotoxin, whereas atropine, propranolol, and cimetidine plus pyrilamine did not affect the response. Capsaicin treatment abolished the depressor response. These results suggest that spinal cord stimulation causes neurogenic vasodilation which is mediated by capsaicin-sensitive nonadrenergic and noncholinergic vasodilator nerves.

Animals↗
PubMed1976

A study of muscarinic receptor heterogeneity with weak antagonists.

A study of heterogeneity among muscarinic receptors was carried out with new rigid molecules, comprising structures in the fused quinuclidine-valerolactone, quinuclidine-cyclohexenone, quinuclidine-cyclohexanone and quinuclidine-cyclohexane derivatives. These are structurally related to the potent muscarinic agent, 3-acetoxyquinuclidine but substantially different from in it conformation. All proved to antagonize acetylcholine-like activity, but to a different extent in different systems. The equipotent molar ratio with respect to atropine (as 1) was: isolated guinea pig ileum, 10,000-1,000; salivary gland (mouse), 1,000-100; superior cervical ganglion (cat), 100-10; CNS (mouse), approximately 10. It is suggested that the rigid structure induces a three-point constrained fit in the receptor (onium group, hydrophobic moiety and carbonyl group), but that not all muscarinic receptors are capable of responding equally. In this case, receptor specificity of the drug is a direct consequence of its graded departure from the preferred conformation of acetycholine and, therefore, is necessarily associated with partial loss of potency.

Animals↗
PubMed1990

Parasympathetic nervous control of intraocular pressure.

Electrical or chemical activation of the oculomotor nucleus (ONC) was performed in pentobarbital anesthetized cats to determine the role of parasympathetic nervous input to the eye in modulating intraocular pressure (IOP). In all animals, the vagosympathetic nerve trunks were sectioned bilaterally at the mid-cervical level. Intracranial stimulation of the ONC produced miosis and a bilateral sustained rise in IOP with little or no cardiovascular response. During stimulation, IOP increased by approximately 35-40%, with an additional small rise seen when the current was turned off. The secondary rise in IOP probably represents the actual pressure level reached which was otherwise masked by intense accommodation due to stimulation. The rise in IOP was not antagonized with gallamine triethiodide. However, both IOP and pupillary responses were blocked by either hexamethonium (1.5 mg kg-1, i.v.) or atropine (0.5 mg kg-1, i.v.). These results provide evidence for a neural parasympathetic mechanism for increasing IOP in cats. In another group, activation of ONC following electrolytic lesion of the preganglionic parasympathetic nerve to one eye, produced a rise in IOP and miosis only on the side with intact oculomotor nerve indicating that the rise in IOP is in part mediated by nerve fibers that travel to the eye along the oculomotor nerve trunk. Microinjection of L-glutamate (2.5 x 10(-7) M) into the ONC produced a bilateral rise in IOP that lasted for more than 15 min. This increase in IOP was greater than 50% of control levels and was accompanied with miosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Actions of cholinergic drugs on cells in the interpeduncular nucleus.

The muscarinic versus nicotinic effects of acetylcholine (ACh) on the activity of cells in the interpeduncular nucleus (IPN) of guinea pig brain slices were investigated using electrophysiologic techniques. Nicotinic and muscarinic drugs acted postsynaptically to increase the firing rate of cells in the IPN. The excitatory actions of ACh were blocked both by atropine and by d-tubocurarine. These results indicated that cholinergic receptors of IPN cells seem to have both nicotinic and muscarinic characteristics.

Acetylcholine↗
PubMed1994

Ca(2+)-dependent cosecretion of adrenomedullin and catecholamines mediated by nicotinic receptors in bovine cultured adrenal medullary cells.

Bovine cultured adrenal medullary cells (4 x 10(6)) contained 4266.5 +/- 370.0 fmol of immunoreactive adrenomedullin and 373.4 +/- 32.6 nmol of catecholamines. Nicotinic (but not muscarinic) receptors mediated the Ca(2+)-dependent co-secretion of adrenomedullin and catecholamines, with the molar ratio of adrenomedullin/catecholamines secreted into the medium being equal to the ratio stored in the cells. The concentration-response curve of carbachol for adrenomedullin secretion (EC50 42 microM) was similar to that for catecholamine secretion (EC50 63 microM). Reverse phase HPLC analysis showed that immunoreactive adrenomedullins in the cells and secreted into the medium were both eluted exclusively at the position almost identical to synthetic human adrenomedullin[1-52]NH2.

Adrenal Medulla↗