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PubMed1982

Progressive isolated segmental anhidrosis.

A patient had progressive segmental anhidrosis, which proved after extensive neurologic and autonomic workup to be an isolated abnormality. Intradermal acetylcholine produced localized sweating in areas of thermoregulatory anhidrosis five months after the onset of symptoms but failed to do so at two years. These findings are consistent with a preganglionic sympathetic lesion affecting a functionally defined subset of sympathetic cells and/or fibers. The alteration of the sudomotor response to intradermal acetylcholine during the course of the illness suggests that the diagnostic utility of pharmacologic sweat tests may be time dependent, limited to a relatively early period following onset of anhidrosis.

Acetylcholine↗
PubMed1982

Cyclic AMP arrhythmias. Inhibition by choline esters.

Ventricular tachycardia (VT) was induced and maintained in open-chested pigs by subepicardial infusion (focal infusion 10 microliters/min) of norepinephrine (NE) (10(-5) M) in solution with CaCl2 (2.5 X 10(-3) M) and NaCl (0.9%). Choline esters and related compounds were then tested for their antiarrhythmic properties. The NE/Ca2+ VT was abolished within 60 sec by carbamylcholine (CCh) or methacholine (each 10(-6) M). Acetylcholine and butyrylcholine were less effective (each 10(-4) M). The fly mushroom poison muscarine had a strong antiarrhythmic effect (10(-6) M). Choline abolished the NE/Ca2+ VT at higher concentrations (10(-2) M). The antiarrhythmic effect of muscarine and CCh (10(-6) M) was blocked by atropine (10(-6) M) but not hexamethonium (up to 10(-4) M). The NE/Ca2+ VT was also abolished by beta-adrenoceptor blocking agents [pindolol (10(-6) M), propranolol (10(-4) M)] and calcium antagonists [isoptin, D-600 (10(-4) M each), MnCl2 (5 X 10(-4) M), NiCl2, CoCl2 (2.5 X 10(-3) M each)]. Tetrodotoxin (up to 10(-5) M) did not protect against NE/Ca2+ VT. Analysis of myocardial tissue obtained from the infusion sites showed that cAMP was increased when the NE/Ca2+ VT ensued and that choline esters in the absence of atropine prevent such accumulation of cAMP. It is concluded that activation of muscarinic receptors by choline esters inhibits ventricular arrhythmias induced by regional adrenergic overstimulation and accumulation of cAMP, possibly by decreasing the slow inward Ca2+ current.

Acetylcholine↗
PubMed1970

Dopamine as a synaptic transmitter and modulator in sympathetic ganglia: a different mode of synaptic action.

An analysis of the role of adrenergic transmission in mediating the hyperpolarizing, slow inhibitory postsynaptic potential has revealed that dopamine is apparently the specific synaptic transmitter for this response. An additional action of dopamine was discovered, namely the selective facilitation of another synaptic response, the slow excitatory postsynaptic potential. (This potential is a depolarizing response to the muscarinic action of acetylcholine.) This second, modulatory, role of dopamine has characteristics strikingly different from other known modes of synaptic action. After a brief initial action by dopamine, the facilitation of the slow excitatory postsynaptic potential response can persist for hours and is unaffected by a delayed blockade of the postsynaptic receptors for dopamine. This suggests that the modulation consists of a long-lasting metabolic and/or structural change induced in the postsynaptic neuron by dopamine. These conclusions are based on the demonstrated actions of dopamine and other catecholamines, as well as on effects (on dopamine actions and on slow postsynaptic potentials of alpha-adrenergic blockers, of blockade, of dopamine oxidase, of depletion of ganglionic catecholamine by muscarinic excitation, and of a selective re-uptake of dopamine after such depletion.

Acetylcholine↗
PubMed1981

Pharmacological responses by different portions of guinea pig vas deferens circular muscle preparation.

The different segments of the guinea pig vas deferens circular muscle exhibit differential response patterns upon pharmacological stimulation. Namely, apart from barium chloride, the affinity and intrinsic activity of certain agonists and the strength of maximum contractions they induce appear to decrease along the path from the epididymis toward the prostate. If one subdivides the vas deferens into 3 parts of equal length such as epididymal, medial and prostatic portions, then adrenaline, acetylcholine, acetyl-beta-methylcholine, dopamine, histamine and bradykinin induce contractions on each of the 3 parts; whereas tyramine, ephedrine elicit responses in the epididymal and medial portions; amphetamine, DMPP, serotonin and PGF2 alpha in turn provoking contractions exclusively on the epididymal portion. The effects of adrenaline and noradrenaline are blocked by phentolamine and tolazoline; the responses to acetylcholine, acetyl-beta-methylcholine and carbamyl-beta-methylcholine are antagonized by atropine over a specific concentration range. The effects of tyramine, ephedrine and amphetamine are inhibited by phentolamine in an remarkably low dose range (pA2 = 13.51 +/- 0.09; 14.54 +/- 0.31; 14.35 +/- 0.12). The situation was the same when tyramine-dibenamine and tyramine-phenoxybenzamine combinations were tested (pD'2 = 14.03 +/- 0.37; 13.26 +/- 0.03). Based on these findings the presence of a peculiar alpha adrenergic receptor is suggested on the sympathetic postganglionic fibres. In addition to the already identified alpha adrenergic, muscarinic cholinergic and histamine H1 receptors, we could show the presence of dopaminergic receptors too in the vas deferens circular muscle.

Acetylcholine↗
PubMed1982

The effect of physostigmine on the vagally induced muscarinic inhibition of noradrenaline release from the isolated perfused rabbit atria.

1. Presynaptic cholinergic-adrenergic interactions were studied on isolated perfused rabbit atria with the extrinsic right vagus and sympathetic innervation intact. The transmitter stores were labelled with 14C-choline and 3H-noradrenaline. The radioactive compounds were separated on columns and determined by scintillation spectrometry. The stimulation-evoked overflow of both transmitters was calcium-dependent and abolished by tetrodotoxin. 2. Methacholine caused a concentration-dependent decrease of atrial tension development and 3H-noradrenaline overflow evoked by 3 Hz sympathetic stimulation. Vagus nerve stimulation (1-20 Hz), although nearly abolishing tension development at 20 Hz, decreased evoked 3H-noradrenaline overflow by not more than 18%. 3. Physostigmine decreased atrial cholinesterase activity by 80% and increased the fraction of stimulation-evoked unhydrolyzed 14C-acetylcholine in the persufates from 58 to 86%. However, the inhibition by vagus stimulation (1-10 Hz) of evoked 3H-noradrenaline overflow was smaller than in the absence of the drug. This was closely related to a decrease in acetylcholine overflow. Yet for a give fractional rate of acetylcholine release the muscarinic inhibition of noradrenaline overflow still did not exceed that observed in the absence of physostigmine. 4. It is concluded that the vagally induced control of noradrenaline release occurs at discrete sites rather than in a diffuse pattern at multiple terminal axon sites as is the case after exogenous muscarinic agonists.

Animals↗
PubMed1983

Studies on the mechanisms of the antisecretory and cytoprotective actions of SCH 28080.

The antisecretory and cytoprotective actions of SCH 28080 (2-methyl-8-(phenylmethoxy)imidazol[ 1,2-a ]pyridine-3-acetonitrile), an antiulcer compound, were characterized. In the isolated guinea-pig gastric mucosa, SCH 28080 at 5 X 10(-8) M abolished the acid secretory responses to histamine and methacholine but at 5 X 10(-7) M also inhibited the responses to dibutyryl cyclic AMP plus theophylline. The data suggest that the antisecretory effect of SCH 28080 involves a direct action on the parietal cells distal to the primary events mediating the cholinergic and H2 histaminergic secretory mechanisms. In the histamine-stimulated dogs, a prolonged suppression of acid secretion was accompanied by only a transient fall in the ratio of mucosal plasma flow to acid output after i.v. dosing of SCH 28080, 1 mg/kg, indicating that the antisecretory action of SCH 28080 was not secondary to changes in gastric blood flow. Mechanisms mediating the cytoprotective effects of SCH 28080 were investigated. SCH 28080 (10 mg/kg p.o.) increased total mucus as determined by measurements of N-acetylneuraminic acid in rat stomach. In the isolated guinea-pig gastric mucosa, bicarbonate secretion was augmented in a dose-dependent (10(-6)-10(-4) M) manner. Concomitant stimulation of the gastric mucus and bicarbonate by SCH 28080 may lead to strengthening of the gastric mucosal barrier and account for its gastric cytoprotective activity against injuring agents. In conclusion, the antisecretory and cytoprotective activities of SCH 28080 are due to a direct action on the parietal cells and a stimulatory effect on mucus and bicarbonate secretion by the mucosal epithelial cells, respectively.

Animals↗