The effect of eserine on the response of the vas deferens to hypogastric nerve stimulation.
(49/481)
In experiments in which the vas deferens together with the hypogastric nerve of the guinea-pig was studied as an isolated preparation, the relation between frequency of electrical stimulation of the nerve and the height of contraction was determined. The optimal frequency was 20 shocks/sec. This value was the same when hyoscine was present to exclude the direct effect of any acetylcholine which might be released. When eserine was added to the bath in the presence of hyoscine, the response to stimulation at a frequency of 5 shocks/sec gradually increased until it became many times greater; the response to a frequency of 10 shocks/sec also increased, though to a less extent, but eserine decreased the amplitude of the contraction at a stimulus frequency of 20 shocks/sec. Neostigmine had the same effect as eserine. These findings indicate that, in the presence of hyoscine, eserine increased the noradrenaline released by low frequency stimulation, but decreased it for high frequency. If this is so, the results are compatible with the belief that there is a cholinergic link in the release of noradrenaline by hypogastric nerve stimulation. (+info)
PHOTOSENSITIVITY OF THE FROG IRIS.
(50/481)
The absorption of quanta by rhodopsin leads to the contraction of frog iris muscle. The contractions reach a maximum after about 8 sec. in the light. When the light is turned off the irises relax exponentially with a half-time of about 6 sec. Membrane polarization is not necessary for the response but calcium movement and membrane permeability changes probably are. The response is not mediated by acetylcholine or epinephrine. The curves of log It vs. log t for constant response amplitude bend progressively upward away from a unit slope line at short times as larger response criteria are used because (a) light influences tension development over longer times and (b) the higher intensity, shorter duration flashes are less effective. (+info)
THE MODE OF ACTION OF NEOSTIGMINE AND PHYSOSTIGMINE ON THE GUINEA-PIG TRACHEALIS MUSCLE.
(51/481)
Neostigmine (2.2 mug/ml.) or physostigmine (3.3 mug/ml.) contracted guinea-pig isolated tracheal chains. The anticholinesterase diisopropylphosphodiamidic fluoride (mipafox) itself caused no contractile response even in concentrations of 100 mug/ml., yet neostigmine or physostigmine still caused contractions after treatment with mipafox. The responses were abolished by hyoscine or atropine. Local anaesthetics, cooling, ionic changes and hemicholinium, all known to inhibit the release of acetylcholine from nerve endings, abolished or much reduced the responses. It seems that the contractile response to physostigmine or neostigmine does not depend on their anticholinesterase activity, but on their ability to release acetylcholine from postganglionic parasympathetic nerve endings. (+info)
THE EFFECTS OF CHOLINE AND OTHER FACTORS ON THE RELEASE OF ACETYLCHOLINE FROM THE STIMULATED PERFUSED SUPERIOR CERVICAL GANGLION OF THE CAT.
(52/481)
When the superior cervical ganglion of the cat was perfused with Locke solution, the amount of acetylcholine released into the perfusate decreased during successive periods of repetitive stimulation of the preganglionic nerve. Addition of choline to the perfusion fluid prevented this decrease. Choline also significantly increased (P<0.01) the initial output of acetylcholine. In contrast, variation of the physostigmine concentration or of the pCO(2) and pH of the perfusion fluid had no statistically significant effect (P>0.05) upon the initial release of acetylcholine. (+info)
EFFECT OF SOME BLOCKING DRUGS ON THE PRESSOR RESPONSE TO PHYSOSTIGMINE IN THE RAT.
(53/481)
Bretylium and guanethidine blocked the pressor effect of physostigmine and potentiated the responses to adrenaline and noradrenaline on the blood pressure of the rat. Morphine and atropine in small doses blocked the pressor effect of physostigmine without interfering with the actions of adrenaline and noradrenaline. Chlorpromazine in small doses (0.5 to 2.5 mg/kg) blocked the pressor effect of physostigmine and potentiated the responses to noradrenaline whilst those to adrenaline remained unaltered. 3,6-Di(3-diethylaminopropoxy)pyridazine di(methiodide) (Win 4981) blocked the pressor effect of physostigmine and, in its early stages, this block was partially reversed by choline chloride. N-Diethylaminoethyl-N-isopentyl-N'N'-diisopropylurea (P-286), in a dose that reduced the effect of dimethylphenylpiperazinium, had no effect on the pressor response to physostigmine or on the responses to adrenaline and noradrenaline. Hexamethonium, even in large doses (100 mg/kg), only blocked partially the effect of physostigmine while mecamylamine produced a complete block; the responses to adrenaline and noradrenaline were potentiated in both instances. (+info)
LEAKAGE OF TRANSMITTERS IN SALIVARY GLANDS.
(54/481)
Salivary secretion evoked by sympathetic stimulation or by injection of guanethidine, adrenaline or synephrine is slightly reduced by parasympathetic antagonists in doses which abolish the secretory responses to stimulation of the parasympathetic nerve. Similarly, an adrenaline antagonist caused a small diminution of the salivary flow elicited by parasympathetic stimulation or by injection of methacholine chloride. Secretion caused by pilocarpine could be accelerated by physostigmine. We conclude that transmitter leaks in subliminal concentrations, as far as secretion is concerned, from the sympathetic and parasympathetic postganglionic nerve endings. (+info)
THE SYMPATHETIC MECHANISM IN THE ISOLATED PULMONARY ARTERY OF THE RABBIT.
(55/481)
The nature of postganglionic sympathetic nervous transmission to vascular muscle in vitro was studied using the recurrent cardiac nerve-pulmonary artery preparation of the rabbit. Experiments, similar to those which in other tissues have provided evidence to support a role for acetylcholine at the sympathetic postganglionic nerve-effector cell junction, were carried out. The contractile response of the isolated artery to acetylcholine was blocked completely by atropine. High concentrations of acetylcholine and of hemicholinium had no effect on the contractile response to sympathetic nerve stimulation. Physostigmine, atropine and hemicholinium were without influence on the relationship between nerve stimulus frequency and response. Yohimbine, bretylium and reserpine blocked completely the response to nerve stimulation but did not affect that to applied acetylcholine. These results support the view that transmission in this preparation at the sympathetic postganglionic nerve-effector cell junction is mediated by an adrenaline-like transmitter and provide no evidence for the view that acetylcholne is involved at this site. (+info)
ALTERATION OF ACETYLCHOLINE PENETRATION INTO, AND EFFECTS ON, VENOM-TREATED SQUID AXONS BY PHYSOSTIGMINE AND RELATED COMPOUNDS.
(56/481)
Choline and neostigmine markedly antagonize the effect of acetylcholine (ACh) on the action potential of the venom-treated squid axon, although they themselves have no effect on conduction. Physostigmine also antagonizes the blocking action of ACh at a concentration well below that which has any effect on conduction. In contrast, d-tubocurarine (curare) increases the effect of ACh on the action potential. Choline, neostigmine, and physostigmine markedly decrease the penetration of C(14)-labeled ACh into the axoplasm of the squid axon. Curare, in contrast, increases the penetration of ACh, whereas dimethylcurare gives variable results. The results provide an explanation why physostigmine and neostigmine do not influence the action of ACh on axonal conduction in a way similar to that observed at the junction. The additive effect of curare and ACh on the action potential may be due either to the greater rate of penetration of ACh or to an additive effect of the two compounds on the receptor, or to a combination of both factors. (+info)