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SOME EFFECTS OF LONG CHAIN POLYMETHYLENE BISONIUM SALTS ON JUNCTIONAL TRANSMISSION IN THE PERIPHERAL NERVOUS SYSTEM.

A survey has been made of the effects on junctional transmission of the complete series of polymethylene bis-trimethylammonium (BTM) and bis-triethylammonium (BTE) salts from the decamethylene compounds (BTM 10 and BTE 10) to those with twenty-one methylene groups in the chain. These were tested for their ability to cause contracture of the isolated chick biventer cervicis preparation, and for their ability to block the twitch responses of this preparation, those of the rat isolated diaphragm preparation, and those of the cat tibialis anterior preparation. They were also tested for their ability to block transmission in the cat superior cervical ganglion, to block the actions of acetylcholine on the guinea-pig isolated ileum, and for ability to inhibit the hydrolysis of acetylcholine by acetylcholinesterase. Their electrical conductivity has been measured in aqueous solution. Ability to cause contracture of the chick biventer cervicis is confined to the compounds BTM 10 to 15; BTE 10, 11 and 12 have some weak activity but the other BTE compounds, and the BTM compounds with more than fifteen methylene groups, have virtually no activity. In the BTE series both neuromuscular blocking and ganglion-blocking activities increase with chain length up to a maximum in the region of BTE 15 to 17 and then decline. In the BTM series ganglion-blocking activity increases with chain length in much the same way as in the BTE series, though the maximum activity is at a slightly longer chain length. At the neuromuscular junction an increase in chain length beyond BTM 10 leads to a decline in activity but this returns to some extent at longer chain lengths, reaching a second maximum at BTM 18, above which it declines further. At the ganglion BTE 16 is only slightly more active than BTM 16 and about five-times as active as hexamethonium; at the neuromuscular junction in the cat BTE 16 is about five-times as active as BTM 16 and about eight-times as active as (+)-tubocurarine. The affinity of the BTE compounds for the postganglionic acetylcholine receptors of the guinea-pig ileum reaches a maximum at BTE 14 but does not decline significantly with further increase in chain length. Anticholinesterase activity, likewise, does not alter significantly between BTM 12 and BTM 21 and the activity of the compounds in the BTE series appears to be similar. This property could conceivably be modifying the actions of some of the intermediate compounds but is not likely to be affecting those of the more active ones. The conductivity experiments indicate that micelle formation could be limiting the actions of the compounds with 20 or 21 methylene groups, but is not likely to be affecting those of the other compounds. The results suggest that there is a regular increase with chain length of the affinity of these compounds for the receptors in the ganglia and at the neuromuscular junction but that efficacy in causing contracture is limited to compounds with three methyl groups in the cationic head and a chain of about ten methylene groups. The connexion between this ability to depolarize and the ability to block transmission by desensitization is discussed.

Acetylcholine↗

Neuroprotective effect of the novel Na+/Ca2+ channel blocker NS-7 on rat retinal ganglion cells.

PURPOSE: To investigate whether NS-7, 4-(4-fluorophenyl)-2-methyl-6-(5-piperidinopentyloxy) pyrimidine hydrochloride, a novel Na(+)/Ca(2+) channel blocker, can protect the rat retina subjected to ischemia-reperfusion insult. METHODS: To evaluate the protective effect of NS-7 against retinal damage, the drug was administered before and after ischemia-reperfusion. Damage to the retina was assessed by measuring the thickness of the inner plexiform layer (IPL) and the outer nuclear layer (ONL) of each eye. In a subsequent experiment, electroretinographic (ERG) evaluation was also used. RESULTS: In histopathologic evaluation, ischemia-reperfusion injury caused a significant reduction of IPL thickness (measured as the IPL/ONL ratio). In the NS-7-treated group, retinal damage was partially prevented by a concentration of 0.25 mg/kg per day. In the ERG evaluation, ischemia-reperfusion injury caused a reduction of A- and B-wave amplitudes. NS-7 treatment significantly prevented the reduction of the B wave at a concentration of 0.1 or 0.3 mg/kg, while the reduction of the A wave was not significantly affected. CONCLUSIONS: NS-7 has neuroprotective effects against retinal damage resulting from subjection to ischemia. In addition, NS-7 can be used as an agent for treating acute ischemic retinopathy, including diseases associated with very high intraocular pressure, such as acute angle-closure glaucoma.

Animals↗

alpha- and beta-adrenoceptor blockade fail to prevent high sodium diet-induced left ventricular hypertrophy.

High sodium diet (HS, 8% NaCl) induces left ventricular hypertrophy (LVH) in normotensive rats without an increase in pressure or volume load or in resting cardiac sympathetic activity. HS may affect LV adrenoceptors density or affinity or their postreceptor pathways, thereby causing LVH. We therefore assessed the effects of HS with and without blockade of alpha1- or beta-adrenoceptors by terazosin or nadolol, alone or in combination, on resting hemodynamics, LV and right ventricular (RV) weights, and LV dimensions of male WKY rats. HS increased LV weight by 14% to 17%, and the ratio of LV wall thickness to radius by 18% to 23%. Singly or in combination, the adrenoceptor antagonists did not prevent HS-induced LVH, but instead aggravated it. The increased ratio of LV wall thickness to radius and of LV to RV were attenuated by terazosin or nadolol alone. Neither the resting LV peak-systolic or end-diastolic pressures nor the right atrial pressure was changed by HS, either alone or in combination with the blockers. The failure of chronic alpha1- or beta-blockade to prevent HS-induced LVH suggests that adrenoceptor activation is not important in evoking the LVH. However, the blockers shifted the LVH from a concentric to an eccentric form, suggesting an involvement of additional trophic factors during adrenoceptor blockade.

Adrenergic alpha-Antagonists↗

Cardiovascular effects of an organophosphate toxin isolated from Ptychodiscus brevis.

The dose-dependent hypotensive and bradycardic effects induced by an ichthyotoxic organophosphate compound isolated from the marine dinoflagellate Ptychodiscus brevis were studied. These effects were not antagonized by atropine, but potentiated by alpha-adrenoceptor blocker and hexamethonium. The toxin abolished the vasopressor effect elicited by phenylephrine, indicating an alpha-adrenergic blocking activity. The cardiovascular depressor responses were antagonized by tetraethylammonium while blockade of cholinergic and histaminergic receptors or inhibition of prostaglandin synthesis failed to modify these effects. The results indicate that the cardiovascular depressor effects of the toxin are probably mediated through alpha-adrenergic and ganglionic blockade accompanied by modulation of potassium channel activity.

Adrenergic alpha-Antagonists↗

ACTIONS OF HEMICHOLINIUM (HC-3) ON NEUROMUSCULAR TRANSMISSION.

Hemicholinium No. 3 (HC-3; alpha,alpha'-dimethylaminoethanol-4, 4'-biacetophenone) produced neuromuscular block of the tibialis anterior muscle-sciatic nerve preparation of the anaesthetized cat which was of slow onset, of long duration and dependent on the nerve stimulus frequency. The failure of the compound to modify the response of the tibialis muscle to close-arterial injections of acetylcholine suggested that the sensitivity of the motor endplate was not changed by it. The neuromuscular block produced by hemicholinium was antagonized by choline but only partly relieved by anticholinesterase drugs. The response to tetanic stimulation of the nerve during the neuromuscular block was well sustained and was followed by a slight posttetanic potentiation. The neuromuscular blocking action of hemicholinium could be relieved by temporary suspension of stimulation. These results suggest that the mode of action of hemicholinium at the neuromuscular junction is different from that of tubocurarine, and indicate that the action of hemicholinium is presynaptic, probably arising from a reduction in acetylcholine released by nerve stimulation.

Acetylcholine↗

THE PRESERVATION OF BRADYKININ BY PHENOTHIAZINES IN VITRO.

Chlorpromazine and phenoxybenzamine have been shown to potentiate the actions of bradykinin in vivo. To test whether this phenomenon could be due to inhibition of the enzymatic destruction of bradykinin, bradykinin was incubated with either tissue extracts or with carboxypeptidase B. Bradykinin was rapidly destroyed by acetonedried powders of brain and serum of various animals as well as by purified carboxypeptidase B. The rate of disappearance of bradykinin activity was decreased in the presence of phenothiazine derivatives, phenoxybenzamine and hydroxyzine, but not by compounds of a larger group including other psychotropic drugs, tranquillizers and ganglionic and adrenergic blocking agents. Spectrophotometric studies of the hydrolysis of hippuryl-L-arginine confirmed the presence of a carboxypeptidase B-like activity in brain. The substances that acted as inhibitors of bradykinin destruction were also enzyme inhibitors as measured by this technique. Previous incubation of carboxypeptidase B with phenothiazines and zinc ions greatly reduced the enzymatic inhibition by the phenothiazines, which indicated a possible chelating action by these inhibitors on the metalo-enzyme carboxypeptidase B.

Animals↗

Dual agonist-antagonist effects of 5-hydroxytryptamine (5-HT) in the guinea pig ileum: evidence for a selective receptor desensitization effect.

The application of 5-HT to strips of whole ileum or the longitudinal muscle-myenteric plexus preparation from guinea pigs caused dose-dependent muscle contractions that were followed by relaxation to baseline tension without washing off the drug (fade). The contractile effect of a subsequent addition of 5-HT, 4 min after a priming dose of 5-HT, was markedly reduced. Increasing priming doses of 5-HT caused proportional increases in the 5-HT Emax50, up to a priming dose that completely abolished the contractile effects caused by further additions of 5-HT. The auto-blockade of the 5-HT responses was selective to drugs acting on serotonergic receptors. 5-HT did not antagonize the effects of acetylcholine, dimethylphenylpiperazinium, nicotine, histamine, prostaglandin E2, substance P or angiotensin II. N-methyl-5-HT was the most potent analogue in mimicking the effects of 5-HT to produce auto-blockade and fade of the contractile responses. Other structural analogues of 5-HT that shared the 5-HT blocking effect were 5-methoxytryptamine, 5,6-dihydroxytryptamine, and N,N-dimethyltryptamine although these compounds were considerably less potent than 5-HT as blockers or as agonists. Results suggest that fade and the auto-blockade are part of a common effect and are discussed in relation to a model of drug-induced selective receptor desensitization.

Animals↗

INNERVATION OF THE LARGE INTESTINE OF THE TOAD (BUFO MARINUS).

The morphology, physiology and pharmacology of the innervation of the toad (Bufo marinus) large intestine have been studied. The large intestine can be divided into the regions colon, rectum and cloaca, on morphological grounds, but acts as a unit in response to nerve stimulation. Of the right and left nerves, each appears to supply the entire large intestine. Autonomic innervation of the large intestine of Bufo marinus is as follows: (1) The 9th and 10th spinal nerves (pelvic) contain predominantly excitatory preganglionic cholinergic fibres, but some inhibitory adrenergic fibres are also present in most preparations. (2) The splanchnic nerves contain inhibitory postganglionic adrenergic fibres from the 3rd to 5th sympathetic ganglia, and a small number of excitatory cholinergic fibres. The pathway of adrenergic inhibitory fibres to the large intestine alongside the posterior mesenteric artery as seen in mammals is rarely present in the toad. Several nonspecific actions of autonomic drugs on the large intestine are discussed. The functional organization of the autonomic innervation of the toad large intestine is similar to that in mammals, that is the large intestine is controlled by antagonistic cholinergic and adrenergic nerves. However, the separation of these two types of nerve fibres into anatomically distinct nerves does not appear to be as complete as in mammals. It is suggested that inhibitory autonomic control of the alimentary canal in vertebrates first appears in the hind-gut region.

Acetylcholine↗

The importance of brainstem cholinergic neurons in the pressor response to cocaine.

After intracisternal injection, 140 nmol (48 microg) of cocaine (but not lidocaine or procaine) evoked an increase in mean arterial pressure (MAP) of 41 mm Hg. The increase in MAP began within 1 min after injection and lasted 10 to 15 min. The pressor response to intracisternal injection of cocaine was not mediated through central alpha-adrenergic receptors, but intracisternal pretreatment with D1 or D2 dopamine receptor antagonists shortened the duration of the response. Pretreatment with intracisternal injection of hemicholinium-3 to deplete medullary acetylcholine produced a dose-dependent inhibition of the pressor and tachycardic responses to intracisternal injection of cocaine. Central pretreatment with hemicholinium-3 also inhibited the pressor response to intravenous injection of 0.5 mg/kg cocaine. Atropine pretreatment was only partly effective in blocking the pressor and tachycardic responses to intracisternal injection of cocaine. However, a single intracisternal injection of the nicotinic ganglionic receptor blocker hexamethonium inhibited the pressor response to cocaine administered intracisternally 24 h later, and on each of the following 4 days. The blocking effect of hexamethonium was not mimicked by the alpha7 selective antagonist methyllycaconitine or by the alpha4beta2 subtype-preferring antagonist dihydro-beta-erythroidine. The data suggest that the pressor response to cocaine is mediated by medullary acetylcholine release on to nicotinic receptors of the ganglionic type, enhancing the output of bulbospinal sympathetic premotor neurons. Our results provide new evidence for the prolonged inactivation of relevant central nicotinic receptors by nicotinic receptor antagonists, and suggest that such compounds might be used safely for cocaine overdose, as well as for antiabuse issues without the concern for autonomic side effects.

Anesthetics, Local↗