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PubMed1975

Control of peripheral vascular resistance in perfused hindquarters of dogs: lack of effect of nicotinic and muscarinic ganglion block.

The effects of nicotinic and muscarinic ganglion blockade were studied on the peripheral resistance of the perfused hindlimbs of the dog. Nicotinic ganglion blockade by chlorisondamine (1 mg/kg) significantly reduced reflex vasomotor responses but did not significantly alter hindlimb peripheral resistance. Combined nicotinic ganglion blockade by chlorisondamine (1 mg/kg) and muscarinic ganglion blockade by atropine (50mug/kg) abolished the reflex vasomotor response but did not alter hindlimb peripheral resistance. It was concluded that autoregulatory mechanisms are capable of maintaining a peripheral resistance after block of both muscarinic and nicotinic ganglion transmission.

Animals↗
PubMed1975

Effects of hexamethonium and other ganglionic blocking agents on electrical activity of the esophagus induced by vagal stimulation in the dog.

Electrical activity of the dog's esophagus was evoked by electrical stimulation of the vagus nerve and recorded by using a suction electrode placed on the serosal surface of the esophagus. Neuromuscular blocking agents (d-tubocurarine and succinylcholine) blocked this activity, while atropine had no effect. Hexamethonium (in doses which did not effect neuromuscular transmission in the diaphragm) and high doses of nicotine significantly depressed the evoked esophageal electrical activity, while lower doses of nicotine facilitated the response. The results suggest that a certain proportion of the striated muscle of the esophagus is innervated by processes from the intermediate ganglion cells in the Auerbach plexus.

Adrenergic alpha-Antagonists↗
PubMed1976

Studies on the mechanism of the cardiovascualr effects of methyldopa.

Oral administration of methyldopa (100 mg/kg, twice daily for 3 days) to mongrel dogs produced a significant decrease in blood pressure and heart rate. The drug treatment affected neither the resting venous tone nor the cardiac output. Thus, the hypotensive effect of the drug was predominantly due to a reduction in total peripheral resistance. Vasoconstrictor responses of the renal vasculature to sympathetic nerve stimulation were significantly impaired after methyldopa at all the frequencies, while mesenteric vasoconstrictor responses to sympathetic nerve stimulation were impaired only at the lower stimulation frequencies. In addition, methylnorepinephrine was a significantly less potent vasoconstrictor than norepinephrine in the renal vasculature, but was equipotent to norepinephrine in the mesentery. The finding of a reduction in the renal vascular resistance of methyldopa-treated dogs, with no such alteration in the mesenteric vascular resistance, is consistent with the nerve stimulation studies. Therefore, the results of the present investigation indicate that in addition to the existing evidence favoring a central site of action for methyldopa, the impairment of peripheral sympathetic neuronal function is also of importance in accounting for the hemodynamic alterations observed following treatment with methyldopa.

Animals↗
PubMed1978

Cardiovascular responses to intraventricular adrenaline in spontaneous hypertensive rats.

The effects of intracerebroventricular (i.c.v.) injections of adrenaline on the blood pressure and heart rate of spontaneous hypertensive (SH) rats have been investigated. Adrenaline induced dose-related falls in blood pressure and heart rate in both conscious and urethane anaesthetised rats. In conscious rats, the hypotension and metoprolol, but were unaffected by pretreatment with phentolamine, piperoxan, fluphenazine or methysergide. However, in urethane-anaesthetised rats, the hypotension and bradycardia induced by i.c.v. adrenaline was not significantly affected by i.c.v. pretreatment with propranolol or oxprenolol, while metoprolol significantly antagonised only the bradycardia. Piperoxan, fluphenazine and methysergide were also without effect. Pretreatment with mecamylamine (i.p.) abolished the cardiovascular depressor effects of i.c.v. adrenaline in both conscious and urethane anaesthetised SH rats. It is concluded that the cardiovascular depressor effects of i.c.v. adrenaline are mediated by central adrenoceptors in SH rats and that, in conscious rats, these depressor effects may be mediated by central beta-adrenoceptors rather than alpha-adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1978

The action of CNS drugs on an isolated sympathetic nerve preparation of rabbit.

The effect of some centrally active drugs on the transmission of nerve impulses through the isolated cervical sympathetic nerve and superior cervical ganglion of the rabbit has been studied by recording both preganglionic and ganglionic responses to single square wave stimuli. Chlorpromazine, trifluoperazine and haloperidol have a greater axonal depressant action than the known local anaesthetics procaine and xylocaine. Chlordiazepoxide and diazepam are similar in local anaesthetic potency to procaine while meprobamate and sodium pentobarbitone possess only slight axonal depressant properties. Meprobamate, sodium pentobarbitone and possibly diazepam have ganglion blocking properties while procaine, chlorpromazine, trifluoperazine, haloperidol and chlordiazepoxide reduce the ganglion potential by virtue of their preganglionic action.

Action Potentials↗
PubMed1978

Plasma cyclic GMP: response to cholinergic agents.

S.c. injections of cholinergic agents, carbachol, methacholine and bethanechol, into fasted rats caused rapid increases in the plasma concentration of cyclic GMP, with a sharp peak at 5--10 min after the injection. Acetylcholine gave rise to a rapid accumulation of cyclic GMP in plasma only when administered together with physostigmine which produced only a slight, if any, potentiation of the action of the cholinesterase-resistant choline esters. Cyclic AMP also increased after these drugs, but only subsequently to the rise of cyclic GMP; the primary action of the cholinergic drugs appeared to be the increase in cyclic GMP. Atropine was effective not only in abolishing the increase in plasma cyclic GMP induced by cholinergic drugs but also in lowering the baseline level of cyclic GMP. It was concluded that the plasma concentration of cyclic GMP could serve as a good parameter of cholinergic activity in rats.

Acetylcholine↗
PubMed1979

Ganglion blocking properties of some bispyridinium soman antagonists.

Various doses of several bispyridinium compounds (HS-6, HI-6, HGG-12, HGG-42, and SAD-128) known to protect animals against the irreversible cholinesterase inhibitor soman were examined to determine their effects on the cardiovascular and respiratory system of cats. Although the potency varied considerably all of the compounds tested lowered the blood pressure, which appeared to be the result of ganglion blocking properties as determined by their reduction of the pressor response to dimethylphenylpiperazinium and the blockage of the contraction of the preganglionically stimulated cat nictitating membrane. Some of the compounds caused cessation of respiration at much lower doses than others but did so at doses greater than those causing ganglion blockage.

Animals↗
PubMed1981

Plasma catecholamines in rats exposed to cold: effects of ganglionic and adrenoreceptor blockade.

Exposure to cold (4 degrees C) of catheterized rats acclimated to 20 degrees C resulted in a progressive increase in plasma noradrenaline (NA) concentrations which reached values consistently more than twice the basal ones (20 degrees C) by about 30 min. No further increase in plasma NA levels were detected when the cold exposure was continued for 24 h. Plasma adrenaline (A) and dopamine levels did not change at any time studied. Adrenalectomized rats exposed to cold exhibited percent rises in plasma NA similar to those in intact rats. An increase in plasma A levels concomitant with that of NA was observed following exposure to cold of rats in which either basal catecholamine release was impaired by chlorisondamine or the vasoconstrictor response was impeded by phentolamine. Propranolol did not modify the acute neurosympathetic response to cold. Exposure to cold (4 degrees C) for short periods of time combined with the measurement of plasma catecholamines is proposed as a useful and reproducible method for studying a pure neurosympathetic response in the rat.

Adrenalectomy↗
PubMed1983

Use of a sympathetic-cholinergic system in the analysis of sympatho-inhibition produced by clonidine and some congeneric derivatives of clonidine.

The effects of clonidine and five analogs of clonidine were tested with regard to their ability to depress centrally and peripherally evoked electrodermal responses (EDR) in control cats, as well as in animals pretreated with yohimbine hydrochloride. With the exception of St-91, all of the clonidine-like substances selectively reduced the amplitude of centrally (hypothalamic) evoked responses in a dose-dependent fashion. Clonidine was found to have no significant inhibitory effect at the level of the sympathetic ganglion. The order of central nervous system sympatho-inhibitory potency of these compounds was clonidine (St-155) greater than St-375 greater than St-606 greater than St-600 greater than St-608 much much greater than St-91. Prior treatment with yohimbine hydrochloride (0.5 mg/kg i.v.) antagonized the depressant effect of all of these drugs. These results indicate that clonidine and the clonidine congeners tested (with the exception of St-91) all produce sympatho-inhibition by an action on a CNS alpha-adrenergic mechanism and demonstrate the usefulness of this electrodermal model system for the analysis of drugs affecting central sympathetic reactivity.

Animals↗
PubMed1984

Potentiation of colonic contractility to cholecystokinin and other peptides.

Changes in colonic contractility were studied in anesthetized cats following the intravenous injection of several peptides. Increases in contractile activity were observed after the octapeptide of cholecystokinin (CCK-8), pentagastrin, substance P or neurotensin. On the other hand, vasoactive intestinal peptide (VIP) caused an inhibition which, in some cases, was followed by an excitatory response. The responses produced by pentagastrin, substance P or neurotensin, but not by CCK-8, were partially inhibited by atropine. Following bethanechol pretreatment, the stimulation in contractile activity elicited by CCK-8, substance P, neurotensin or pentagastrin was markedly enhanced. Responses were also increased by pretreatment with eserine, hexamethonium or mecamylamine. This potentiation was blocked by atropine. It is concluded that, following treatments which cause an increase in the level of cholinergic input to the colon, an exaggerated motor response to some peptides can develop.

Animals↗
PubMed1986

Antagonism of the emetic action of xylazine by alpha-adrenoceptor blocking agents.

The intramuscular injection of xylazine (2 mg/kg) evoked vomiting in 81% of the dogs studied. Adrenoceptor antagonists showing alpha 2-blocking activity, yohimbine, tolazoline and phentolamine, antagonized the xylazine-induced vomiting in a dose-dependent manner. Of these antagonists, yohimbine was the most effective, since the maximal antagonistic effect was seen at 0.5 mg/kg yohimbine, a dose at which the other drugs had less or no effect. The adrenoceptor antagonists showing alpha 1-blocking activity, prazosin and phenoxybenzamine, at the doses studied did not prevent the emesis induced by xylazine. A beta-adrenoceptor antagonists, propranolol, was ineffective in reducing xylazine-induced vomiting. The dopamine receptor antagonists, metoclopramide and domperidone, did not prevent xylazine-induced vomiting nor did yohimbine antagonize apomorphine-induced vomiting. The xylazine-induced vomiting was not prevented by atropine, naloxone or hexamethonium. These results indicate that the xylazine-induced vomiting is mediated by alpha 2-adrenoceptors and does not appear to involve beta-adrenoceptors, cholinoceptors, dopamine or opiate receptors in the emetic pathway.

Adrenergic alpha-Antagonists↗
PubMed1988

Adrenergic-induced hyperglycemia in anaesthetized rats: involvement of peripheral alpha 2-adrenoceptors.

The selective alpha 2-adrenoceptor agonist, UK 14.304, induces a time- and dose-dependent hyperglycemic response in the anaesthetized rat. This hyperglycemia seems to be mediated through the pancreas because lesions of the pancreatic beta-cells induced with streptozotocin completely abolished this hyperglycemic response to UK 14.304 while ganglionic blockade by chlorisondamine did not affect the response. The non-selective agonist, adrenaline, induces a similar hyperglycemic response which is antagonized selectivity by the alpha 2-adrenoceptor antagonist, idazoxan. Combined alpha 1- and beta-adrenoceptor blockade resulted in an increase in the alpha 2-adrenoceptor-mediated hyperglycemic response to adrenaline. Since adrenaline is known not to cross the blood-brain barrier it is concluded that alpha 2-adrenoceptor stimulation induces hyperglycemic responses through a peripheral effect that involves postsynaptic alpha 2-adrenoceptors in the pancreatic beta-cell which are linked to the inhibition of insulin release.

Anesthesia↗