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PubMed1976

Effects of nicotinic and muscarinic compounds on biting attack in the cat.

Predatory-like biting attack on a rat, as well as hissing, growling, and other threat behaviors, could be induced in normally non-aggressive cats by systemic administration of the muscarinic agonist, arecoline (7-12 mg/kg). In contrast to arecoline, nicotine was found to suppress aggressive behaviors. Systemic administration of nicotine (0.5 mg/kg) prior to arecoline injection resulted in a significant reduction in elicited attack and threat behaviors. Furthermore, nicotine (0.075-0.500 mg/kg) was found to produce a dose-dependent suppression of natural predatory behavior as well. This nicotine-produced suppression of attack did not appear to be due to the induction of general malaise, since attack suppression could be seen in the absence of general behavioral inhibition, and doses of nicotine resulting in complete suppression of attack had little effect on food intake. Results indicate that muscarinic and nicotinic compounds can exert antagonistic control over some types of aggressive behaviors.

Aggression↗
PubMed1978

Pharmacological studies on 3-[gamma-(p-fluorobenzoyl)propyl]-2,3,4,4a,5,6-hexahydro-1-(H)-pyrazino (1,2-a) quinoline (compound 69/183). Part I: Hypotensive activity.

3-[gamma-(p-Fluorobenzoyl)propyl]-2,3,4,4a,5,6-hexahydro-1-(H)-pyrazinol(1,2-a)quinoline (compound 69/183, centpyraquin) has been found to possess promising hypotensive activity in anaesthetised cat, dog and monkey- It also lowers the blood pressure of unanaesthetised cat, dog and hypertensive rat. The effective doses are between 0.5 to 2.0 mg/kg in all the species except rat, in which doses of 10.0 and 20.0 mg/kg are effective. The compound potentiates epinephrine and norepinephrine pressor responses but inhibits carotid occlusion, tyramine and DMPP induced pressor responses. The contraction of the nictitating membrane due to pre- as well as post-ganglionic sympathetic nerve stimulation is blocked equally. In mice the compound produces ptosis which is antagonised by N-benzyl-N-methylguanidine. Localisation of the compound either to the superior cervical ganglion of cat or to the central cardiovascular loci has no effect on the activities of either of them. No evidence of an initial catecholamine release by the compound could be obtained. It has weak smooth muscle relaxant activity. The mechanism of hypotensive action seems to be the blockade of adrenergic neurones along with direct smooth muscle relaxation.

Adrenal Glands↗
PubMed1979

Haemodynamic effects of the quaternary ammonium compound QX 572 in anaesthetized cats. II. Studies on the mechanism for the cardiac chronotropic effects.

The antiarrhythmic compound, QX 572, has been shown to increase heart rate both in patients and experimental animals. In anaesthetized cats the positive cardiac chronotropic effects were mainly due to increased sympathetic activity. The present experiments were designed to localize the active sites within the sympathetic nerve system. It was found that QX 572 caused an increased heart rate in response to electrical stimulation of the cardiac sympathetic nerves, but this was not due to effects on the CNS, the sympathetic ganglia or the cardiac adrenergic beta-receptors. It is concluded that QX 572 by some action increased the amount of noradrenaline released from the cardiac sympathetic nerve endings. The mechanism for this effect has not been clarified.

Adrenalectomy↗
PubMed1977

Possibilities for a cholinergic action on smooth musculature and on sympathetic axons in brain vessels mediated by muscarinic and nicotinic receptors.

A pharmacological identification and characterization of cholinergic receptors was carried out in pial arteries of cats. In one series of experiments, the middle cerebral artery was suspended in an organ bath for recording fo circular motor activity. Parasympathomimetic compounds produced either a relaxation or a contraction. The relaxation occurred at low doses (up to 10(-6) M), and the response was inhibited in a competitive manner by atropine. The mean KB value (determined with acetylcholine as agonist) was 3.85 X 10(-11) M, and the corresponding pA2 value 10.43. At higher doses, the parasympathomimetics produced a contraction. This effect, too, was inhibited in a competitive manner with atropine. The calculated mean KB value with acetylcholine as agonist was 1.12 X 10(-11) M, and pA2 was 10.07. The motor responses did not require an intact perivascular sympathetic innervation, which shows that the effects were mediated by muscarinic type of cholinergic receptors present in the smooth musculature. In another series of experiments, pial arteries were preincubated in the presence of 3H-norepinephrine, and the amount of tritium efflux was measured in a superfusion system before or during electrical field stimulation (12 V, 1 msec pulse duration, 10 Hz). The efflux was minimized by sympathetic denervation, and the effect of transmural stimulation abolished by bretylium and guanethidine, which shows that the bulk of tritium overflow during stimulation originated from the perivascular sympathetic nerves. The marked elevation of tritium efflux during stimulation was enhanced by hexamethonium, and it was inhibited by nicotine and acetylcholine, whose effects were counteracted by hexamethonium (but not by atropine). This finding indicates the presence of nicotinic type of cholinergic receptors on the perivascular adrenergic nerves, allowing inhibition of norepinephrine by acetylcholine that may be liberated from the adjacent cholinergic terminals in the autonomic nerve plexus.

Acetylcholine↗
PubMed1976

Interaction of hexafluorenium with human plasma cholinesterase in comparison with hexamethonium.

1. The influence of the 2 alkane-bis-onium compounds hexafluorenium (HF1) and hexamethonium (C6) on human plasma cholinesterase (ChE) was studied with respect to the type of inhibition. 2. HF1 and C6 are reversible inhibitors of ChE. The inhibitory potency of HF1 (pI50 = 6.96; Ki = 2.4 x 10(-9)) is about 40 000-fold higher than that of C6 (pI50 = 2.4; Ki = 6.7 x 10(-2)). 3. The kinetic analysis displayed a competitive (C6) and a non-competitive (hf1) mechanism of action. 4. The inhibition of ChE by C6 is induced by a binding of C6 to the anionic site of the active center thus impairing the primary formation of the enzyme-substrate complex. HF1, however, is most probably bound to anionic side receptors in the vicinity of the active center; by that a conformational change of the enzyme protein is induced impairing the acylation step of the esteratic site.

Binding Sites↗
PubMed1979

Similarities in effects of acetylcholine and dopamine on horizontal cells in the fish retina.

The effect of acetylcholine (ACh) on cone- and rod-connected horizontal cells (generating photopic and scotopic L-type S-potentials, respectively) in the fish (Eugerres plumieri) retina was compared with that of dopamine (DA), and some similarities were found in the effects. About two-thirds of the L-type horizontal cells examined were sensitive to a test solution containing ACh (10 mM in concentration) and BW-anticholinesterase (BW; 1.0 mM). ACh with BW augmented a center response and attenuated a surround response as did DA (0.2 mM), although the latter effect was more pronounced and longer-lasting. ACh with BW frequently produced oscillations of the horizontal cell membrane potential, as did DA with clonidine (alpha-adrenergic stimulant). Phentolamine (alpha-adrenergic blocker) interrupted both the effects of DA and ACh on the center and surround responses, while hexamethonium (cholinergic antagonist) appeared to interfere selectively with the effect of ACh. Therefore, the ACh-induced changes observed in the horizontal cell membrane potential are assumed to be mediated by the adrenergic system in the fish retina.

Acetylcholine↗
PubMed1979

Comparison of the cardiostimulatory effects of acetylcholine and nicotine on the working guinea-pig heart.

The isolated working guinea-pig heart was used to compare the cardiostimulatory effects of acetylcholine and nicotine observed in the presence of atropine. Both agonists increased aortic pressure, left ventricular pressure, left ventricular dP/dt, cardiac output, and ventricular cyclic AMP levels. These responses were qualitatively and quantitatively similar to the effects of exogenous norepinephrine. Hexamethonium treatment abolished the responses to acetylcholine and to nicotine. However, several differences in the responses of the two agonists were also observed with respect to: 1) the effect of propranolol pretreatment, 2) selective effects on coronary and aortic flow rates, 3) coefficients of correlation between ventricular cyclic AMP and changes in dP/dt, and 4) the "autoinhibition" effect. The results support the view that the cardiostimulatory effects of acetylcholine are due entirely to endogenous catecholamine release, but that the effects of nicotine may involve an additional action.

Acetylcholine↗
PubMed1975

Studies on the mechanism of the action of morphine on the peristalsis of guinea pig ileum in situ.

The influence of some drugs on the effect of morphine on the threshold pressure required to elicit peristalsis in the guinea pig ileum in situ was studied, in order to test the hypothesis that this effect of morphine is mediated by catecholamine release. Tachyphylaxis to this effect of morphine was confirmed. Pretreatemnt with two 8 mg/kg doses of reserpine, 24 and 48 hrs before the experiment, significantly reduced the effect of morphine on the pressure threshold. The i.v. administration of 10 mg/kg dl-Dopa re-established the effect of morphine in reserpinized animals to the level of the untreated controls. Pretreatment with guanethidine (15 mg/kg) decreased and even prevented this effect of morphine. Phentolamine pretreatment (10 mg/kg) also significantly inhibited the effect of morphine. Neither DCI nor propranolol influenced this morphine effect. Pretreatment with reserpine, guanethidine or phentolamine reduced the basic pressure threshold needed to elicit peristalsis. The possibility that the decrease of local circulation induced by hypotenison would reduce the local concentration of morphine was rejected because the same doses of guanethidine or phentolamine did not modify the effect of hexamethonium given i.v. in this preparation. All these results support the idea that the effect of morphine on intestinal peristalsis is mediated by a catecholamine acting on alpha-receptors, e.g. norepinephrine.

Animals↗
PubMed1976

Hypothalamic superfusion with muscarinic drugs: their effects on pressor responses to hypothalamic stimulation.

The posterior hypothalamus of cats anaesthetized with pentobarbital sodium was superfused with artificial cerebrospinal fluid through a push-pull cannula and electrically stimulated with the noninsulated tip of the cannula. The effects of muscarinic drugs on the pressor response to stimulation of the hypothalamus were investigated. Superfusion with muscarine, oxotremorine or N-benzyl-3-pyrrolidyl acetate methobromide (AHR 602) decreased the pressor responses to hypothalamic stimulation. Superfusion with methylatropine did not influence the pressor responses to hypothalamic stimulation; however, superfusion with methylatropine 60 min prior to and during superfusion with the muscarinic drugs abolished the inhibitory effects of muscarine and oxotremorine and temporarily reversed that of AHR 602 on the pressor responses. Superfusion of the posterior hypothalamus with arecoline enhanced the rise of blood pressure elicited by hypothalamic stimulation. When the hypothalamus was superfused with hexamethonium 60 min prior to and during superfusion with arecoline, arecoline reduced the pressor responses to electrical stimulation of the hypothalamus. Superfusion with methylatropine prior to and together with an ineffective concentration of arecoline increased the rise of blood pressure elicited by hypothalamic stimulation. From the drugs studied here only oxotremorine caused a fall of the "resting" arterial blood pressure; it was abolished by the intravenous injection of methylatropine. From these results it was concluded that superfusion of the posterior hypothalamus with muscarinic drugs impairs the pressor responses to hypothalamic stimulation. Drugs possessing both nicotinic and muscarinic properties either enhance or diminish the pressor responses according to their relative potencies on the two types of receptor.

Alkaloids↗