The Effects of Drugs on the Release of Vasopressin

Dyball, R. E. J.

doi:10.1111/j.1476-5381.1968.tb00994.x

Cited by 20 publications

(7 citation statements)

References 26 publications

(30 reference statements)

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“…phentolamine, reduced central angiotensin pressor activity approximately 33% [14]. Phenoxy benzamine, however, can partially inhibit vasopressin release [1] in addi tion to blocking a-adrenergic receptors. The observation that IVT phentol-amine essentially abolishes central angiotensin pressor activity suggests an adrenergic link in both the vasopressin-releasing and sympathetic path ways influenced by IVT angiotensin.…”

Section: Discussionmentioning

confidence: 99%

Influence of Adrenergic Blocking Drugs on Central Angiotensin Effects

Severs¹,

Summy-Long²,

Daniels-Severs³

et al. 1971

Pharmacology

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The central effects of angiotensin in unanes thetized rats were studied before and after administration of adrenergic blocking drugs. Intraventricular injections of prevented angiotensin-induced drinking, sympathetic stimulation, and vasopressin release. Administration Phentolamine of various β-adrenergic blocking drugs, either intraarterially or intraventricularly, did not alter central angiotensin activity in a manner which could be correlated with β-adrenergic blockade. Local anesthetics inhibited central angiotensin pressor and drinking effects. Centrally administered phentolamine or tetracaine appear to be useful tools for further studies of the actions of angiotensin on the central nervous system.

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Section: Discussionmentioning

confidence: 99%

Influence of Adrenergic Blocking Drugs on Central Angiotensin Effects

Severs¹,

Summy-Long²,

Daniels-Severs³

et al. 1971

Pharmacology

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“…Unlike TFP, Prometh does not have antipsychotic activity and does not inhibit vasopressin release (Dyball et al, 1968) (a hormone whose circulating levels are increased by nicotine administration, Seyler et al, 1986 (Connelly & Littleton, 1983;Takano et al, 1983;Schulz & Zigmond, 1989;Rapier et al, 1990;Brazell et al, 1990). It therefore seems possible that TFP could block presynaptic nicotinic ACh receptors and diminish their contribution to dopamine release.…”

Section: Sensitivity Of Neuronal Acetylcholine Receptors To Psychoactmentioning

confidence: 99%

α4‐β2 and other nicotinic acetylcholine receptor subtypes as targets of psychoactive and addictive drugs

Connolly

Boulter

Heinemann

1992

British J Pharmacology

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1 Xenopus oocytes were injected with various muscle and neuronal nicotinic acetylcholine receptor (ACh receptor, cholinoceptor) subunit RNA combinations and their pharmacological properties studied using two-electrode voltage clamp. The functional expression of one of these combinations, rat a4-2fi2, has not been previously described. The a4-2 mRNA is a splicing variant transcribed from the a4 gene. In the experiments reported here, the a4-2#2 subtype was functionally indistinguishable from the a4-1#2 subtype.2 For each subtype, the relative potency of nicotine compared with acetylcholine was obtained by estimating the relative concentration of nicotine which would elicit the same current response as 0.1JIM ACh. The ratios of these concentrations (nicotine: ACh) for the mouse muscle ACh receptor-(alily6) was 96.1:1. In contrast, the ratios for the rat neuronal subtypes were: a2fi2, 1.01:1; a3fi2, 2.01:1; a4f2, 0.76:1 and a4-2#2, 0.76:1. The much greater relative nicotine sensitivity of the neuronal subtypes as compared with muscle receptors illustrates their potential to mediate the psychoactive and addictive effects of nicotine. However, it does not appear that the differences in relative nicotinic sensitivity among the neuronal receptors themselves can be used as a simple discriminative tool in neuronal tissue. 3 The slopes of the log dose-log response curves at low ACh concentrations were all greater than 1 but less than 2, suggesting that at least two agonist binding sites mediate the functional response of each hetero-oligomer. 4 The response of all the neuronal subtypes to ACh could be inhibited by the psychoactive drugs mecamylamine, amitriptyline, phencyclidine, trifluoperazine and promethazine. With the exception of the very potent antagonist, mecamylamine, the degree of block of the peak current to ACh produced by 10pM concentrations of these drugs was remarkably similar (around 50%). 5 The degree of inhibition produced when the antipsychotic drug, trifluoperazine, was co-applied with ACh increased as the duration of application increased. Such an effect was not observed with promethazine, a related phenothiazine derivative which does not have antipsychotic actions.

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“…The dissociation in the levels of oxytocin and vasopressin observed in different experiments (as after intravenous administration of nico¬ tine) suggests that under certain conditions these hormones may be released independently from the neurohypophysis (Caldeyro-Barcia & Heller, 1961). The situation is complicated by the fact that adrenaline, which is secreted as a response to the stimulation of the nicotine injection, produces some degree of inhibition of vasopressin release (Dyball, 1968).…”

Section: Methodsmentioning

confidence: 99%

Effect of Nicotine on the Motility of the Oviducts in the Rhesus Monkey: A Preliminary Report

Neri¹,

Marcus²

1972

Reproduction

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Summary. Tubal activity under the influence of nicotine was studied in vivo in six mature rhesus monkeys throughout the various phases of the menstrual cycle, using an open-ended catheter technique. The activity monitoring response during the first half of the menstrual cycle was of two types, an early and a delayed response. The first was of higher tone and amplitude, and the second was followed within 1 to 2 min by complete inhibition of tubal activity which lasted for the next 5 to 30 min. During the second half of the menstrual cycle, intravenous nicotine had no significant effect on tubal tonus and the amplitude was only slightly and occasionally affected. The possible mechanism of action of nicotine, both direct and indirect, on tubal activity is discussed.

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The Effects of Drugs on the Release of Vasopressin

Cited by 20 publications

References 26 publications

Influence of Adrenergic Blocking Drugs on Central Angiotensin Effects

Influence of Adrenergic Blocking Drugs on Central Angiotensin Effects

α4‐β2 and other nicotinic acetylcholine receptor subtypes as targets of psychoactive and addictive drugs

Effect of Nicotine on the Motility of the Oviducts in the Rhesus Monkey: A Preliminary Report

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