Doris Nutto

Effect of transection of subfornical organ efferent projections on vasopressin release induced by angiotensin or isoprenaline in the rat.

Transection of subfornical organ efferents in the rat prevented the vasopressin release in response to intravenous angiotensin II infusion or following a small dose of the beta-sympathomimetic amine isoprenaline (30 micrograms/kg i.m.). In contrast, this lesion had no effect on vasopressin release after hypertonic saline injection or a high dose of isoprenaline (480 micrograms/kg i.m.). We conclude that blood-borne angiotensin II induces vasopressin release by acting on the subfornical organ; depending on the dose of isoprenaline, activation of the endogenous renin-angiotensin system may mediate isoprenaline-induced vasopressin release.

Evidence for Inhibition by β-Endorphin of Vasopressin Release during Foot Shock-Induced Stress in the Rat

This study was to ascertain the effect of naloxone and dexamethasone on vasopressin and beta-endorphin release in the rat during inescapable electric foot shock stress. Plasma vasopressin concentrations were not affected by electric foot shock in vehicle-treated rats, but were raised significantly by the stress in animals pretreated with naloxone. The stress-induced increase in plasma beta-endorphin-like immunoreactivity (beta-EI) was similar whether the rats had received naloxone or not. Plasma beta-EI consisted of equal amounts of beta-endorphin-like and beta-lipotropin-like material as revealed by gel filtration. Dexamethasone almost abolished the foot shock-induced increase in plasma beta-EI and, in the presence of dexamethasone, stress was now effective in elevating plasma vasopressin concentrations. These results are consistent with the hypothesis that beta-endorphin, released from the anterior pituitary, inhibits the release of vasopressin from the posterior lobe of the pituitary gland during foot shock-induced stress.

Stimulation of Adrenocorticotropin/β-Endorphin Release by Synthetic Ovine Corticotropin-Releasing Factor in vitro

Vasopressin analogs, which markedly differed in the ratio of pressor versus antidiuretic activity and also in ACTH/β-endorphin-releasing activity, were used in the present study. The ability of vasopr

Vasopressin and β-endorphin release after osmotic and non-osmotic stimuli: effect of naloxone and dexamethasone

The purpose of this study was to determine whether or not vasopressin release in response to various stimuli in the conscious rat is controlled by endogenous opioid peptides, in particular beta-endorphin. Naloxone (1 mg.kg-1 i.m.) promoted vasopressin release in response to both an angiotensin II infusion (500 ng . kg-1 . min-1) or an isosmolar, nonhypotensive hypovolaemia achieved by polyethylene glycol injection (PEG, 20% solution i.p.); however, naloxone was without effect when vasopressin release was induced by hypertonic saline injection (2.5% solution i.p.) or a severe fall in arterial blood pressure following trimethidinium (10 mg . kg-1 i.m.) induced ganglionic blockade. Vasopressin release was accompanied by an increase in plasma beta-endorphin-like immunoreactivity (beta-EI) following an angiotensin II infusion of PEG administration, but not after hypertonic saline or trimethidinium injection. Dexamethasone pretreatment (0.5 mg . kg-1 twice i.p.) prevented the increase in plasma beta-EI following an angiotensin II infusion or PEG administration. The simultaneous angiotensin II- or PEG-induced increase in vasopressin release was unaffected or potentiated, respectively, by the glucocorticoid. In contrast, vasopressin release in response to hypertonic saline or trimethidinium injection was significantly inhibited by dexamethasone. We conclude that an inhibitory control by endogenous opiates is involved in some, but not all of the different pathways leading to vasopressin release. The results obtained do not prove but can be reconciled with the proposal that hypophyseal beta-endorphin is the compound responsible.

Vasopressin stimulates release of ?-lipotropin and ?-endorphin in conscious rats as measured by radioimmunoassay of unextracted plasma

SummaryUsing a newly developed radioimmunoassay to determine the β-endorphin-like immunoreactivity (β-EI) in unextracted plasma, the effect of vasopressin injections on plasma β-EI was investigated in conscious rats. Arginine vasopressin caused a dose-dependent increase of plasma β-EI from 34.5±7.8 fmol ml−1 (n=6) in vehicle-treated animals to 205.0±36.1 fmol ml−1 (n=7) after injection of the highest vasopressin dose employed (486 ng/100 g b.w.). In view of the appreciable cross-reactivity of β-lipotropin (β-LPH) in the radioimmunoassay used, plasma was extracted and subjected to gel chromatography on a Sephadex G-50 column. On average, about 70% of the β-EI co-eluted with human β-LPH and about 30% with human β-endorphin in plasma extracts obtained from both control and vasopressin-treated rats. No peripheral conversion of human β-LPH occurred under the experimental conditions, since after i.v. bolus injection of human β-LPH 97% of the β-EI comigrated with human β-LPH during gel filtration. A similar blood pressure increase to that induced by the vasopressin injections, when elicited by noradrenaline or angiotensin II i.v., was not followed by an elevation of plasma β-EI.These data indicate that vasopressin stimulates β-lipotropin and β-endorphin release into the systemic circulation in vivo.

Evidence for the involvement of a GABA-mediated inhibition in the hypovolaemia-induced vasopressin release

The influence of GABA and of drugs, known to alter GABA-metabolism, on the hypovolaemia-provoked vasopressin release was investigated in rats. Blood volume was decreased without altering plasma osmolality or arterial blood pressure by i.p. injection of polyethylene glycol and the resulting plasma vasopressin concentration was measured using a radioimmunoassay. I.c.v. injections of GABA (0.4–2 mg) markedly suppressed the hypovolaemia-induced vasopressin release. The central inhibitory effect of GABA could not be related to appropriate changes in peripheral parameters believed to regulate vasopressin release (arterial blood pressure, renin-angiotensin system). Aminooxyacetic acid (9–81 mg kg−1, i.m.) and gamma-vinyl-GABA (1.5 g kg−1, i.p.), two potent inhibitors of GABA aminotransferase and known to increase brain GABA content, reduced vasopressin release to a comparable as did GABA (i.c.v.). On the other hand, 3-mercaptopropionic acid (10–90 mg kg−1, i.p.), an inhibitor of the GABA synthetizing enzyme glutamic acid decarboxylase, promoted the release of vasopressin when the rats were killed prior to the onset of convulsions. These results, on the whole, intimate the existence of a GABA-mediated inhibition in the central control of vasopressin release.

Cholecystokinin releases β-endorphin from the anterior pituitary gland

Abstract The effect of cholecystokinin on the release of β-endorphin immunoreactivity from anterior pituitary quarters and from cultures of dispersed anterior pituitary quarters was investigated. Cholecystokinin (> 10 −7 M) caused a slight release of β-endorphin immunoreactivity from the pituitary quarters only. It is concluded that the direct effect of cholecystokinin on the anterior pituitary is not likely to have a functional significance in the release of β-endorphin and the co-secreted ACTH.

Evidence that vasopressin is involved in the isophrenaline-induced β-Endorphin release

Abstract We investigated in conscious rats, whether vasopressin, whose release was stimulted by isoprenaline (i.m.), caused the stimultaneous increase in plasma β-endrophin-like immunoreactivity (β-EI). The increase in plasma β-EI following isoprenaline administration was diminished by about 50% in rats pretreated with a vasopressin antagonist and also in rats with a hereditary absolute lack of vasopressin. We conclude that the isoprenaline-induced release of β-EI is mediated in part by vasopressin.

β-Endorphin controls vasopressin release during foot shock-induced stress in the rat

This study tested the possibility that beta-endorphin is involved in the regulation of vasopressin release during stress induced by inescapable electric foot shock. To this end, a specific anti-beta-endorphin antiserum or a control serum lacking the specific anti-beta-endorphin antibodies was administered to male rats. Plasma vasopressin concentrations, measured by radioimmunoassay, were not affected by brief foot shock stress in control rats, but were raised significantly by the stress in animals which had received an intracerebroventricular (i.c.v.) injection of the anti-beta-endorphin antiserum. In contrast, when the same volume of the anti-beta-endorphin antiserum was injected into a tail vein, foot shock stress produced only a slight effect on vasopressin release. I.c.v. injection of the antiserum changed neither basal nociceptive threshold nor stress-induced analgesia as revealed by the tail-flick latency. Vasopressin release induced by an osmotic stimulus was not influenced by the anti-beta-endorphin antiserum given i.c.v. The opiate antagonist naloxone or the glucocorticoid dexamethasone raised plasma vasopressin concentration in stressed rats which had received the control serum (i.c.v.); however, after i.c.v. injection of the anti-beta-endorphin antiserum neither naloxone nor dexamethasone elevated the plasma vasopressin concentration beyond the level reached by the anti-beta-endorphin antiserum (i.c.v.) alone. These results suggest that beta-endorphin inhibits the release of vasopressin during foot shock-induced stress in the rat.

The effect of isoprenaline on plasma concentrations of immunoreactive β-endorphin and β-lipotropin in the conscious rat

SummaryThe effect of the β-adrenoceptor agonist isoprenaline on the plasma concentrations of β-endorphin (β-E) and β-lipotropin (β-LPH) was investigated in conscious rats. Isoprenaline (i.m.) elevated plasma β-endorphin-like immunoreactivity (β-EI) as measured by radioimmunoassay of unextracted plasma, with peak values 24 min after drug administration. This effect was dose-dependent. The lowest effective dose of isoprenaline was 15 μg kg−1; 240 μg kg−1 exerted a maximum effect, raising plasma β-EI about ten-fold above control values. Plasma vasopressin concentrations also increased in response to isoprenaline following a timecourse identical to that of plasma β-EI. (±)-Propranolol (1 mg kg−1) but not phentolamine (10 mg kg−1) rendered isoprenaline (240 μg kg−1) injections almost ineffective. Because of the cross-reactivity of β-LPH in the radioimmunoassay used, plasma was extracted by means of a cation exchange resin and subjected to gel chromatography on a Sephadex G-50 column, avoiding artefactual degradation of the peptides. In isoprenaline-treated rats about 50% of the β-EI behaved similar to human β-LPH, whereas 45% co-migrated with human β-E; immunoreactivity corresponding to β-LPH or β-E comprised about 70% or 30%, respectively, in the plasma extract of vehicle-treated rats. Dexamethasone pretreatment reduced the isoprenaline-induced increase in plasma β-EI by 87%, but left the simultaneous elevation of plasma vasopressin concentrations unchanged.These data demonstrate that isoprenaline stimulates β-LPH and β-E release in vivo. The possibility of an interrelationship between vasopressin and β-E release is discussed.