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The effect of the dopamine antagonist, haloperidol, on arginine-vasopressin (AVP) release induced by angiotensin II was studied in six dehydrated conscious dogs. Angiotensin II (10 ng/kg per min) alone caused a twofold increase (P<0·05) in plasma AVP concentration, a 25 mmHg increase (P<0·01) in mean arterial blood pressure (ABP) and a 70% decrease (P<0·01) in plasma renin activity (PRA). In the presence of haloperidol (3 μg/kg per min), angiotensin II caused similar changes in mean ABP (+25 mmHg; P<0·01) and PRA (−65%, P<0·01), but a small insignificant decrease in plasma AVP (−22%). The AVP response to angiotensin II in the presence of haloperidol was significantly (P<0·05) different from its response to angiotensin II alone. Neither haloperidol alone nor the two vehicles had any effect on plasma AVP or mean ABP but PRA dropped slightly. The results suggest that a dopaminergic mechanism may be involved in angiotensin II-induced AVP release.
Search for other papers by P. J. BENTLEY in
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SUMMARY
Ethacrynic acid inhibited short-circuit current (SCC, Na transport) across the toad bladder. Some structural analogues had similar effects and their potency varied with their ability to combine with SH groups. The Na-K ATPase inhibitor ouabain was more effective than ethacrynic acid and its action and that of ethacrynic acid was additive.
The natriferic and hydro-osmotic effects of vasopressin were inhibited by ethacrynic acid (10−5 and 10−4 m); the antagonism was competitive at 10− and 10−4 m (but not at 10−3 m). Certain analogues of ethacrynic acid also exhibited this effect but it was not clearly related to their SH-combining ability.
The natriferic and hydro-osmotic effects of caffeine and cyclic AMP were not changed by 10−4 m-ethacrynic acid.
Ethacrynic acid (10−4 m), which does not affect basal sodium transport in bladders pretreated for studying the action of aldosterone, prevented the initiation of the increase in sodium transport by aldosterone but was without effect when added to a toad bladder already under the influence of aldosterone. This suggests that ethacrynic acid interferes with metabolic processes underlying the action of aldosterone. Dihydroethacrynic acid which has no SH-binding activity was without effect.
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SUMMARY
The vasopressor and milk ejection activities were estimated in the supraoptic region of the hypothalamus of rats which had been hypophysectomized 30 min, 4 and 8 days earlier. Both pressor and milk ejection activities were significantly greater 4 days after hypophysectomy than those in sham-operated control rats. Eight days after hypophysectomy, pressor activity decreased below control values but milk ejection activity was still significantly raised. Increased biological activity after hypophysectomy is thus associated with the previously observed increase in neurosecretory material within the supraoptic nucleus so these results provide additional evidence that neurosecretory material represents stored hormone. Milk ejection activity increased relatively more than pressor activity which supports the suggestion that the final stage in the formation of neurohypophysial hormones occurs as they pass from the hypothalamus to the neural lobe. If this final maturation normally occurs more slowly for oxytocin than for vasopressin, the obstruction to the flow of hormones down the neural stalk caused by hypophysectomy would result in a greater increase in milk ejection than pressor activity.
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ABSTRACT
Young, middle-aged and aged rats received s.c. testosterone implants for 50–52 days in order to investigate whether supplementation of testosterone in aged rats could normalize the reported reduction of kidney arginine vasopressin (AVP)-binding sites and increase the plasma concentration of AVP. Receptor number, which was measured by means of a membrane-binding assay with [3H]AVP as ligand, was below the detection level in the untreated aged rat. Following testosterone treatment, no effects were seen in the youngest groups, but in the aged group AVP receptors became clearly detectable, albeit with a lower affinity. A remarkable observation was the increase in affinity for renal AVP binding in the middle-aged compared with the young rat. Plasma levels of AVP in control aged rats tended to be higher. Such a tendency was completely absent in the testosterone-treated aged rats. Possible mechanisms underlying the restoration of reduced AVP-binding sites in the kidney of the aged rat by testosterone treatment are discussed.
Journal of Endocrinology (1989) 123, 59–63
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SUMMARY
The recoveries from portal blood of Pitressin and Azovan blue injected into the superior mesenteric artery in neurohypophysectomized rats were determined. The ratio of the recoveries of Pitressin and Azovan blue was 1·00±0·15. In rats with intact neurohypophyses and anaesthetized with urethane, the concentration of antidiuretic hormone in arterial blood was not different from that in portal blood. It is therefore concluded that vasopressin and endogenous antidiuretic hormone are not cleared rapidly from the circulation in the intestines. The pressor responses to 20 mu. Pitressin given intraportally were smaller than those obtained with 10 mu. given intravenously, suggesting rapid clearance of Pitressin from the circulation in the liver.
A technique is described for determining the renal clearance of test substances infused intravenously into conscious rats followed by sampling of the arterial blood. In six rats the urinary clearance of Pitressin was 1·24±0·06 times the clearance of inulin. In two rats in which urine flow was unusually low, clearance of Pitressin was respectively 0·161 and 0·325 times the inulin clearance. It is calculated that the rate of clearance of Pitressin from the circulation in conscious rats corresponds to a half-life of 42 sec.
Search for other papers by A V Sirotkin in
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Abstract
The effects of growth hormone (GH) and prolactin (PRL) (1, 10, 100, 1000 or 10 000 ng/ml medium) on oxytocin, vasopressin, progesterone, cAMP and cGMP release by cultured bovine granulosa cells were studied. It was found that GH significantly stimulated oxytocin, vasopressin and cAMP but suppressed progesterone secretion. PRL tended to have the same pattern of action on nonapeptide, cAMP and steroid release, but its effect was not as great, with only a high supraphysiological dose (10 000 ng/ml) producing a statistically significant effect. No significant influence of GH on cGMP output was observed. Physiological doses of PRL (1, 10, 100 or 1000 ng/ml) significantly inhibited cGMP production whilst a high dose (10 000 ng/ml) resulted in stimulation.
These observations suggested that GH may regulate ovarian oxytocin, vasopressin, progesterone and cAMP secretion. The effects of PRL on the release of these substances appeared to be non-specific, possibly resulting from its structural similarity to GH.
Journal of Endocrinology (1994) 143, 417–422
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ABSTRACT
The plasma concentration of arginine vasopressin (AVP) is increased in diabetic ketoacidosis (DKA) in man and the rat. Although haemodynamic changes and nausea/emesis may account for the increased secretion of AVP in severe human DKA, they appear not to be responsible in moderate DKA. Streptozotocin-treated rats were studied to investigate other factors possibly involved in the secretion of AVP in DKA.
Wistar rats were injected i.p. with streptozotocin (150 mg/kg body weight). Diabetic rats were maintained on 3–4 units protamine–zinc insulin (PZI)/day for 11 days, after which PZI was withdrawn for 3 days in half the rats. The plasma concentration of AVP was greater in rats with DKA than in normal controls (mean 11·4 pmol/l compared with 1·6 pmol/l; P <0·05). Rats with DKA had higher plasma osmolality and concentrations of blood glucose, β-hydroxybutyrate and acetoacetate, but lower plasma carbon dioxide content than diabetic and normal controls (P <0·05). There were no differences in plasma levels of sodium, urea or haematocrit between rats with DKA and controls. In a separate study involving the same procedures, daily systolic blood pressure was measured using a tail cuff to occlude arterial inflow to the tail, and subsequent detection of the cuff pressure at which the first arterial pulsation appeared. No significant differences were detected between normal and diabetic rats and rats with DKA. Exponential relationships between plasma osmolality and plasma AVP (correlation coefficient, r = +0·75; P <0·01), and plasma ketone bodies and plasma AVP (r= +0·60; P <0·05) were obtained. The increase in plasma AVP in the DKA group was not due to haemodynamic changes or nausea/emesis. The results suggest that in early DKA in the rat, increases in the plasma concentration of AVP are related to the metabolic consequences of insulin deficiency and not to hypovolaemia or hypotension.
J. Endocr. (1988) 116, 343–348
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ABSTRACT
The cerebrospinal fluid level of arginine vasopressin (AVP) or vasoactive intestinal polypeptide (VIP) was enhanced chronically by implantation of a device for controlled drug delivery in the lateral ventricle of the rat. Urine production, water consumption, urine osmolality as well as urinary AVP excretion were then measured for a period of 26 days. During this period the rats were studied under normal hydration and under conditions of osmotic stress induced by water deprivation (2 days) and the drinking of 2% (w/v) NaCl (6 days), in order to see whether the capacity of central systems to react adequately to osmotic stimuli was affected by high central peptide levels.
Immediately after the central AVP treatment was started, a temporary increase was found in urinary AVP levels which was not accompanied by a change in any of the other parameters but which decreased again to control levels within 10 days. After this burst of AVP excretion, AVP-treated rats showed a tendency during periods of normal hydration for a lower urine osmolality, combined with a higher water intake and urine production without changes in urinary AVP excretion. Since there was no clear-cut correlation between urinary AVP excretion and body water turnover, this could still indicate a slowly acquired and slight inhibition of pituitary AVP release by long-term centrally administered AVP. However, the capacity of these rats to respond to osmotic stimuli was not different from the controls.
In the VIP-treated rats a slight but significant reduction in urine production was found in all three periods of normal hydration. During the osmotic stress induced by the drinking of 2% NaCl the VIP-treated rats showed a lower increase in urine production and fluid intake and a lower decrease in urine osmolality when compared with the response of the control rats. This has tentatively been interpreted as a potentiation by VIP of the activation of pituitary AVP release under these conditions.
J. Endocr. (1988) 117, 207–214
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ABSTRACT
To investigate whether hyperglycaemic ketoacidotic diabetic rats continue to osmoregulate the secretion of arginine vasopressin (AVP), male Wistar rats were injected with streptozotocin (150 mg/kg body weight). Rats rendered diabetic were maintained on protamine–zinc insulin (PZI) for 11 days (insulin-treated rats; n = 35), after which PZI was withdrawn for 72 h in half the rats (insulin-withdrawn rats). Insulin-withdrawn and -treated rats were divided into two groups; one was injected i.p. with distilled water (20 ml/kg) and the other with hypertonic saline (500 mmol NaCl/l; 20 ml/kg), and killed 30 min after injection. Insulin-withdrawn rats (water loaded and osmotically stimulated) were hyperglycaemic (16·5 ± 0·8 and 16·5 ± 0·9 mmol glucose/l respectively) and ketotic (2077 ± 664 and 1474 ± 170 μmol acetoacetate/l respectively). Insulin-treated rats were euglycaemic and non-ketotic. Osmotic manipulation caused similar changes in plasma sodium in both insulin-withdrawn and -treated rats. Plasma AVP was low in the water-loaded rats (0·6 ± 0·1 and 4·5 ± 0·9 pmol/l in the insulin-treated and -withdrawn rats respectively) and increased in rats injected with hypertonic saline (1·2 ± 1·8 and 35·2 ± 17·9 pmol/l respectively). There was no evidence of hypotension and hypovolaemia in any group of rats. Linear regression analysis defined the functions: plasma AVP = 2·56 (plasma Na – 141), r = +0·63, P < 0·01 for hyperglycaemic ketotic rats; plasma AVP = 0·83 (plasma Na – 146), r = +0·78, P < 0·001 for insulin-treated animals. The slopes and abscissal intercepts were significantly (P < 0·05) different. We conclude that the hyperglycaemic ketotic diabetic rat retains the ability to osmoregulate AVP secretion.
Journal of Endocrinology (1989) 123, 413–419
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The ageing process in animals and humans is thought to be accompanied by a gradual impairment of corticosteroid receptor function, which is reflected by increased pituitary-adrenocortical hormone secretion at baseline and a number of aberrant neuroendocrine function test results. The latter include the ACTH and corticosteroid responses to a combined dexamethasone (DEX)/corticotropin-releasing hormone (CRH) challenge. The excessive hormonal response to this test among aged individuals has been taken as indirect evidence of enhanced endogenous arginine vasopressin (AVP) release, which - together with peripherally administered CRH - is capable of overriding DEX-induced ACTH suppression. The current study was designed to explore the role of endogenous AVP in mediating excessive hypothalamic-pituitary-adrenocortical (HPA) activity in ageing. The combined DEX/CRH test was administered to aged (22-24 months old) Wistar rats and the effect of the AVP type 1 (V1) receptor antagonist, d(CH(2))(5)Tyr(Me)AVP, on ACTH release was studied. Infusion of the V1 receptor antagonist after DEX pretreatment and before CRH administration prevented the CRH-induced rise in ACTH secretion in comparison with vehicle-treated aged rats (area under the concentration-time curve: 699+/-479 versus 2896+/-759; P<0.01). This difference was absent in young (3 months old) control rats. In situ hybridization showed an increased number of AVP mRNA-expressing neurons in the parvocellular but not the magnocellular, portion of the hypothalamic paraventricular nucleus in DEX-pretreated aged rats. The number and synthetic activity of parvocellular neurons expressing CRH mRNA was also increased. We have concluded that the increased HPA activity in aged rats involves enhanced synthesis and release of AVP from parvocellular neurons, possibly secondary to impaired corticosteroid receptor function.
