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SUMMARY
The effect of intravenous injections of vasopressin upon sexual behaviour was studied in both intact and castrated, testosterone-treated rabbits. A high dose of vasopressin reduced the number of ejaculations and lengthened the latency to the first mount and ejaculation. A low dose of vasopressin had no significant effect on the sexual behaviour in either intact or castrated rabbits. The volume of ejaculates and the number of sperm cells were also determined. It was found that vasopressin (200 or 40 mu./animal) significantly increased both volume and sperm content in the ejaculates. The possibility that vasopressin is of physiological importance in male sexual functions is discussed.
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SUMMARY
The results support previous findings that vasopressin produces dephosphorylation of a toad bladder membrane protein of 50000 mol. wt. At vasopressin concentrations of 50 mu./ml phosphorylation of this protein was 60 ± 7% of the control level, and maximal natriferic and hydro-osmotic responses were observed in intact bladders. However, at concentrations of vasopressin of 10 mu./ml when a maximal natriferic response but no significant hydro-osmotic response were observed, there was no significant difference in phosphorylation of the proteins from control or vasopressin-treated bladders.
We conclude that the 50000 mol. wt membrane protein is likely to be associated with the hydro-osmotic response of the toad bladder to vasopressin.
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SUMMARY
Intracarotid injection of 0·25 ml of a hyperosmotic (1 m) sodium chloride solution into hydrated rats was an effective stimulus for vasopressin release. The effects of autonomic blocking drugs on this stimulus and on the release of vasopressin by intracarotid injections of acetylcholine were studied.
Anti-adrenergic compounds (reserpine and phenoxybenzamine), ganglion-blocking agents (pempidine and pentolinium) and atropine were shown to be effective in preventing the vasopressin release caused by hyperosmotic stimulation.
Acetylcholine-induced release of vasopressin was inhibited by pempidine but not reserpine.
Based on these findings the nervous pathway(s) involved in the release of vasopressin induced by hyperosmolarity of the plasma is discussed.
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ABSTRACT
The plasma concentration and the 24-h urinary excretion of vasopressin were studied in normal black and white men and women on a normal sodium (150 mmol/day) diet for 3 days and a low sodium (9 mmol/day; furosemide, 1 mg/kg on first day) diet for 4 days. During the normal sodium diet, the 24-h urinary excretion of vasopressin was significantly (P<0·05) higher in men than in women and higher (P<0·05) in black than in white subjects. Corresponding differences in plasma vasopressin concentrations (P<0·05 to 0·01) were observed, with the exception that the difference between white men and women was not statistically significant. These data suggest that under basal conditions the secretion of vasopressin is higher in men and black subjects than in women and white subjects, although differences in the metabolic clearance of vasopressin cannot be ruled out. Reduction in sodium intake resulted in a significantly (P<0·01) decreased excretion of vasopressin in all groups except black women, but had no effect on plasma vasopressin concentrations. Significant (P<0·01) differences with respect to sex and race persisted for vasopressin excretion, but not for plasma vasopressin concentrations. Sex- and race-related differences in vasopressin could not be attributed to differences in blood pressure, plasma volume or plasma sodium concentration. The physiological consequences of these differences in vasopressin remain to be determined.
J. Endocr. (1986) 108, 191–199
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Arginine vasopressin (AVP) is a major antidiuretic hormone, the overproduction of which causes diluting hyponatremia in humans and is called the syndrome of inappropriate antidiuresis (SIAD). To study physiological changes resulting from AVP overproduction and to develop an animal model of hyponatremia, the human AVP gene was expressed under the control of the metallothionein promoter in transgenic (Tg) rats. Analyses of AVP immunoreactivity (irAVP) in the tissues revealed that the transgene is expressed mainly in the central nervous system. Gel filtration showed that irAVP in the brain and plasma was properly processed AVP. AVP purified from the brains of both Tg and control rats also exerted equal bioactivity to generate cAMP in LLC-PK1 cells. The founder rats did not show any physical or anatomical abnormalities. Under basal conditions, Tg rats had high plasma AVP levels (Tg 13.8 +/- 2.5 pg/ml; control 2.7 +/- 1.2 pg/ml; n=6 in both groups; means +/- S.E.M.), decreased urine volume, and normal plasma [Na(+)]. Hypertonic saline injected i.p. did not affect AVP secretion in Tg rats. In response to a zinc-supplemented liquid diet, plasma AVP decreased in control rats, but increased in Tg rats (Tg 32.7 +/- 2.7 pg/ml; control 1.0+/-0.1 pg/ml; n=6), resulting in hyponatremia (Tg 135.2 +/- 2.5 mEq/l; control 140.8 +/- 0.4 mEq/l; n=6). To our knowledge, this is the first transgenic animal to show diluting hyponatremia. This transgenic rat may therefore provide a useful model in which to investigate various physiological alterations resulting from the oversecretion of AVP which involve SIAD, stress response, behavior, and blood pressure.
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Introduction
At physiological concentrations of arginine vasopressin (AVP) in plasma, a principal target organ of AVP is the kidney where its function is the regulation of water excretion. It has become recognized in the last few years that AVP acts not only upon the collecting tubules but also upon other sites of the renal tubular system and parts of the kidney tissue, in particular the medullary thick ascending limb of Henle's loop.
Vasopressin receptors
The actions of AVP are mediated by two distinct biochemical intracellular mechanisms. Vasopressor glycogenolytic activities of AVP are associated with an increase in the concentration of calcium and metabolism of phosphatidylinositol via activation of the V1 receptor. Antidiuretic activity is associated with an increase in the intracellular generation of cyclic AMP (cAMP) after activation of the V2 receptor.
V1 receptor
Occupancy of V1 receptors by AVP activates the breakdown of membrane phosphoinositides
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Neurophysin is considered to act as a carrier protein for oxytocin and arginine vasopressin (AVP) in the neurohypophysis, and recent evidence has suggested that neurophysin is released into the blood together with the neurohypophysial hormones in response to various stimuli (Cheng & Friesen, 1970). Neurophysin, extracted from bovine pituitary posterior lobes, consists of two major components designated neurophysin I and II (Hollenberg & Hope, 1968) both of which bind oxytocin and AVP in vitro, although neurophysin II appears to be located specifically in neurosecretory granules containing AVP (Dean, Hope & Kazie, 1968).
We now report results relating to the release of neurophysin, oxytocin and vasopressin into the blood in response to hand-milking, mating and haemorrhage in the goat. Consecutive serial blood samples (approximately 25 ml each) were taken from an indwelling jugular cannula during hand-milking in one goat and during mating in four oestrous female goats (McNeilly & Folley, 1970).
Medical Microbiology and
Biochemistry, Faculty of Medicine and Health Sciences, United Arab Emirates University, PO Box 17666, Al Ain, United Arab Emirates
Department of Obstetrics and Gynecology, University Hospital, SE 221 85, Lund, Sweden
Zoonoses and Emerging Infections Group, Clinical Virology, University of Veterinary Medicine, Clinical Department of Diagnostic Imaging, Infectious Diseases and Clinical Pathology, Vienna, Veterinärplatz 1, A-1210 Vienna, Austria
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Medical Microbiology and
Biochemistry, Faculty of Medicine and Health Sciences, United Arab Emirates University, PO Box 17666, Al Ain, United Arab Emirates
Department of Obstetrics and Gynecology, University Hospital, SE 221 85, Lund, Sweden
Zoonoses and Emerging Infections Group, Clinical Virology, University of Veterinary Medicine, Clinical Department of Diagnostic Imaging, Infectious Diseases and Clinical Pathology, Vienna, Veterinärplatz 1, A-1210 Vienna, Austria
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Medical Microbiology and
Biochemistry, Faculty of Medicine and Health Sciences, United Arab Emirates University, PO Box 17666, Al Ain, United Arab Emirates
Department of Obstetrics and Gynecology, University Hospital, SE 221 85, Lund, Sweden
Zoonoses and Emerging Infections Group, Clinical Virology, University of Veterinary Medicine, Clinical Department of Diagnostic Imaging, Infectious Diseases and Clinical Pathology, Vienna, Veterinärplatz 1, A-1210 Vienna, Austria
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Medical Microbiology and
Biochemistry, Faculty of Medicine and Health Sciences, United Arab Emirates University, PO Box 17666, Al Ain, United Arab Emirates
Department of Obstetrics and Gynecology, University Hospital, SE 221 85, Lund, Sweden
Zoonoses and Emerging Infections Group, Clinical Virology, University of Veterinary Medicine, Clinical Department of Diagnostic Imaging, Infectious Diseases and Clinical Pathology, Vienna, Veterinärplatz 1, A-1210 Vienna, Austria
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Medical Microbiology and
Biochemistry, Faculty of Medicine and Health Sciences, United Arab Emirates University, PO Box 17666, Al Ain, United Arab Emirates
Department of Obstetrics and Gynecology, University Hospital, SE 221 85, Lund, Sweden
Zoonoses and Emerging Infections Group, Clinical Virology, University of Veterinary Medicine, Clinical Department of Diagnostic Imaging, Infectious Diseases and Clinical Pathology, Vienna, Veterinärplatz 1, A-1210 Vienna, Austria
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Medical Microbiology and
Biochemistry, Faculty of Medicine and Health Sciences, United Arab Emirates University, PO Box 17666, Al Ain, United Arab Emirates
Department of Obstetrics and Gynecology, University Hospital, SE 221 85, Lund, Sweden
Zoonoses and Emerging Infections Group, Clinical Virology, University of Veterinary Medicine, Clinical Department of Diagnostic Imaging, Infectious Diseases and Clinical Pathology, Vienna, Veterinärplatz 1, A-1210 Vienna, Austria
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Introduction The neurohypophyseal peptide hormones, oxytocin (OT) and vasopressin (VP), have potent uterotonic effects in both pregnant and non-pregnant humans and rats ( Bossmar et al. 1994 , 1995 , Chan et al. 1996
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Abstract
The influence of volume status on the effect of physiological doses of vasopressin on sodium excretion was assessed in anaesthetized Brattleboro rats. Following a 1 h control period, animals were divided into four groups. Group 1 (control) rats were kept in water balance throughout (by adjustment of the rate of i.v. glucose infusion) and received no vasopressin. In group 2 rats, vasopressin (20 μU/min) was infused i.v. for 2 h, then withdrawn during the following 2 h; the vasopressin-induced antidiuresis and subsequent return to water diuresis were matched by appropriate changes in the i.v. infusion, thus maintaining water balance. In this group, vasopressin had no effect on sodium excretion. Group 3 rats received the same dose of vasopressin, but the infusion rate of the glucose solution was not reduced; consequently these rats became water-loaded. In this group, sodium excretion increased significantly during vasopressin infusion, and rapidly returned to baseline values when the vasopressin was discontinued. Group 4 rats were treated in the same way as group 3 animals except that the vasopressin infusion was maintained (but without additional water loading) for a further 2 h; this did not prevent the fall in sodium excretion during the final 2 h of the experiment. We conclude that the natriuretic effect of physiological levels of vasopressin reported elsewhere may be dependent on an accompanying acute volume expansion during infusion of the hormone.
Journal of Endocrinology (1996) 151, 49–54
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1. The decrease of antidiuretic potency in the blood was studied in anaesthetized rats after the intravenous injection of vasopressin (100 mU/100 g) and was shown to follow an exponential course.
2. Removal of the kidneys retarded the rate of disappearance of injected vasopressin from the circulation, and so did tying of the coeliac and mesenteric arteries.
3. In rats in which the kidneys had been removed and the coeliac and mesenteric arteries had been tied, the disappearance of vasopressin was almost entirely prevented.
4. It was concluded that under the experimental conditions used, the extraction of vasopressin was almost complete after the passage of blood through the kidneys and the splanchnic vascular bed.
5. The kidneys accounted for about 50 % of the vasopressin cleared, and the splanchnic vascular area for at least 40 %.
6. The antidiuretic activity found in the urine after the intravenous injection of vasopressin into unanaesthetized rats was equivalent to 6·7 % of the dose administered.
