Rise In Plasma Vasopressin Research Articles

Cardiovascular effect of the antidiuretic hormone arginine vasopressin

The two major biological actions of vasopressin are antidiuresis and vasoconstriction. The antidiuretic action of low concentrations of vasopressin is well established and concentrations 10 to 100 times above those required for antidiuresis elevate arterial blood pressure. Antidiuresis is mediated by V2-receptors at the kidney, whereas vasopressin constricts arterioles by binding at V1-receptors. Pharmacological effects of specific antagonists of the vasoconstrictor activity of vasopressin (vascular or V1-receptor antagonists) are presented. Low concentrations of vasopressin do have significant hemodynamic effects. Physiological concentrations of vasopressin cause vasoconstriction and elevate systemic vascular resistance. In subjects with intact cardiovascular reflex activity, however, cardiac output falls concomitantly and blood pressure therefore does not change. In animals with baroreceptor deafferentation or in patients with blunted baroreceptor reflexes (autonomic insufficiency) a rise in plasma vasopressin causes vasoconstriction and an increase in blood pressure, because cardiac output does not fall under these conditions. Vasopressin contributes substantially via increase in systemic vascular resistance to maintain blood pressure during water deprivation. During hemorrhage and hypotension vasopressin has a major role to restore blood pressure. In experimental hypertension vasopressin contributes to the development and maintenance of high blood pressure in DOCA, but not in genetic hypertensive rats. The role of vasopressin in human hypertension is not yet clear. Vasopressin in extrahypothalamic areas of the brain affects circulatory regulation by interaction with central cardiovascular control centers. The exact mechanism of how vasopressin is involved in central regulation of blood pressure remains to be established. In contrast to our previous opinion vasopressin is a vasoactive hormone also at low plasma concentrations. Its cardiovascular action is more complex than previously assumed.

Plasma vasopressin, cortisol, and growth hormone concentrations in relation to surgery in the suprasellar region.

Posterior and anterior pituitary functions were assessed in 8 patients before, during, and after surgery for tumors in the suprasellar region. Preoperatively, all patients but one responded adequately to an osmotic stimulus with a rise in plasma vasopressin (AVP) and all but one showed adequate cortisol response to adrenocorticotropic hormone (ACTH) and hypoglycemia. During surgery a transient rise was seen in plasma levels of AVP (5 out of 8 patients), cortisol (7 out of 8 patients) and growth hormone (4 out of 8 patients). This response could be predicted from the preoperative stimulation tests. Postoperatively the AVP response to osmotic stimuli was impaired in 4 out of 5 patients, although urine volume had returned to normal after a transient polyuric phase. The response of plasma cortisol to ACTH was still adequate but lower than preoperatively.

Contribution of vasopressin to the maintenance of blood pressure during dehydration.

Normal Long-Evans rats, when dehydrated for up to 72 h, have a progressive rise in plasma vasopressin that is associated with a fall in body weight and urine volume, a rise in plasma and urine osmolality, and the maintenance of normal systolic blood pressure. In contrast, Brattleboro diabetes insipidus rats, genetically deficient in vasopressin, when dehydrated to achieve an equivalent body weight loss, have a significant 15 mmHg fall in systolic blood pressure. Even when fluid balance is corrected in the Brattleboro rats by the continuous administration of 1-desamino-8-D-arginine vasopressin, a synthetic vasopressin analogue with potent antidiuretic properties but minimal pressor activity, blood pressure still falls when the animals are dehydrated. In contrast, Brattleboro rats infused with exogenous arginine vasopressin to produce a plasma vasopressin level of 18.9 +/- 3.5 pg X ml-1 are able to maintain normal blood pressure during 48 h of dehydration. This level of vasopressin is comparable to the level found endogenously in dehydrated Long-Evans rats and is nonpressor in normal rats. These results suggest that both the antidiuretic and vasoconstrictor properties of vasopressin are important in the cardiovascular response to dehydration.

Hypothalamic integration of dopaminergic and opiate pathways controlling vasopressin secretion.

Lesions of the circumventricular organs were produced by administration of monosodium-L-glutamate to neonatal rats. At 16 weeks of age these rats were given different stimuli to vasopressin release. In control rats, morphine (50 micrograms) injected into the third ventricle resulted in a rapid increase in plasma vasopressin concentrations at 10 min, followed by a reduction at 20 min. The circumventricular organ-lesioned rats, however, showed a pronounced fall in vasopressin secretion both at 10 and 20 min after 50 micrograms morphine. A similar abolition of the morphine-elicited rise in plasma vasopressin could also be achieved by the iv infusion of small doses of dopamine in normal rats. Hypoxic stimuli, which result in a marked rise in vasopressin in normal rats, failed to elicit any increase in circumventricular organ-lesioned animals. Vasopressin release after stimulation with 9% saline, however, was augmented in the lesioned animals. These results suggest that circumventricular organs have an important role in controlling neurohypophyseal secretion and that they differentially control different stimuli to vasopressin release via dopaminergic and opiate pathways.

Effect of ethanol ingestion on plasma vasopressin and water balance in humans.

The effects of 75 ml ethanol ingested over 60 min on plasma osmolality (Posmol) and plasma vasopressin (PAVP) in four normal subjects were studied. In the 1st h of the investigation PAVP fell, then rose, even though plasma ethanol levels were still rising. The rise in PAVP was preceded by a rise in Posmol corrected for the influence of ethanol. The fall in PAVP was followed by an increase in free water clearance and a decrease in urine osmolality, while the later rise in PAVP was followed by a decrease in free water clearance (CH2O) and a rise in urine osmolality. The relationship between PAVP and Posmol was then studied during intravenous (iv) hypertonic saline infusion in five subjects. The results were compared with those from a second infusion in the same subjects after ingestion of ethanol (0.5 ml/kg). Ethanol reduced vasopressin release in response to iv hypertonic saline infusion, and this correlated with a reduced decrease in CH2O. We conclude that ethanol inhibits PAVP release by decreasing the response of the osmosodium receptors to changes in plasma tonicity.

Arginine vasopressin response to insulin-induced hypoglycemia in man.

Insulin-induced hypoglycemia causes an increase in plasma vasopressin concentration in man and rat. To assess the mechanism by which this occurs, the effect of hypoglycemia was studied in healthy adults. After insulin injection, a 7-fold rise in plasma immunoreactive arginine vasopressin to 8.2 +/- 3.6 pg/ml was observed in 10 normal subjects. This was associated with a rise in plasma sodium of 2 meq/liter, but no significant change in mean arterial pressure or hematocrit was observed. The significance of the plasma sodium rise was assessed by observing the vasopressin response to hypoglycemia in a patient shown previously to have a selective loss of the vasopressin response to osmotic stimulation. His plasma vasopressin rose from 1.6 to 12.5 pg/ml with no fall in blood pressure or volume. beta-Adrenergic blockade with propranolol before repeat insulin-induced hypoglycemia did not reduce the vasopressin response (peak plasma vasopressin, 8.1 +/- 1.7 pg/ml), despite suppression of PRA. Linear regression analysis showed that the rise in plasma vasopressin and the percentage decline in plasma glucose correlated significantly (r = 0.57, P less than 0.001). In conclusion, hypoglycemia releases vasopressin nonosmotically by a mechanism that appears to be independent of factors currently known to effect vasopressin secretion.

Human plasma vasopressin response to potent loop-diuretic drugs.

To investigate the effect of potent loop diuretic drugs on the factors that control water excretion, immunoreactive plasma arginine vasopressin was measured at regular intervals for 6 h after intravenous administration of frusemide (40 mg) and piretanide (12 mg) in healthy adults. Despite a large diuresis there was no significant rise in plasma vasopressin compared to controls. Diuretic drug treatment caused small increases in plasma osmolality comparable to the control group, but no change in mean arterial blood pressure. The fall in blood volume of 7% within 1 h of frusemide administration was insufficient to stimulate vasopressin secretion. We conclude that loop diuretic drugs in the dose given have little effect on plasma vasopressin and osmolality but cause a small fall in blood volume in healthy adults.

Vasopressin function in familial cranial diabetes insipidus

A family suffering from cranial diabetes insipidus, that extends over 4 generations, is described. Inheritance of polyuria was autosomal dominant. Vasopressin function was studied in members of the last 2 generations, 4 of whom had polyuria. Osmoregulation of vasopressin secretion was assessed by infusion of hypertonic saline. Plasma vasopressin remained undetectable in one patient, while 2 others had very blunted vasopressin responses to osmotic stimulation. Three non-osmotic stimuli were applied. Controlled hypotension produced by trimetaphan infusion and insulin-induced hypoglycaemia did not increase plasma vasopressin but apomorphine-induced nausea caused a minimal rise in plasma vasopressin to 0.7 pg/ml. Polyuria and thirst resolved with antidiuretic therapy in all patients studied. Congenital absence of vasopressin as in Brattleboro rats is unlikely to account for diabetes insipidus in this disorder since small increases in vasopressin have been demonstrated in these patients. In view of previous post-mortem findings, familial cranial diabetes insipidus is most likely to be due to degeneration of vasopressin-synthesizing neurones.

Vasopressin release induced by hemorrhage in the goat.

AbstractEffects of moderate hemorrhage were studied in normovolemic and hydrated conscious goats. Plasma arginine vasopressin (AVP) in jugular vein blood did not rise in response to bleeding of 8 and 12 ml/kg b.wt. After a blood loss of 16 ml/kg an abrupt and conspicuous rise in plasma AVP (to > 10 times basic level) was seen in 50% of the experiments, whereas no rise in AVP occurred in the remaining experiments. Bleeding at 20 and 24 ml/kg gave a more consistent AVP response. Hydration did apparently not reduce the AVP‐responsiveness to bleeding. The plasma vasopressin concentration returned to pre‐hemorrhage level about 3 h after bleeding, i.e. before the blood was re‐transfused. A minor, and inconsistent rise in plasma renin activity occurred in response to bleeding. Central venous pressure fell during hemorrhage and stayed depressed until the blood was re‐transfused. Since the depression was of the same order in all experiments, and was still present when plasma AVP had returned to pre‐hemorrhage level, the fall in venous pressure was obviously not the main cause of the AVP‐response. However, the pronounced rise in plasma vasopressin was correlated to a fall in the arterial pressure and to hyperventilation. No urge to drink developed during any of the hemorrhage experiments. It is concluded that the goat does not readily respond to hemorrhage with vasopressin liberation. When it happens, pressor amounts of the hormone are released, and a fall in arterial pressure and/or increased stimulation of respiratory chemoreceptors (hypoxia?) appear(s) to be the ultimate cause(s) of the release. This thirst‐independent regulation of vasopressin secretion is obviously of no importance in day to day control of water balance, but may help to maintain the arterial blood pressure in emergency situations.

Development and clinical application of a new method for the radioimmunoassay of arginine vasopressin in human plasma.

A radioimmunoassay has been developed that permits reliable measurements of plasma arginine vasopressin (AVP) at concentrations as low as 0.5 pg/ml in sample volumes of 1 ml or less. Nonhormonal immunoreactivity associated with the plasma proteins is eliminated by acetone precipitation before assay, leaving unaltered a component that is immunologically and chromatographically indistinguishable from standard AVP. Storage of plasma results in a decline in AVP concentration and, thus, must be carefully regulated. The plasma AVP values obtained by our method approximate the anticipated levels and vary in accordance with physiologic expections. In recumbent normal subjects, plasma AVP ranged from (mean +/-SD) 5.4+/-3.4 pg/ml after fluid deprivation to 1.4+/-0.8 pg/ml after water loading, and correlated significantly with both plasma osmolality (r=0.52; P<0.001) and urine osmolality (r=0.77; P<0.001). After fluid restriction, plasma AVP was uniformly normal relative to plasma osmolality in patients with nephrogenic diabetes insipidus and primary polydipsia but was distinctly subnormal in all patients with pituitary diabetes insipidus. The infusion of physiologic amounts of posterior pituitary extract caused a dose-related rise in plasma vasopressin that afterwards declined at the expected rate (t(1/2)=22.5+/-4 min). We conclude that, when used appropriately, our radioimmunoassay method provides a useful way of assessing AVP function in man.