Plasma ADH Levels Research Articles

Vasopressin release during nonhypotensive hemorrhage and angiotensin II infusion.

These experiments were designed to determine whether angiotensin II (AII) could potentiate the increase in plasma vasopressin (ADH) concentration produced by continuous, nonhypotensive hemorrhage in nephrectomized dogs. Infusion of AII (10 ng/kg.min) into a common carotid artery in nonbled dogs did not increase plasma ADH levels, suggesting that increases in carotid arterial plasma AII concentration alone do not stimulate an increase in ADH release. Subsequently, nephrectomized dogs subjected to nonhypotensive hemorrhage (0.44 ml/kg.min) were infused as follows: 0.9% saline intravenously, AII (10 ng/kg.min) intravenously, or AII (10 ng/kg.min) into the carotid. The Plasma ADH concentration increased in all three groups of dogs during hemorrhage. Although the AII-infused dogs demonstrated significant increases in plasma ADH levels earlier during hemorrhage, these changes were small; there were no statistically significant differences in plasma ADH concentrations among the three groups. These results suggest that increases in plasma AII concentration have little or no significant effect on the volume control of ADH release.

急性及び慢性大静脈狭窄とADH

Plasma ADH levels were studied during acute and chronic constriction of the inferior or superior caval vein in dogs. Mongrel dogs weighing 9.5 to 29 Kg were used. ADH was extracted from plasma according to Yoshida's method and bioassay was carried out using experimental diabetes insipidus rats.Plasma ADH level increased 2 to 5 folds 10 minutes after the caval vein obstruction with balloon inflation as the result of slight decrease in the venous return to the heart. In this case the left ventricular pressure did not change and the stretch receptor in the left atrium would be stimulated. Plasma ADH increased 8 to 30 folds when the venous return decreased markedly, the left ventricular pressure lowered significantly after balloon inflation and the baroreceptor in the carotid sinus or in the arterial system would be stimulated. There was no correlation between plasma ADH levels and peripheral venous pressure except in one case.In only 2 out of 11 dogs with chronic thoracic inferior caval vein constriction plasma ADH increased. In one case hyponatremia occurred one week after the constriction of caval vein. There was no correlation between plasma ADH levels and degree of ascites. ADH seems not to be a primary factor in occurrence of ascites or edema in these experimental models. But it will increase secondary to the change in distribution of the body fluid to keep the“effective circulating blood volume”.

Hemodynamic effects of moderate increase of the plasma vasopressin level in conscious dogs

The influence of moderate increase of the plasma ADH level on aortic and central venous pressures, heart rate, cardiac output, stroke volume, central blood volume, systemic peripheral resistance and plasma volume was examined in conscious dogs. The animals were given 0.75 mU ADH/kg b.w. in single intravenous injection as a priming dose. This was followed by a constant infusion of the hormone at a rate of 0,12 mU/min/kg/0.2 ml 0.9% NaCl solution lasting one hour. Plasma ADH level measured at 30 min of the infusion was equal to 22 ± 4 μU/ml. A significant increase of aortic (mean systolic and diastolic) and central venous pressures, systemic peripheral resistance and of plasma volume was observed in the course of the infusion. It was accompanied by a decrease of heart rate, cardiac output and central blood volume. Changes of stroke volume were not significant.

Potentiation by angiotensin II of the vasopressin response to an increasing plasma osmolality.

An investigation was made of the effect of angiotensin II on the release of ADH in response to an osmotic stimulus. Dogs anesthetized with pentobarbital were hydrated initially by the infusion of 4% glucose iv, in order to bring the plasma concentrations of ADH and renin to low levels. Subsequent infusion of 2.5M NaCl iv, 1.38 ml/kg per min, resulted in a progressive increase in the plasma ADH concentration in response to the increasing plasma osmolality. The relationship between the plasma ADH concentration and plasma osmolality appeared to be rectilinear over the range studied. When the hypertonic saline infusion was accompanied by an infusion of angiotensin II, 10 ng/kg per min, into a common carotid artery, the increase in the plasma ADH concentration was significantly greater. Infusion of angiotensin II alone in the dose tested and under the reported experimental conditions was without a significant effect on the plasma ADH level. It is concluded that angiotensin II can potentiate the release of ADH ...

The activity of the hypothalamo-hypophysial antidiuretic system in conscious dogs. I. The influence of isoosmotic blood volume changes.

The influence of isoosmotic changes of blood volume on the plasma vasopressin level, osmotic reactivity of the antidiuretic system, arterial blood pressure, central venous pressure and heart rate was examined in 13 conscious intact dogs. The rate of disappearance of exogenous vasopressin under control conditions and during hypovolemia was also investigated. A moderate decrease of blood volume produced a clear cut and persistent increase of the plasma vasopressin level, and a fall of central venous pressure. The same blood loss did not change the rate of disappearance of vasopressin from the plasma. Moderate blood volume expansion produced a decrease of plasma ADH level and of the osmotic reactivity of the antidiuretic system. Hypervolemia produced a marked increase of central venous pressure and central blood volume. The result suggest that moderate changes of blood volume modify the activity of the hypothalamo-hypophysial antidiuretic system and support the hypothesis of Gauer and Henry (see [7]) that impulses influencing the activity of the hypothalamo-hypophysial antidiuretic system arise in the central low-pressure part of the circulatory system.

Plasma levels of antidiuretic hormone in man during halothane anaesthesia and surgery.

Effects of halothane-nitrous oxide and oxygen anaesthesia alone for 11/2 hours and of surgery on plasmaadh, serum osmolality, urine volume and urine osmolality were studied in 14 patients. The mean plasmaadh level after premedication with pentobarbitone, pethidine and atropine was 2.8 μu/ml, which was within normal limits (0.4–3.5 μu/ml). It increased significantly by as much as 2.7 times the control level after 11/2 hours of halothane anaesthesia. Surgical stress further increased it (7.5 times). Serum osmolality remained relatively stable.adh secretion appears to play a role on the decreased urine volume and elevated urine osmolality. The clinical application of the present study is also discussed.

Plasma ADH levels following a decrease in mean atrial transmural pressure in dogs.

ARTICLESPlasma ADH levels following a decrease in mean atrial transmural pressure in dogsKL Goetz, GC Bond, AS Hermreck, and JW TrankKL Goetz, GC Bond, AS Hermreck, and JW TrankPublished Online:01 Nov 1970https://doi.org/10.1152/ajplegacy.1970.219.5.1424MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByExogenous vasopressin dose-dependently modulates gastric microcirculatory oxygenation in dogs via V1A receptor12 November 2019 | Critical Care, Vol. 23, No. 1Hyponatremia in a neonate: a case reportCurrent Opinion in Pediatrics, Vol. 17, No. 4Effekte der Beatmung auf Nieren- und LeberfunktionEffekte der Beatmung auf Nieren- und LeberfunktionAtrial receptors, vasopressin and blood volume in the dogLife Sciences, Vol. 36, No. 14Mathematical simulation of the body fluid regulating system in dogJournal of Theoretical Biology, Vol. 99, No. 2Inappropriate secretion of antidiuretic hormone in infants with respiratory infections.Archives of Disease in Childhood, Vol. 56, No. 5Mechanism of impaired water excretion in acute right ventricular failure in conscious dogs.Circulation Research, Vol. 42, No. 6Syndrome of inappropriate antidiuretic hormone secretion in neonates with pneumothorax or atelectasisThe Journal of Pediatrics, Vol. 91, No. 3LiteraturMechanism of diuretic response to increased left atrial pressure in the anesthetized dogKidney International, Vol. 8, No. 6The contribution of atrial stretch receptors to salt and water homeostasis in the humanBasic Research in Cardiology, Vol. 70, No. 4The Relationship of Antidiuretic Hormone to the Control of Volume and Tonicity in The HumanLeft Atrial Receptor Discharge during Atrial Arrhythmias in the DogCirculation Research, Vol. 33, No. 6Impaired Atrial Receptor Responses in Dogs with Heart Failure Due to Tricuspid Insufficiency and Pulmonary Artery StenosisCirculation Research, Vol. 32, No. 4Reflex Diuresis during Tachycardia in the DogCirculation Research, Vol. 32, No. 4The Influence of Intrathoracic Pressure on Fluid and Electrolyte BalanceChest, Vol. 62, No. 5Recent Trends in the Physiology of the Posterior Pituitary More from this issue > Volume 219Issue 5November 1970Pages 1424-1428 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.219.5.1424PubMed5473129History Published online 1 November 1970 Published in print 1 November 1970 Metrics

Plasma levels of antidiuretic hormone in man during diethyl ether anaesthesia and surgery.

The present study was undertaken to determine the plasma antidiuretic hormone (adh) during ether anaesthesia and surgery by utilizing a bioassay technique. The measurements of osmolality in serum and urine, and of urine output, were performed simultaneously. The present study clearly demonstrated a remarkable participation of adh in decreased urine output and in elevation of urinary concentration in 11 patients. Plasma adh level was increased markedly from 2.9 ± 0.93 to 16.9 ± 3.5 μu/ml, which was a sixfold elevation from preinduction concentration after 30 minutes of ether anaesthesia alone. This was followed by gradual decline almost to preinduction levels in two hours after the start of anaesthesia but before the operation. Plasma adh levels increased again to 34.5 ± 11.7 μu/ml ten minutes after the start of operation. A decrease in urinary output and an increase in urinary osmolality were also observed. The increase in plasma adh level was less marked during deep ether anaesthesia. In operations on the extremities or in orthopedic procedures, elevation in the plasma adh level was less prominent than in laparotomy. Our study clearly indicates that the raised ADH secretion during anaesthesia and surgery contribute in part to the decreased urine formation.

Plasma ADH level in patients with chronic congestive heart failure.

Plasma ADH levels in patients with chronic congestive heart failure were determined. In about half cases with moderate to severe right heart failure, ADH increased and it normalized after the cardiac function had improved. There were some cases where ADH increased in response to decreased circulating blood volume. In chronic congestive heart failure, ADH seems to play a role in edema formation together with aldosterone or change in the renal circulatlon.

Antidiuretic hormone release in the monkey during hypo- and hyper-osmotic dehydration.

Release of antidiuretic hormone in two types of dehydration was studied in monkeys. It was found that dehydration with high plasma osmolarity led to a tremendous elevation of plasma ADH level, and dehydration with low plasma osmolarity also led to a significant increase of plasma ADH level though less marked in degree.

3. Antidiuretic Hormone in Congestive Heart Failure

In the present series of patients, no consistent correlations were observed between the plasma ADH level and the severity of congestive heart failure or the stadium of decompensation. However, a positive correlation was observed between the plasma ADH level and the venous pressure. A positive correlation was also observed between the serum osmolality and the venous pressure. There seemed to be a positive correlation between the plasma ADH level and the serum osmolality, and this correlation was remarkable in the course of a patient. The plasma ADH activity after over 14 hours' deprivation of water was usually within the normal limit in patients with congestive heart failure examined in the present study. High levels were observed, however, under certain conditions. There were no consistent data which indicated the impaired osmoreceptor function. The serum osmolality after water deprivation was within normal limits and the decrease in serum osmolality after hydration was accompanied by an inhibition of plasma ADH activity in most cases. Although there was no hyponatremic case in this series, it might be presumed that in some cases of hyponatremia, except for the cases in which the homeostasis mechanism is extremely exhausted, the regulation to maintain the circulating blood volume predominates over the regulation of osmolality. The venous pressure is set at a higher level by cardiac decompensation. An elevation in venous pressure leads to an increase in extravasation of body fluid and a decrease in venous return with an increased oncotic pressure of the venous blood. These changes in body fluid stimulate the release of ADH, which leads to hypervolemia and elevation in venous pressure, thus constituting a vicious circle. Even in this case the ADH seems to act homeostatically together with mineral corticoids in adjusting to the high venous pressure set by cardiac failure. In conclusion, the ADH system seems to play a role in homeostasis of the body fluid in congestive heart failure. The mode of action seems to be a physiological one even in cases with congestive heart failure in the present study. And the action of the ADH is thought to have some-thing to do not only with mineralocorticoids but also with cortisol.

Studies on Antidiuretic Hormone

The present paper deals with a modified sensitive means for the measurement of plasma ADH and the experimental results of the application in human subjects.Weinstein's extraction method for ADH was modified and likewise Share's bioassay method for ADH was also modified. By using these methods, it was possible to detect 2.5 μU, where the measurement hitherto has been about 20μU.Studies were made on normal human subjects who were administered intravenously with nicotine bitartrate and hypertonic saline solution to compare the difference in mode of stimulation of the agents on the supraoptic nuclei and also to compare the resulting ADH release from the neurohypophysis.It was demonstrated in these studies that the plasma ADH levels were between 0.7 to 7.2 μU per c.c. after nicotine injections and 1.2 to 12.1μU per c.c. after hypertonic saline infusions. At the beginning of the negative free water clearance, the plasma ADH levels were higher after nicotine injections than that after hypertonic saline infusions, and then gradually decreased. After hypertonic saline infusions, however, the plasma ADH levels gradually increased and reached a state of equilibrium after approximately 30 minutes.These results suggest that nicotine directly stimulates the supraoptic nuclei for a short period, and as a result, a large amount of ADH is released from the neurohypophysis into the blood. On the other hand, hypertonic saline stimulates the osmoreceptor to set up nerve impulses, which reflexly stimulates the supraoptic nuclei and in turn the neurophypophysis.