http://www.icapture.ubc.ca/projects/trials/vasst/physiology.pdf

Physiology of Vasopressin Relevant to Management of Septic Shock

Antunes-Rodrigues, Jose, Margaret de Castro, Lucila L. K. Elias, Marcelo M. Valenca, and Samuel M. McCann. Neuroendocrine Control of Body Fluid Metabolism. Physiol Rev 84: 169–208, 2004; 10.1152/ph...

Neuroendocrine Control of Body Fluid Metabolism

Publisher Summary
This chapter describes anti-diuretic hormone arginine vasopressin (AVP), lysine vasopressin (EVP), urinary AVP, plasma AVP-osmolality, and the chromatographic behavior of purified bovine AVP on Sephadex G-15 with different eluting solvents or sample composition. As immunoassay methods can be used successfully to develop simple and accurate assays, plasma AVP has re-stimulated much investigative interest and, as a consequence, many other laboratories are beginning to develop their own assay procedures. It has been known for almost 30 years that the secretion of AVP can be influenced by a number of factors, including changes in blood osmolality, volume, and pressure. However, the relative potency of these variables and the way in which they interact in regulating secretion of the hormone under different conditions of salt and water balance has been a subject of some dispute. The advent of the immunoassay technique has now made it possible to begin to define these aspects of AVP physiology in more precise and comprehensive terms. The osmoregulation of AVP can be readily understood by analyzing the relationship between plasma AVP and plasma osmolality under different conditions of water balance.

The regulation of vasopressin function in health and disease.

Neurophysiology and neuropharmacology of hypothalamic magnocellular neurons secreting vasopressin and oxytocin.

https://www.amjmed.com/article/0002-9343(82)90825-7/pdf

Neurogenic disorders of osmoregulation

A new specific RIA for a-human atrial natriuretic hormone (ahANP) was used to determine whether changes in plasma volume elicited by acute water loading, hypertonic saline infusion, and furosemide administration caused changes in ANP release and resultant changes in renal and cardiovascular function in normal subjects. In addition, changes in plasma arginine vasopressin (AVP), PRA, and aldosterone concentrations were studied simultaneously. Mean plasma ahANP and AVP levels were 51.3 ± 16.0 (±SE) and 3.1 ± 0.6 pg/ml, respectively, in the basal state. Plasma ahANP rose to 77.8 ± 27.6 in response to a 4.5% increase in plasma volume induced by water loading, increased further to 134.1 ± 28.9 in response to a 23% volume increase induced by hypertonic saline, and fell to 70.2 ± 15.8 pg/ml in response to a decrease in plasma volume after furosemide treatment (P 〈 0.01–0.05). On the other hand, plasma AVP fell to 1.8 ± 0.1 pg/ml after the water load, rose to 4.1 ± 0.6 after hypertonic saline, and rose further to ...

Effects of acute water load, hypertonic saline infusion, and furosemide administration on atrial natriuretic peptide and vasopressin release in humans.

Four patients with central diabetes insipidus were studied to clarify the mechanism of antidiuretic action of carbamazepine (Tegretol). Oral administration of Tegretol to these patients resulted in a significant decrease in urine volume and in an elevation of U/P osmolar ratio to greater than 1. Antidiuretic hormone (ADH) concentrations in plasma also increased to normal range after the treatment. These studies indicated that the drug was acting through the release of endogenous ADH and thereby induced antidiuresis. During the course of therapy, an acute water load did not suppress ADH release, free water clearance remaining negative. Accordingly, it was concluded that the release of ADH during Tegretol therapy was controlled by the drug itself, not by physiological osmo- and volume-regulations. Tegretol was also effective in reducing polyuria in a patient with compulsive water drinking, but danger of water intoxication was great in this patient. Thus, Tegretol should not be given to this type of...

Mechanism of carbamazepine (Tegretol)-induced antidiuresis: evidence for release of antidiuretic hormone and impaired excretion of a water load.

In order to investigate the role of central alpha 1- and alpha 2-adrenoceptors in the control of vasopressin (ADH) release and the cardiovascular system, norepinephrine (NE) (1.4 microgram/kg), methoxamine (1.4 microgram/kg), yohimbine (60 micrograms/kg), and prazosin (40 micrograms/kg) were administered via the cerebral ventricles in urethane-chloralose-anesthetized dogs after morphine sedation (n = 42). In the control study 0.9% saline was administered. NE resulted in a significant fall in blood pressure, heart rate, and ADH release. Methoxamine tended to activate the cardiovascular system, but did not affect the release of ADH significantly. Prazosin decreased blood pressure significantly with a significant rise in heart rate and ADH release. Pretreatment with prazosin did not block significantly the effect of NE on blood pressure, heart rate, and ADH release. Yohimbine did not affect the cardiovascular system and ADH release significantly. Pretreatment with yohimbine completely blocked the effect of NE on ADH release, and brought about a slight rise in blood pressure and heart rate. In none of the experiments could changes in ADH release be attributed to changes in plasma osmolality. These results indicate that central alpha 1-adrenoceptors might act to activate the cardiovascular system, but have no effects on ADH release in anesthetized dogs. On the other hand, central alpha 2-adrenoceptors might act to reduce ADH release and to depress the cardiovascular system.

The Role of Central α1- and α2-Adrenoceptors in the Regulation of Vasopressin Release and the Cardiovascular System*

The clearance of vasopressin (VP) by the kidneys and splanchnic viscera was studied in the anesthetized dog. VP is bound to plasma protein, 10% at basal plasma VP levels and 40% at plasma VP concentrations greater than 20 microU/ml. The urinary clearance of VP is 70-100% of the glomerular filtration rate; the renal organ clearance of the hormone is 20-30% greater than its urinary clearance. There is evidence that the renal organ clearance of VP is affected by changes in both glomerular filtration rate and renal blood flow. The renal clearance of VP is a result of glomerular filtration, degradation, or reabsorption in the proximal nephron, and secretion into the distal nephron. In the short term, the renal clearance of VP is unaffected either by changes in the plasma VP concentration over a broad range or by moderate hemorrhage. The splanchnic clearance of VP is accomplished almost equally by the intestine and the liver. Because the sum of the splanchnic and renal clearances of VP is less than estimates of its metabolic clearance rate, there may be a physiologically significant clearance of VP by organs in addition to the kidneys and splanchnic viscera.

Metabolism of vasopressin.

A new method was developed for the estimation of arginine vasopressin (AVP) in plasma and urine. Samples were extracted by a microcolumn of resin and assayed radioimmunologically using a highly sensitive antiserum to AVP. Ion-exchange resin, CG-50, H+ form, packed in a small column (diameter 4 mm, height 6 mm), was proved effective to remove the interfering substances and to concentrate the AVP in the sample. The application of 80% acid acetone successive to diluted HCl brought about a consistent recovery of AVP from the resin column. Recoveries were 66.4 +/- 8.5% for plasma and 85.4 +/- 9.7% for urine. In normal subjects plasma AVP levels were 3.9 +/ 0.3 pg/ml (mean +/- S.D.) in ambulatory states, 4.9 +/- ).6 after overnight fast, and 0.4 +/- 0.2 after water lading. High levels of 2.0 +/- 24.2 pg/ml were obtained in patinents with syndrome of inappropriate secretion of ADH (SIADH), low values of 0-1.8 pg/ml in diabetes inipidus. Urinary excretions of AVP were 117.4 +/- 59.4 ng/24/hr (mean +/- S.D.) in normal controls, 191 +/- 177.0/24 hr in SIADH, and 17.0 +/- 12.0/24 hr in diabetes insipidus.

Kuniaki Matsui

Papers

Effects of acute water load, hypertonic saline infusion, and furosemide administration on atrial natriuretic peptide and vasopressin release in humans.

Mechanism of carbamazepine (Tegretol)-induced antidiuresis: evidence for release of antidiuretic hormone and impaired excretion of a water load.

The Role of Central α1- and α2-Adrenoceptors in the Regulation of Vasopressin Release and the Cardiovascular System*

Metabolism of vasopressin.

Radioimmunoassay of arginine vasopressin in human plasma and urine, a resin microcolumn method.