The Role of Antidiureric Hormone in Congestive Heart Failure

Abstract

Part II. Urinary antidiuretic hormone (ADH) and congestive heart failure.
A clinical entity, congestive failue has been subjected to physiologic reinterpretation. This reinterpretation has been due for the most part to the fact that this entity is one involving a complex series of events occuring over a considerable period of time between the initiating factors and the final remarkable condition of the edematous state and there is no direct correlation between initiating factors and final condition.
It is no doubt that the edema is a state of abnormal retention and distribution of Na and water in the decreased their excretion from kidney, therefore many investigators emphasized the role of the kidney in the development of congestive failure, and impaired glomerular filtration has been considered principal renal abnormality. Lately many peports has pointed out the abnormal function of the kidney tubules, and this in turn admitt the humoral factors which control the reabsorption of Na and water.
As regard to the Na reabsorption aldosterone play an important role and evidence has shown that in congestive failure it's excretion is much greater than normal. On the other hand posterior pituitary antidiuretic hormone (ADH) is the potent water conservatory hormone and control water reabsoption in the kidney.
In spite of many researchs, we are far from a final conclusion in regard to the role of posterior pituitary hormone. In the pervisous literature author has reported the reliable extraction and estimation method of this hormone from urine.
Employing this method hospitalized valvular, congenital heart failure in various grade were used for the estimation of urinary antidiuretic hormone (ADH), and observed the changing pattern of ADH under the treatment of digitalis and diuretics. Secretion mechanism of ADH was examined by water load. Inactivation of ADH in the serum of congestive failure was compaired to liver cirrhosis and using portal vein constricted rabits.
The conclusions thus obtained as follows.
1) Urinary excretion of ADH in congestive heart failure were remarkably increased than the normal subject and as the grade of failure advance ADH increased.
2) There was no direct correlation between the ADH excretion and the initial diuresis which was caused by the digitalis and diuretic therapy, but as the congestive failure improve urinaly ADH decreased.
3) In contrast with normal subject no decrease or disappearance in urinary ADH was found after the administration of water in congestive failure. This in turn, proved