Dahl's hypothesis that a saluretic substance may be responsible for a sustained rise in arterial pressure: Its possible role in essential hypertension

Dahl's original hypothesis, that the kidney's control of sodium excretion is paramount in the control of blood pressure, is used to form a possible explanation for the origins of essential hypertension.

Abstract

Dahl's hypothesis that a saluretic substance may be responsible for a sustained rise in arterial pressure: Its possible role in essential hypertension In 1969, Dahi, Knudsen, and Iwai [1] were the first to propose that a circulating saluretic substance might cause a sustained rise in arterial pressure in salt-sensitive hypertensive rats.Haddy and Overbeck [2], in 1976, extended this hypothesis to include the rise in blood pressure that occurs with volume expansion, including primary aldosteronism, cortisone administration, chronic renal failure, and some forms of experimental hypertension.Recently, Blaustein [3] described how a rise in the concentration of a circulating inhibitor of sodium transport might cause a rise in arterial pressure.Blaustein's hypothesis and the increasing evidence on the nature of hypertension in animals and man, and of the nature of natriuretic hormone [4], enable us to use Dahi's original hypothesis [1], and Borst and Borst de Geus's [5] main tenet, that the kidney's control of sodium excretion is paramount in the control of blood pressure, to form a possible explanation for the origins of essential hypertension.The following account outlines the relevant animal work and then describes parallel observations that have been made in man. Rat studiesIn rats, hypertension of an unknown cause is known as spontaneous hypertension.Its incidence in rat colonies varies from 11 to 55% [6, 7], and it is related linearly to age and to the amount of sodium in the diet [8].Dahi [9] noted, however, that some rats on a high intake of salt did not develop hypertension.By selective in-breeding of young rats on a high-sodium diet, his group was able to show that this difference was determined genetically.They developed one strain, known as "sodium sensitive," that develops hypertension on a high-sodium intake, and another, known as "salt resistant," that does not [10,11].Others also have demonstrated that hypertension in rats is determined genetically by selective in-breeding from rats that develop hypertension on a normal-sodium diet (the spontaneously hypertensive rat") and from those that do not