Role of the Kidney in the Pathogenesis of Congestive Heart Failure

Abstract

The pathogenesis of sodium retention in congestive heart failure has been a difficult problem to elucidate. The production in dogs of cardiac valvular lesions of increasing severity has enabled investigators to study the sequential alterations in salt and water balance in the same animal from the normal state through the progressive stages of cardiac impairment until frank failure is present. The findings in dogs suggest that: 1. Abnormalities in sodium metabolism are detectable in mild heart disease long before overt failure is present. 2. Total exchangeable sodium may be increased in animals with mild valvular damage. These animals have normal exercise tolerance and normal basal glomerular filtration rates. 3. Increased sympatho-adrenal (adrenergie) activity is responsible, in large measure, for the decreased sodium and water excretion in dogs with cardiac impairment. 4. Preliminary experiments suggest that the carotid sinus may be the receptor organ initiating the reflex increase in sympatho-adrenal tone, and may be the elusive "volume receptor" for which investigators have been searching. 5. Evidence is also available that the carotid sinus may play a major role in the regulation of the zona glomerulosa of the adrenal cortex, the site of aldosterone production.