ABSTRACT
This chapter reviews the mechanisms responsible for renal sodium retention in heart failure. Four aspects, as they relate specifically to heart failure, will be considered: the afferent stimulus that initiates the process; the afferent receptors that signal the kidney to retain sodium; the efferent limb involved in this process; and the nephron sites where tubular function is altered. Some evidence exists as well for the presence of volume or pressure receptors in the high pressure arterial circulation which may affect urinary sodium excretion. Irrespective of the initiating afferent stimulus in congestive heart failure and where it is perceived, stimulation of the efferent limb produces two major alterations in renal function; a reduction in renal blood flow, and a reduction in sodium excretion. There is considerable evidence that sodium reabsorption along the proximal tubule varies with the peritubular physical factors, particularly the peritubular oncotic pressure.
