The pivotal role of the renin-angiotensin-aldosterone complex in the body's hemodynamic regulation has prompted many studies and has given rise to a number of theories on the mechanism of renin release from its source in the juxtaglomerular cells. What is the nature of renal sensors, and to what stimuli do they respond?
Having abandoned Goldblatt's original hypothesis, which ascribed renin release to renal ischemia, investigators are now focusing mainly on the two mechanisms postulated in the "baroceptor" and the "macula densa" theories. The former links renin release with the response of juxtaglomerular cell pressor receptors to arteriolar stretch, whereas the latter theory relates the release to chemical and, possibly, volume changes in the macula densa fluid. Vander1 suggests that the macula densa responds to changes in the total delivered sodium load rather than to fluctuations in sodium concentration or fluid volume. Nash and associates2 provide cogent evidence in