Physiology of the renomedullary depressor system

THE LOCATION OF A DEPRESSOR MECHANISM IN THE RENAL MEDULLA: The late Eric Muirhead was the first to identify a depressor mechanism in the renal medulla. He located it in the renomedullary interstitial cells and was able to extract a lipid substance with the properties of a blood-pressure lowering hormone from papillary tissue, from renomedullary interstitial cells grown as monolayer tissue culture and from the venous outflow of high-pressure perfused kidneys.

The reversal of Goldblatt renovascular hypertension induces a reduction in blood pressure associated with an unchanged or slightly decreased heart rate, reduced efferent sympathetic activity and a decrease in vascular resistance in the splanchnic region. If the renal medulla is destroyed chemically by 2-bromoethylamine hydrobromide the blood pressure does not fall to normal levels. Extracorporeal crossperfusion of an isolated normal kidney at high pressure activates the renal depressor mechanism, inducing a decrease in blood pressure, also in association with reduced heart rate and sympathetic nervous activity in the normotensive assay rat. Diuresis and natriuresis are also increased when the mechanism is activated, as when the lipid extracts are given intravenously.

Stimulation of efferent sympathetic activity to the kidney can block the initiation of the depressor mechanism. Also, if nitric oxide synthase is blocked, the depressor mechanism cannot be activated.

The renomedullary depressor mechanism, together with the renin-angiotensin system, provides the kidney with the ability to perfectly control blood pressure homeostasis. The antihypertensive effect of this hormonal system is brought about by sympathetic inhibition (cardioprotective), vascular relaxation (vasoprotective) and increased diuresis/natriuresis (renoprotective), which are the characteristics of modern treatment of hypertension.