Another Humoral Substance that enhances Adrenergic Responsiveness during Acute Renal Ischaemia

Abstract

RENAL hypertension consists of an early humoral period in which angiotensin concentrations are increased¹ followed by a period of sustained hypertension. The latter seems to be maintained largely through the sympathetic nervous system^2–4, but the mechanism is not fully understood^5–7. The interaction between angiotensin and the sympathetic nervous system has received attention^8,9; that increased angiotensin-like activity has not been detected in blood^10,11 and that renin and angiotensin concentrations are often not increased in chronic hypertension^1,12,13 suggests that something other than the renin–angiotensin system accounts for the facilitation of neurogenically mediated vasoconstriction observed during sustained hypertension^14–16. The neurogenic contribution to renal hypertension could develop if the ischaemic kidney produces another factor which acts like angiotensin or which potentiates the effects of undetectable amounts of angiotensin. Here we describe the release during acute reduction of renal perfusion pressure of a new humoral factor with actions like those of angiotensin. The factor, released into renal venous blood, elicits hind paw adrenergic vasoconstrictor responses beyond the level produced by the infusion of angiotensin alone.