The autoregulation of renal blood flow involves a neuroendocrine mechanism related to the juxtaglomerular apparatus in the kidney.
Figure: Structure of the juxtaglomerular apparatus in mammals
When the afferent arterial blood pressure is low, the stretch sensitive receptors of the arterioles initiate nerve impulses which induce the secretion of a proteolytic enzyme called renin by the juxtaglomerular cells into the blood. This enzyme causes the release of a decapeptide called angiotensin-I from a large globular plasma protein known as angiotensinogen. Another proteolytic enzyme from the plasma, the converting enzyme, removes two amino acids from angiotensin-I to form an octapeptide called angiotensin-II. Angiotensin-II is about 200 times more powerful than norepinephrine in its lasopressor activity. It increases the blood pressure by two mechanisms. Firstly, it acts on the smooth muscle of the arterioles and causes strong vasoconstriction. Secondly, it stimulates the secretion of aldosterone by the adrenal cortex. Aldosterone enhances the uptake of Na+ by the kidney tubules and hence causes a rise in the plasma Na+ level. This results in an increase in the extracellular fluid volume and consequently an elevation in blood pressure. Angiotensin-II is degraded by an enzyme called Angiotensinase, present in plasma.