Regulation of Kidney Function

Glomerular filtration rate, blood volume, blood pressure and the concentration of the urine finally produced are not fixed quantities; they are continuously monitored and adjusted through a set of interlinked hormonal feedback mechanisms, centred on the kidney itself, the adrenal cortex, the heart and the pituitary gland.

The starting point for one of the most important of these mechanisms is the juxtaglomerular apparatus (JGA), the specialised patch of cells formed where the ascending limb of the loop of Henle passes close to the afferent arteriole of its own nephron, described earlier in this chapter. When glomerular blood flow or blood pressure falls — for instance following blood loss, dehydration, or a drop in blood Na+ — the juxtaglomerular cells of this apparatus respond by releasing the enzyme renin into the blood. Renin acts on angiotensinogen, an inactive plasma protein continuously secreted by the liver, converting it into angiotensin I; angiotensin I is then further converted, chiefly as blood passes through the capillaries of the lungs, into angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a powerful vasoconstrictor, narrowing blood vessels throughout the body and so directly raising blood pressure, and it also travels to the adrenal cortex, where it stimulates the release of the steroid hormone aldosterone. Aldosterone acts on the distal convoluted tubule, promoting the active reabsorption of Na+ (and, following it osmotically, water), which increases blood volume and further raises blood pressure. Together, this sequence — renin, angiotensin II and aldosterone — makes up the renin-angiotensin-aldosterone system (RAAS), a self-correcting loop that restores blood pressure and blood volume toward normal whenever they fall too low, and in doing so also restores glomerular filtration rate toward its normal level.

A separate hormone provides an opposing check on this system when blood volume or blood pressure rises too high rather than too low. Atrial natriuretic factor (ANF), also called atrial natriuretic peptide, is secreted by the muscular walls of the atria of the heart when they are stretched more than usual by an excessive volume of blood returning to the heart. ANF causes the blood vessels to dilate (vasodilation) and increases the excretion of Na+ and water by the kidney, both of which act to lower blood volume and blood pressure back toward normal — the direct physiological opposite of the renin-angiotensin-aldosterone system, so that the two mechanisms together keep blood pressure and blood volume from drifting too far in either direction. …