Renal Blood Flow

Renal Blood Flow

Blood flow to the two kidneys is normally about 22 per cent of the cardiac output, or 1100 ml/min. The renal artery enters the kidney through the hilum and then branches progressively to form the interlobar arteries, arcuate arteries, interlobular arterie and afferent arterioles, which lead to the glomerular capillaries, where large amounts of fluid and solutes (except the plasma proteins) are filtered to begin urine formation. The distal ends of the capillaries of each glomerulus coalesce to form the efferent arteriole, which leads to a second capillary network, the peritubular capillaries, that surrounds the renal tubules. The renal circulation is unique in that it has two capillary beds, the glomerular and peritubular capillaries, which are arranged in series and separated by the efferent arterioles, which help regulate the hydrostatic pressure in both sets of capillaries.

High hydro-static pressure in the glomerular capillaries (about 60 mm Hg) causes rapid fluid filtration, whereas a much lower hydrostatic pressure in the peritubular capillaries (about 13 mm Hg) permits rapid fluid reabsorption. By adjusting the resistance of the afferent and efferent arterioles, the kidneys can regulate the hydrostatic pressure in both the glomerular and the peritubular capillaries, thereby changing the rate of glomerular filtration, tubular reabsorption, or both in response to body homeostatic demands. The peritubular capillaries empty into the vessels of the venous system, which run parallel to the arteriolar vessels and progressively forms the interlobular vein, arcuate vein, interlobar vein, and renal vein, which leaves the kidney beside the renal artery and ureter.

Each afferent artery has a region of renin-secreting granular Cells which form part of the Juxtaglomerular apparatus of the nephron. This specialized apparatus is involved with the renin angiotensin System. And also consists of extraglomerular mesangial cells and the macula densa region of the thick ascending limb.

In the normal kidney, the control of renal blood flow and its distribution within the kidneys are determined by a complex interaction of neurological factors and endocrine and locally released vaso active substances. The afferent and efferent renal arterioles have sympathetic innervations from T4 to L2. Increasing sympathetic activity, e.g. in response to shock, preferentially causes vasoconstriction of the afferent artery, thereby reducing renal blood flow.

Renal vessel vasodilators increase renal blood flow and include prostaglandins (PGI2, PGE2), nitric oxide, bradykinin and dopamine. Many of these vasoactive compounds are synthesized within the kidney and, in addition to their effects on total renal blood flow, many alter the distribution of blood flow between the cortex and the medulla. In normal health, many of these mediators probably have a minimal influence on the regulation of renal blood flow and its distribution. However, in disease or in states of stress (e.g. hemorrhage), they play a significant role in maintaining adequate renal perfusion. For example, administration of a no steroidal anti-inflammatory drug (NSAID) to a hypotensive patient may have disastrous consequences on renal function due to inhibition of prostaglandin synthesis.