Cardiac output (CO) is about 5-6 L/min.  The kidneys receive approximately 25% of cardiac output, which is more blood than most organs in the body receive.  The blood is carried to the kidneys via the renal arteries with a pressure of 70-100 mmHg.  Maintenance of high afferent arteriolar pressure and, therefore, regulation of the afferent arteriolar diameter are important to regulating glomerular filtration pressure.  Without sufficient afferent arteriolar pressure, filtration is compromised!  The kidney must be protected against extreme elevations in blood pressure as well as against hypotension.  Remember, due to endothelial fenestrations, there is very little resistance across the capillary network of the glomerulus.  A sufficient reduction in blood pressure, therefore, may allow blood to flow freely through the glomeruli, but can severely impair glomerular filtration and compromise kidney function!

Renal Artery & Afferent Arteriolar Vasoconstriction: (protection from high b.p.)

Over the physiological range of b.p., GFR remains relatively constant.  The renal artery is sympathetically innervated and, with increases in b.p., sympathetic activity will cause vasoconstriction (neurogenic) to prevent increased blood flow in the renal artery.  This prevents increased perfusion so that GFR will not be increased in the face of routine increases in b.p.  There is also some myogenic control and over-expansion of the afferent arterioles will lead to their constriction; this local myogenic response help protect afferent arterioles, and the glomeruli downstream, from overstretch or rupture in the face of elevated blood pressure.

The Juxtaglomerular Apparatus: (protection from high or low b.p.)

The distal tubule of the nephron returns to the cortex and contacts its own glomerulus.  The point of contact between the distal convoluted tubule and the glomerulus is right where the afferent and efferent arteriole enter and leave the glomerular capsule.  Sandwiched between the contact point of the distal convoluted tubule and afferent arteriole are several populations of cells collectively known as the juxtaglomerular apparatus.  Using this juxtaglomerular apparatus, individual nephrons have the ability to maintain relatively constant perfusion pressures such that consistency of overall renal function is normally well maintained.

Both the distal tubule and the afferent arteriole contribute cells to the juxtaglomerular apparatus.  Macula densa cells are tall epithelial cells surrounding the distal tubule.  Macula densa are "sandwiched against" granular cells (also known as juxtaglomerular cells) of the afferent arteriole. 

 The macula densa cells act indirectly as pressure receptors, by sensing the amount of NaCl being filtered.  As pressure in the glomerulus increases, the amount of plasma (and therefore NaCl) filtered will increase.  The macula densa sense this increase and release paracrine signals causing:

i) constriction of the afferent arteriole in the face of elevated blood pressure (to prevent over filtration or damage to the glomerulus) and dilation of the afferent arteriole in the face of reduced blood pressure (to increase glomerular pressure and filtration)

ii) the granular cells (juxtaglomerular cells of the afferent arteriole) to release renin in the face of decreased blood pressure (see the Renin-Angiotensin System, below).

Mesangeal cells are specialized connective tissue cells found within the glomerulus, itself.  Mesangeal cells have contractile fibrillar components that communicate with capillaries of the glomerulus.  Elevations in fluid pressure sensed by the macula densa cause fibrillar mesangeal cells to contract.  As the fibrils of the mesangeal cells tighten around the capillaries, there is a temporary decease in GFR. This is a means of regulating individual nephron function in the juxtaglomerulus area, and helps protect the glomerular capillaries from high b.p.

The Renin-Angiotensin System (protection against low b.p.)

ANG II is a potent peripheral vasoconstrictor.  ANG II attempts to increase renal perfusion pressure by increasing peripheral resistance, through vasoconstriction, to maintain GFR.  ANG II also increases the release of ADH to increase H₂O re-absorption in the distal tubules and collecting ducts to indirectly increase blood pressure.  In the hypothalamus, ADH acts as a "thirst transmitter."  ADH makes you want to drink to increase H₂O intake and blood pressure.  ANG I is the principal hormonal stimulus for adrenal production of aldosterone.  Aldosterone increases Na⁺ re-absorption from the distal tubule and collecting duct in exchange for increased K⁺ secretion.  Increased Na⁺ re-absorption leads to additional passive H₂O re-absorption in the kidney and increased blood pressure.  Finally, ANG II slowly reduces renin secretion so that the renin-angiotensin system will not drive blood pressure dangerously high!