The intrinsic autoregulation of renal function is complex and involves several systems, which modulate the vascular smooth muscle tone and diameter of the afferent and efferent arterioles. The three major mechanisms involved in renal autoregulation are: myogenic factors intrinsic to the pre- and postglomerular arterioles , the tubuloglomerular feedback (TGF) mechanism , and various vasoactive hormones produced in and out side the kidney acting on the smooth muscle cells in the arterioles.
The myogenic response: The myogenic mechanism is probably the most important component of renal autoregulation and refers to the active contraction of vascular smooth muscle elicited by an increased in intravascular pressure. An increase in wall tension, e.g. caused by increased arterial blood pressure, leads to an activation of the vascular smooth muscle cells and a decrease in vascular diameter and wall tension. The myogenic response probably represents one of the principle means by which many organs and tissue autoregulate blood flow. The phenomenon is well known and was described already in 1902 by Bayliss .
Tubuloglomerular feedback: TGF is a phenomenon unique to the kidney, by which a change in GFR induce a change in flow and/or pressure [32-34] and/or composition of tubular fluid flowing past the macula densa region of the nephrons [23,35]. The structural basis for the TGF is located in the juxtaglomerular apparatus, where the contact between the thick ascending limb of Henle and the vascular pole of the glomerulus are located.
It is thought that macula dense is a sensor, which is able to send at signal to the afferent and efferent arteriole, which leads to a change in the wall tension in the arterioles, when the flow and/or pressure and/or NaCl concentration and/or osmolality in the thick ascending limb of Henle change  and, thus, correct the initial changes in GFR.
Intra- extrarenale vasoactive hormones: Even though studies indicate that vasodilatation and vasoconstricting intrarenal hormones such as prostaglandin's and hormones in the renin-angiotensin system contribute to autoregulation of GFR [36,37], information is as yet inconclusive [38-40]. However, The setting of the above-mentioned intrinsic systems is believed to be under influence from the sympathetic nervous system  and various systemic and local hormones (long-term regulation of GFR and shift in autoregulation interval (fig. 1)) .
There are advocates for a singular mechanism mediating autoregulation by the myogenic response [43,44], whereas others suggest that TGF is the most important mechanism . However, there is emerging consensus that a complicated interplay between both myogenic and TGF mechanisms best explains the efficient autoregulatory response typical of the renal vasculature [30,32,46]. Difference in response time to change in perfusion pressure  and to location of the two components [47,48] may be part of the dispute.
Regardless of the precise mechanisms, the arteriole ability to change the diameter is the key to autoregulation of GFR when perfusion pressure change. Autoregulation of flow requires that resistance increase or decrease in parallel with changes in perfusion pressure. If efferent arteriolar resistance declined significantly when perfusion pressure is reduced, glomerular capillary pressure and GFR would also fall. Consequently, it is the afferent arteriole, which plays a pivotal role in regulating glomerular capillary pressure, renal plasma flow and consequently GFR [26,49-52].
The range of renal autoregulation in animal studies is from 75-95 mm Hg [28,46,53,54] to 180 mm Hg  of renal arterial pressure. The range of systemic BP for normal renal autoregulation in healthy humans is partly unknown. But a mean arterial blood pressure (MABP) of 80 mm Hg is usually suggested as the lower limit for normal autoregulation of GFR [56,57]
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