Myogenic autoregulation & tubuloglomerular autoregulation

The myogenic mechanism is how arteries and arterioles react to an increase or decrease of blood pressure to keep the blood flow within the blood vessel constant.

The smooth muscle of the blood vessels reacts to the stretching of the muscle by opening ion channels, which cause the muscle to depolarize, leading to muscle contraction. This significantly reduces the volume of blood able to pass through the lumen, which reduces blood flow through the blood vessel. Alternatively when the smooth muscle in the blood vessel relaxes, the ion channels close, resulting in vasodilation of the blood vessel; this increases the rate of flow through the lumen.

This system is especially significant in the kidneys, where the glomerular filtration rate (the rate of blood filtration by the nephron) is particularly sensitive to changes in blood pressure. However, with the aid of the myogenic mechanism, the glomerular filtration rate remains very insensitive to changes in human blood pressure.

Myogenic mechanisms in the kidney are part of the autoregulation mechanism which maintains a constant renal blood flow at varying arterial pressure. Concomitant autoregulation of glomerular pressure and filtration indicates regulation of preglomerular resistance. Model and experimental studies were performed to evaluate two mechanisms in the kidney, myogenic response and tubuloglomerular feedback. A mathematical model showed good autoregulation through a myogenic response, aimed at maintaining a constant wall tension in each segment of the preglomerular vessels. Tubuloglomerular feedback gave rather poor autoregulation. The myogenic mechanism showed 'descending' resistance changes, starting in the larger arteries, and successively affecting downstream preglomerular vessels at increasing arterial pressures. This finding was supported by micropuncture measurements of pressure in the terminal interlobular arteries. Evidence that the mechanism was myogenic was obtained by exposing the kidney to a subatmospheric pressure of 40 mmHg; this led to an immediate increase in renal resistance, which could not be prevented by denervation or various blocking agents.


One of the most striking characteristics of the renal circulation is the ability of the kidney to maintain a constant renal blood flow (RBF) and glomerular filtration rate (GFR) as renal perfusion pressure is altered. The dual regulation of both RBF and GFR is achieved by proportionate changes in the preglomerular resistance and is believed to be mediated by two mechanisms, tubuloglomerular feedback (TGF) and the renal myogenic response. TGF involves a flow-dependent signal that is sensed at the macula densa, and alters tone in the adjacent segment of the afferent arteriole via a mechanism that remains controversial, but likely involves adenosine and/or ATP. The myogenic response involves a direct vasoconstriction of the afferent arteriole when this vessel is presented with an increase in transmural pressure. The current view is that these two mechanisms act in concert and that their primary role is to stabilize renal function by preventing pressure-induced fluctuations in RBF, GFR and the delivery of filtrate to the distal tubule (“distal delivery”).

Over the last two decades, evidence has accrued to indicate that this “autoregulatory” response plays a concurrent role in protecting the kidney from hypertensive injury (14, 15). This view is based on the strong link between autoregulatory capacity and susceptibility to hypertensive injury. In the presence of intact autoregulation, minimal injury is observed despite substantial hypertension. However, when blood pressure (BP) is elevated beyond the upper limit of normal autoregulatory capacity, renal damage develops rapidly. Conversely, if autoregulatory capacity is diminished, susceptibility to hypertensive renal damage is greatly enhanced and injury is observed with even moderate hypertension. Nevertheless, the primary function of the renal vascular responses to pressure, and of the myogenic and TGF mechanisms, is believed to be “regulatory”, as reflected in the very term “autoregulation”. Thus “renal protection” is lost when “renal autoregulation” fails. However, as discussed below, the requirements for maintaining a constant GFR and for protecting the glomerulus from hypertensive injury differ, even though both involve a regulation of glomerular capillary pressure (PGC). Moreover, the myogenic response and TGF system clearly sense different signals and, therefore, may play distinct roles in “protection” and “regulation”. This review presents the authors' perspective on the role of vascular responses to pressure in regulating renal function and in protecting the kidney against the adverse effects of elevated systemic BP.

The answer is much too long for handing into my teacher.