Three different mechanisms are thought to contribute to the process of cerebral autoregulation.

Cerebral autoregulation plays an important role in maintaining an appropriate blood flow to that region.

However, autoregulation only partially accounts for the expression pattern of Fis.

Measuring and understanding cerebral autoregulation remains a big challenge.

Fine-tuning of tubulin levels during the cell cycle occurs by autoregulation.

Capillary beds may control their blood flow via autoregulation.

While most systems of the body show some degree of autoregulation, the brain is very sensitive to over- and underperfusion.

However, the autoregulation of AsnC is not affected by asparagine.

Treatment of the loss of autoregulation of the brain's blood vessels may be difficult or impossible.

Cerebral autoregulation is the ability of the blood vessels in the brain to maintain a constant blood flow.

Brain blood flow autoregulation is abolished when abnormally high CO2 levels persist.

The Bowditch effect is an autoregulation method by which myocardial contractility increases with an increase in heart rate.

It also regulates its own expression (autoregulation).

Carbon dioxide is one of the mediators of local autoregulation of blood supply.

Autoregulation of nodulation controls nodule numbers per plant through a systemic process involving the leaf.

It has been shown that people who suffer from chronic hypertension can tolerate higher arterial pressure before their autoregulation system is disrupted.

Cerebral autoregulation refers to the physiological mechanisms that maintain blood flow at an appropriate level during changes in blood pressure.

There is "autoregulation" of renal blood flow and glomerular filtration rate in isolated kidneys.

This autoregulation falters when hypertension becomes excessive.

These arteries, when healthy, are capable of autoregulation to maintain coronary blood flow at levels appropriate to the needs of the heart muscle.

Cerebral autoregulation is a process in mammals, which aims to maintain adequate and stable cerebral blood flow.

Failure of normal autoregulation and an abrupt rise in systemic vascular resistance are typical initial components of the disease process.

This positive autoregulation by stimulating its own transcription may be a mechanism for prolonging the signals from extracellular stimuli.

Cerebral autoregulation usually ensures the brain has priority to cardiac output, though this is impaired slightly by exhaustive exercise.

Affected arteries develop endothelial dysfunction and impairment of normal vasodilation, which alter renal autoregulation.