Autoregulation

Autoregulation is the intrinsic ability of an organ or tissue to maintain a relatively constant blood flow or function despite changes in perfusion pressure or metabolic demand. In physiology, autoregulation most often refers to regulation of blood flow to organs such as the brain or kidney, ensuring stable oxygen delivery and filtration across a range of mean arterial pressures. Autoregulation can be achieved through several mechanisms that sense pressure, flow, or metabolic activity and adjust vascular resistance accordingly.

Myogenic mechanisms involve blood vessels responding to stretch by constricting when pressure rises (and dilating when pressure falls) to keep flow steady. Metabolic or functional autoregulation relies on local metabolic signals—such as CO2, H+, adenosine, and potassium—that rise with tissue activity and promote vasodilation to increase blood flow. Endothelial factors, including nitric oxide, prostacyclin, and endothelin, modulate vascular tone in response to shear stress and signaling cues. In the brain, autoregulation combines myogenic and metabolic inputs with neurogenic influences to maintain cerebral blood flow across a typical mean arterial pressure range of roughly 60–150 mmHg.

Renal autoregulation stabilizes glomerular filtration rate through myogenic responses in the afferent arteriole and tubuloglomerular feedback from the macula densa, maintaining filtration across a mean arterial pressure roughly 80–180 mmHg.

Clinical relevance and limitations: impaired autoregulation can worsen ischemic injury or hypertensive damage, and certain drugs or disease states can shift or blunt the autoregulatory range. Autoregulation is not universal; it varies by organ and species.

Autoregulation can also refer to gene expression control, where a gene product regulates its own expression through negative feedback loops to stabilize protein levels.