Local and humoral control of blood flow !
- Regulation
- Exam priority: medium
Each tissue adjusts its own arterioles to get the blood it needs, even when arterial pressure changes.
Updated 2026-11-01
Also called: Autoregulation of blood flow
See it in 3D: Kidneys · Vessels inside the kidney · Carotid arteries
What it is
Each organ's flow follows its metabolism: when a tissue works harder, its arterioles dilate. Many organs also hold flow nearly constant over a wide range of arterial pressure (autoregulation). On top of this local control, circulating substances constrict or dilate the vessels.
How it works, step by step
- Active tissue uses more O₂ and makes more CO₂, H⁺, K⁺ and adenosine.
- These metabolites relax the smooth muscle of arterioles and precapillary sphincters.
- Local resistance falls and flow rises (active hyperemia) until the metabolites are washed out.
- If flow is cut off for a while, on release it overshoots well above normal (reactive hyperemia) and repays the oxygen debt.
- Higher flow raises shear stress on the endothelium, which releases nitric oxide and dilates the larger feeding arteries.
- In the long run, sustained ischemia drives the growth of new vessels and collaterals (angiogenesis).
Regulation
- +Local metabolites (adenosine, CO₂, H⁺, K⁺, lactate) and low PO₂: Vasodilation of working tissue: more flow.
- +Endothelial nitric oxide and prostacyclin: Relax smooth muscle; sustain flow-mediated dilation.
- +Bradykinin and histamine: Dilate arterioles and raise capillary permeability (inflammation, anaphylaxis).
- +Epinephrine at β2 receptors in skeletal muscle: Muscle vasodilation at low physiological levels.
- −Norepinephrine and epinephrine at α1 receptors: Vasoconstriction of skin, viscera and kidney.
- −Angiotensin II, vasopressin and endothelin: Constrict arterioles and raise peripheral resistance.
What controls flow in each organ
| Organ | Dominant control | Detail |
|---|---|---|
| Heart | Metabolic (adenosine, low PO₂) | High O₂ extraction at rest: more demand needs more flow |
| Brain | CO₂ and H⁺; myogenic autoregulation | Hyperventilation lowers CO₂ and constricts cerebral vessels |
| Kidney | Myogenic and tubuloglomerular feedback | Keeps filtration steady |
| Skeletal muscle | Metabolic in exercise; sympathetic at rest | Flow can rise more than 20-fold |
| Lung | Alveolar hypoxia constricts | Diverts blood to well-ventilated alveoli |
Clinical notes
- In peripheral artery disease the arterioles are already fully dilated: walking finds no flow reserve and claudication appears.
- In sepsis and anaphylaxis massive vasodilation wipes out peripheral resistance: distributive shock.
- In diabetic retinopathy the retinal capillaries lose autoregulation.
Test yourself
Think of the answer, then tap the question to see it.
Why does a muscle released from a tourniquet turn red and get more flow than normal?
During ischemia vasodilator metabolites build up and O₂ runs out; when flow returns the arterioles stay dilated (reactive hyperemia) until the oxygen debt is repaid.
What keeps renal blood flow nearly unchanged when mean arterial pressure rises from 100 to 140 mmHg?
Autoregulation: wall stretch triggers myogenic contraction of the afferent arteriole, and tubuloglomerular feedback reinforces it.
Why does hypoxia dilate systemic arterioles but constrict pulmonary ones?
In tissues hypoxia means poor supply and more flow fixes it; in the lung it means poorly ventilated alveoli, and constricting those vessels diverts blood to areas that do oxygenate.
Why does a patient with peripheral artery disease hurt when walking but not at rest?
The stenosis caps maximal flow; at rest it is enough, but in exercise the arterioles are already dilated and there is no reserve for the extra demand.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- Coronary circulation and myocardial ischemia
- Skin blood flow
- Muscle blood flow and the cardiovascular response to exercise
- Nervous control of the circulation and the CNS ischemic response
- Flow, pressure and resistance: Poiseuille and turbulent flow
- The renin–angiotensin–aldosterone system
Related conditions
In Biochemistry
- Eicosanoids: prostaglandins, thromboxanes and leukotrienes
- Adrenaline
- Angiotensin-converting enzyme (ACE)
- Lactate
- ATP (adenosine triphosphate)
In Pharmacology
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: 20.4 Homeostatic Regulation of the Vascular System (OpenStax (Rice University), 2022); 20.2 Blood Flow, Blood Pressure, and Resistance (OpenStax (Rice University), 2022); Peripheral Arterial Disease (StatPearls (NCBI Bookshelf), 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 17). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
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Representative model, for educational purposes only.