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Vascular physiology

Last updated: November 18, 2020

Summarytoggle arrow icon

The circulatory system, which is also called the vascular system or cardiovascular system, consists of the systemic circulation, pulmonary circulation, the heart, and the lymphatic system. Blood flow through the circulatory system is generated by the heart. Vascular resistance is the amount of resistance in the systematic circulation that must be overcome to create blood flow. The Poiseuille equation describes the relationship between vascular resistance, the length and radius of the vessel, and the viscosity of blood. Blood pressure is generated by the heart, creating a pulsatile blood flow that leads to systolic blood pressure (maximum pressure reached during a cardiac cycle) and diastolic blood pressure (minimum pressure reached during a cardiac cycle) within the circulatory system. The pressure gradient across the circulatory system drives the blood flow from high pressure to low pressure. Blood pressure regulation involves a complex interaction of various sensors (baroreceptors, volume receptors, chemoreceptors) and mechanisms, including the autonomic nervous system, the renin-angiotensin-aldosterone system (RAAS), and atrial reflex and diuresis reflex. Perfusion is the passage of the blood through the circulatory system to the capillary bed to deliver oxygen and nutrients to the tissue and remove waste products (e.g., removal of CO2 to the lungs, removal of urea to the kidneys). Perfusion levels differ in organs and fluctuate depending on the activity (e.g., rest, physical activity). Autoregulatory mechanisms (myogenic autoregulation, local metabolite production), as well as central regulatory mechanisms, modulate perfusion levels in organs. The exchange of substances in the microcirculation occurs via diffusion, filtration, and reabsorption. Capillary fluid exchange is described by the Starling equation, which states that the net fluid flow is dependent on the capillary and interstitial hydrostatic pressures, oncotic pressures, and the vascular permeability to fluid and proteins.

The heart and cardiac physiology, as well as the lymphatic system, are discussed in separate articles.

Pressure, flow, and resistance

The relationship between pressure, flow, and resistance in the circulatory system is expressed as ΔP = Q x R

Blood flow

The capillaries have the largest total cross-sectional area of all blood vessels (4,500–6,000 cm2) and, therefore, have the slowest body velocity (0.03 cm/s). The aorta, on the other hand, has the smallest cross-sectional area (3–5 cm2) but the highest blood velocity (40 cm/s).

Laminar and turbulent blood flow

Blood flow in vessels is either laminar or turbulent depending on the smoothness of the blood vessel walls, the viscosity of the blood, the blood velocity, and the diameter of the lumen.

  • Laminar blood flow
    • Definition: a layered flow pattern
    • Effect: The layer with the highest velocity flows in the center of the vessel lumen.
    • Reynolds number: low
    • Occurrence: throughout the vascular system
  • Turbulent blood flow

Vascular resistance

Poiseuille equation

Vascular stenosis (e.g., coronary artery disease) increases systemic vascular resistance significantly! When the length of the vessel and viscosity of the blood remain constant, the relationship between systemic vascular resistance and the radius of the vessel can be simplified to R ∼ 1/r4. So, if there is a 50% reduction in radius, R = 1/(0.5 x r)^4 → 1/(0.0625 x r4) → 16/r4, there is a 16x increase in resistance (1600%).

Serial and parallel circuits

The total resistance in blood vessels depends on whether these vessels are arranged as serial or parallel circuits.

Serial circuit Parallel circuit
  • Total resistance is the sum of individual resistors (Rx = R1 + R2 + R3 … + RN).
  • Total resistance is greater than individual resistors.
  • Blood flow is the same in each vessel in a series circuit.
  • Total resistance is the sum of reciprocals of individual resistors (1/Rx = 1/R1 + 1/R2 + 1/R3 + 1/RN) .
  • Total resistance can be smaller than individual resistors.
  • Pressure is the same in each vessel in a parallel network.

Arterioles are the blood vessels that contribute most to TPR and, therefore, also to blood pressure regulation.


Wall tension

  • Definition: the force within vessel walls that counteracts vessel rupture during expansion, thus holding the vascular wall together
  • Laplace's law
    • Equation: σt = (Ptm × r) / 2h
      • σt = wall tension (mm Hg)
      • Ptm = transmural pressure (mm Hg)
      • r = inner radius (cm)
      • h = wall thickness (cm)
    • Interpretation:
      • Increases in wall tension are proportional to increases in pressure across the vessel wall (transmural pressure).
      • Wall tension increases with decreasing wall thickness, increasing transmural pressure and/or increasing the inner diameter.
      • Given a constant transmural pressure, the smaller the vascular radius and thicker the vascular wall, the less wall tension generated.

Vessels of the high-pressure system (arteries) have thick vessel walls and smaller internal diameters that enable them to withstand high internal pressures, while vessels of the low-pressure system (veins) have thin vascular walls and larger diameters.

Blood vessel elasticity

  • Definition: the ability of a blood vessel to return to its original shape after expanding

Vascular compliance

  • Definition: the ability of a vessel to expand in response to changes in pressure
  • Equation: C = ΔV/ΔP
    • C = compliance (mL/mm Hg)
    • ΔV = change in volume (mL)
    • ΔP = change in pressure (mm Hg)
  • Greater compliance: greater increase in vascular volume during an increase in pressure (e.g., elastic arteries)
  • Less compliance: less increase in vascular volume during an increase in pressure (e.g., muscular arteries)

Vascular elastance

  • Definition: the ability of a vessel to adapt to intraluminal pressure in response to changes in volume (i.e., the reciprocal of compliance)
  • Equation: E' = ΔP/ΔV
    • E' = elastance (mm Hg/mL)
    • C = compliance (mL/mm Hg)
    • ΔP = change in pressure (mm Hg)
    • ΔV = change in volume (mL)
  • Greater elastance: greater change in blood pressure during blood volume change
  • Less elastance: less change in blood pressure during blood volume change

Compliance is mainly determined by the muscle tone of vessel walls. Arterioles, which are abundant in smooth muscle, have low compliance and are, therefore, considered resistance vessels. Veins are less abundant in smooth muscle, have much higher compliance, and are considered capacitance vessels.

Sensors of blood flow regulation


Volume receptors


If the baroreceptors of the carotid sinus are too sensitive, even small stimuli, such as turning the head or the pressure of a shirt collar, can lead to excessive blood pressure reduction and even fainting. This is referred to as carotid sinus syndrome.

Carotid massage, which stimulates the baroreceptors in the carotid sinus, is an effective way of reducing the heart rate by increasing the refractory period of the AV node.

Peripheral chemoreceptors are more effective in responding to chronic hypoxia than central chemoreceptors.

Central blood pressure regulation

Sympathetic stimulation Parasympathetic stimulation

Atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) regulation

Atrial reflex

  • Definition: a physiologic reflex characterized by an increased heart rate in response to atrial distention (increased venous return to the heart). It is mediated by stretch receptors in the atria.
  • Mechanisms of action: ↑ Volume → ↑ atrial stretch receptors stimulation activation of stretch receptors (B-fibers) in the atria sympathetic innervation and no change in parasympathetic innervation ↑ HR

Atrial natriuretic peptide (ANP) secretion pathway

Diuresis reflex (Gauer-Henry reflex)

  • Definition: a physiological reflex that adapts ADH release in the hypothalamus according to blood pressure
  • Mechanisms of action
    • ↑ BP: Atrial stretch receptors inhibit ADH release via afferent vagal fibers → ↑ water excretion by the kidneys
    • ↓ BP: ADH release → ↓ water excretion by the kidneys

Renal regulation

The RAAS plays a key role in long-term blood pressure regulation and is, therefore, an ideal target for the treatment of arterial hypertension. While beta blockers decrease renin release by the kidneys, the conversion of angiotensin I to angiotensin II by angiotensin-converting enzyme (ACE) can be influenced by ACE inhibitors (e.g., ramipril, enalapril). The effect of angiotensin II on target cell receptors can be inhibited by AT1 receptor antagonists (e.g., candesartan, losartan).


Definition: the passage of the blood through the circulatory system to the capillary bed to deliver oxygen and nutrients to the tissue and remove waste products (e.g., removal of CO2 to the lungs)

Perfusion levels of various organs
Organs % of cardiac output at rest % of cardiac output during exercise
Viscera (hepatic-splanchnic circulation) 24 1
Skeletal muscle 20 88
Kidneys 19 1
Brain 13 3

Other organs

10 1
Skin 8 2
Heart muscle 3 4

Regulation of organ perfusion

Although blood pressure is the main determinant of perfusion, various other mechanisms maintain constant blood flow within organs.


Central regulation

Autoregulation of specific organs

The lungs are the only organs in which hypoxia causes vasoconstriction. This is to ensure that perfusion only occurs in areas that are well ventilated. In all other organs, hypoxia leads to vasodilation to improve perfusion and maintain oxygen supply.

Hypoperfusion of vital organs (e.g., hypovolemic shock, cardiogenic shock) is detected by baroreceptors and volume receptors, leading to an increase in sympathetic tone. Autoregulatory mechanisms are then triggered and lead to centralization of blood flow away from the extremities (skeletal muscle, skin), the GI tract, and other internal organs to maintain perfusion of the heart and brain. In addition, vasoconstriction of precapillary resistance vessels raises systemic vascular resistance and reduces hydrostatic pressure in capillaries, increasing the reabsorption of interstitial fluids into vessels.

To remember the local metabolites used in autoregulation of skeletal muscle, consider to “CAll HuLK”: CO2, Adenosine, H+, Lactate, K+.


Starling forces

For information on the Starling equation for the glomerulus see measurement of renal function in physiology of the kidney.

Edema is caused by the net movement of fluid into the interstitium if there is an increase in capillary hydrostatic pressure (due to heart failure or Na+ retention), an increase in interstitial fluid oncotic pressure (due to lymphatic stasis) or a decrease in capillary oncotic pressure (due to cirrhosis, nephrotic syndrome, heart failure).

Burns, infections or toxins can affect vessel permeability (increased Kf) and can, therefore, result in the formation of edema.

  1. Rosen IM and Manaker S. Oxygen delivery and consumption. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/oxygen-delivery-and-consumption#H4.Last updated: May 9, 2019. Accessed: July 20, 2020.