LC5 - Arterioles and Resistance

Vocabulary flashcards covering the core concepts of flow, pressure, resistance, arterioles, autoregulation, and control of vascular tone from the lecture.

Flow

The movement of fluid, such as blood, through a vessel, primarily driven by a pressure difference between two points (a pressure gradient). In the cardiovascular system, blood flow (Q) is governed by the principles of fluid dynamics, where Q = \frac{\Delta P}{R}. For laminar flow, it's particularly influenced by Poiseuille’s relation, showing a dramatic proportionality to the fourth power of the vessel's radius (Q \propto r^4).

Pressure gradient (ΔP)

The difference between the pressure at the arterial end (upstream, e.g., Pa) and the venous end (downstream, e.g., Pv) of a vessel or circulatory segment. This pressure difference (\Delta P) is the primary force that propels blood forward against resistance, with flow always occurring from an area of higher pressure to an area of lower pressure.

Resistance (R)

The opposition to blood flow within a vessel. Resistance (R) is a crucial determinant of blood flow and is significantly influenced by three main factors: the length (L) of the vessel, the viscosity (\eta) of the blood, and most critically, the radius (r) of the vessel. According to Poiseuille's Law, R \propto \frac{\eta L}{r^4}. This inverse relationship means that a small increase in radius leads to a disproportionately large decrease in resistance, and consequently, a large increase in flow (Q \propto \frac{1}{R}).

Poiseuille’s equation

A fundamental equation in fluid dynamics that describes the laminar flow (Q) of an incompressible fluid through a cylindrical pipe. The equation is expressed as: Q = \frac{(\Delta P \times \pi \times r^4)}{(8 \times \eta \times L)}. This formula highlights that flow (Q) is directly proportional to the pressure difference (\Delta P) and the fourth power of the vessel's radius (r), and inversely proportional to the fluid's viscosity (\eta) and the vessel's length (L). It underscores the profound impact of vessel radius on blood flow.

Radius (r) effect (r^4)

The exponential relationship (r^4) between a vessel's radius (r) and blood flow (Q), derived from Poiseuille's law. This relationship means that even a small change in vessel radius results in a dramatic change in flow: doubling the radius of a vessel increases blood flow by a factor of 2^4 = 16-fold, while simultaneously decreasing resistance by 16-fold. This principle is vital for the physiological regulation of blood flow through vasodilation and vasoconstriction.

Laminar flow

A type of fluid flow characterized by smooth, parallel layers, with the fluid moving in an orderly fashion without significant mixing between layers. This highly efficient flow pattern is typical in most blood vessels under normal physiological conditions and strictly adheres to Poiseuille’s law. It minimizes energy expenditure for blood propulsion.

Turbulent flow

A disordered, chaotic pattern of fluid flow where streamlines are irregular and fluid layers mix, leading to eddies and swirling motions. Unlike laminar flow, it does not follow Poiseuille’s law and requires significantly greater driving pressure to maintain flow. Turbulent flow often occurs at high blood velocities, in large vessels, or just distal to obstructions (like stenotic valves), and can generate audible sounds such as murmurs (e.g., Korotkoff sounds in blood pressure measurement).

Peripheral Arterial Occlusive Disease (PAOD)

A common circulatory condition characterized by the buildup of atherosclerotic plaques in the large and medium-sized arteries, most frequently affecting arteries in the legs. This plaque accumulation leads to narrowing (stenosis) and hardening of the arteries, reducing blood flow to the limbs. Symptoms often include intermittent claudication (pain, cramping, or numbness in the legs during exercise, relieved by rest) due to inadequate blood supply (ischaemia) to the muscles.

Atherosclerotic plaque

A pathological accumulation of lipids, cholesterol, fibrous tissue, and inflammatory cells within the inner lining (intima) of arteries. This buildup leads to the hardening and narrowing (stenosis) of the arterial lumen, obstructing blood flow and reducing distal perfusion to tissues and organs. It is the underlying cause of conditions like PAOD, coronary artery disease, and stroke.

Korotkoff sounds

Distinct tapping, pulsating sounds heard through a stethoscope over the brachial artery when taking blood pressure with a sphygmomanometer. These sounds are generated by the turbulent flow of blood through the artery when it is partially compressed by the inflated cuff. As the cuff pressure gradually decreases, the changes in these sounds indicate systolic and diastolic blood pressure readings.

Cardiac output (Q)

The total volume of blood pumped by the left ventricle of the heart into the systemic circulation per minute. It is a critical measure of the heart's pumping efficiency and is calculated as the product of heart rate (HR, beats per minute) and stroke volume (SV, volume of blood pumped per beat): Q = HR \times SV. At rest, typical cardiac output is about 5 liters per minute, adjusting significantly during activity or stress to meet the body's metabolic demands.

Autoregulation

Intrinsic regulatory mechanisms within an organ or tissue that maintain relatively constant blood flow despite fluctuations in arterial blood pressure. This allows organs to protect themselves from excessive pressure or ensure adequate perfusion. Autoregulation is primarily achieved through metabolic and myogenic components, which adjust vascular tone locally to keep flow stable across a range of systemic pressures.

Metabolic autoregulation (functional hyperemia)

A local regulatory mechanism where blood flow to a tissue increases in direct proportion to its metabolic activity. During increased metabolic demand (e.g., muscle exercise), tissues produce metabolic byproducts such as potassium ions (K^+), adenosine, lactate, and carbon dioxide (CO_2). These substances act as potent vasodilators, causing local arterioles to relax and increase blood flow (functional hyperemia) to deliver more oxygen and nutrients and remove waste products.

Myogenic autoregulation

A local regulatory mechanism intrinsic to vascular smooth muscle. When intravascular pressure increases, stretching the vessel wall, the smooth muscle cells respond by constricting, which helps to resist the pressure increase and maintain consistent blood flow. Conversely, a decrease in pressure leads to vasodilation. This direct response of the blood vessel itself helps to stabilize capillary pressure and maintain constant flow despite fluctuations in arterial perfusion pressure.

Endothelial control of vascular tone

The active role played by the endothelial cells (the inner lining of blood vessels) in regulating the contractile state (tone) of underlying vascular smooth muscle. Endothelial cells respond to various stimuli, including shear stress from blood flow, circulating hormones, and local factors, by releasing vasoactive substances. These include vasodilators like nitric oxide (NO), prostacyclin (PGI_2), and endothelium-derived hyperpolarizing factor (EDHF), as well as vasoconstrictors like endothelins, thereby finely controlling vessel diameter and blood flow.

Endothelial factors (NO, PGI2, EDHF)

Vasoactive substances produced and released by endothelial cells that primarily cause relaxation of vascular smooth muscle, leading to vasodilation. Key examples include: 1. Nitric Oxide (NO): A potent vasodilator produced in response to shear stress. 2. Prostacyclin (PGI_2): A prostaglandin that also causes vasodilation and inhibits platelet aggregation. 3. Endothelium-Derived Hyperpolarizing Factor (EDHF): A less well-defined family of substances that lead to vasodilation by hyperpolarizing smooth muscle cells.

Endothelins

A family of potent vasoconstricting peptides released by endothelial cells. Endothelins, particularly endothelin-1 (ET-1), act on specific endothelin receptors (e.g., ETA and ETB) on vascular smooth muscle, causing prolonged and powerful constriction of blood vessels. They play a role in regulating vascular tone and are implicated in conditions like hypertension and heart failure.

Shear stress

The frictional force exerted by flowing blood on the endothelial cells lining the inner surface of blood vessels. Shear stress acts parallel to the vessel wall and is a crucial mechanical stimulus for endothelial cells. It triggers the release of various vasoactive substances, most notably nitric oxide (NO), which promotes vasodilation and plays a significant role in maintaining vessel health and regulating local blood flow.

Adrenaline (epinephrine) receptors

Receptors located on vascular smooth muscle cells that bind to adrenaline (epinephrine) and noradrenaline (norepinephrine), mediating their effects on blood vessel tone. Two main types exist: 1. \alpha1 receptors: Activation generally causes vasoconstriction, predominantly in many systemic vascular beds. 2. \beta2 receptors: Activation causes vasodilation, notably in skeletal muscle and coronary arteries, preparing these beds for increased blood flow during 'fight or flight' responses. The net effect of circulating adrenaline on overall resistance depends on the distribution and relative density of these receptor types in different tissues.

Sympathetic nerve activity (SNA)

The activity of the sympathetic nervous system, a division of the autonomic nervous system, which plays a major role in the central neural control of arteriolar tone and overall systemic vascular resistance. Increased SNA generally leads to generalized vasoconstriction, primarily through activation of _1 adrenergic receptors on vascular smooth muscle. This widespread vasoconstriction helps to redistribute blood flow, increase total peripheral resistance, and elevate arterial blood pressure, especially during stress or exercise. While generally constrictive, some vascular beds, like skeletal muscle, can exhibit _2 mediated vasodilation under specific conditions.

Hormonal mechanisms

Mechanisms involving circulating hormones that modulate arteriolar resistance and systemic blood pressure over a longer duration compared to neural or local controls. Key hormones include: 1. Adrenaline/Epinephrine: Released from the adrenal medulla, it has widespread effects on vasculature via _1 and _2 receptors. 2. Angiotensin II (Ang II): A potent vasoconstrictor produced by the RAAS, acting on AT1 receptors. 3. Vasopressin (ADH): Primarily known for water reabsorption, it also causes vasoconstriction via V1 receptors. These hormones provide systemic, coordinated control of blood flow and pressure.

Angiotensin II (Ang II)

A highly potent vasoconstrictor peptide formed in the blood from Angiotensin I by the enzyme ACE. Angiotensin II acts on specific AT_1 receptors found on vascular smooth muscle, causing strong contraction and leading to increased total peripheral resistance and arterial blood pressure. It is a key component of the Renin-Angiotensin-Aldosterone System (RAAS), which plays a critical role in long-term blood pressure regulation and fluid-electrolyte balance.

ACE (Angiotensin-converting enzyme)

Angiotensin-converting enzyme (ACE) is a crucial enzyme, primarily found in the lungs and kidney, that catalyzes the conversion of the inactive Angiotensin I into the highly active vasoconstrictor Angiotensin II. ACE also inactivates bradykinin, a vasodilator. Its dual role makes it a key target for medications (ACE inhibitors) used to treat hypertension and heart failure, by reducing the formation of Angiotensin II and promoting vasodilation.

Vasopressin (ADH)

Also known as Antidiuretic Hormone (ADH), Vasopressin is a hormone primarily produced by the hypothalamus and released by the posterior pituitary gland. Its main role is to regulate water balance by increasing water reabsorption in the kidneys. However, at higher concentrations, vasopressin also acts as a potent vasoconstrictor by binding to V_1 receptors on vascular smooth muscle, thereby contributing to increased systemic vascular resistance and elevation of arterial blood pressure, especially during conditions of severe dehydration or hemorrhage.

ABP = CO × TPR

This fundamental equation, often referred to as a rearranged version of Ohm's Law for the cardiovascular system, states that Arterial Blood Pressure (ABP) is directly proportional to the product of Cardiac Output (CO) and Total Peripheral Resistance (TPR): ABP = CO \times TPR. This relationship is crucial for understanding how the body maintains blood pressure. For example, during standing or hemorrhage, changes in CO and/or TPR are rapidly coordinated to prevent a precipitous drop in ABP and ensure adequate perfusion to vital organs.

Total Peripheral Resistance (TPR)

The combined resistance to blood flow offered by all the systemic blood vessels within the systemic circulation. TPR is primarily determined by the degree of vasoconstriction or vasodilation of the thousands of arterioles, which act as 'resistance vessels' due to their ability to dramatically alter their radius. Changes in TPR directly impact arterial blood pressure, as described by the equation ABP = CO \times TPR.

Active (functional) hyperemia

An increase in blood flow to a tissue that occurs in direct proportion to an increase in its metabolic activity. This physiological phenomenon, also called functional hyperemia, ensures that active tissues, such as skeletal muscle during exercise or glands during secretion, receive an adequate supply of oxygen and nutrients and efficient removal of waste products to meet their heightened metabolic demands. It is primarily mediated by the local accumulation of metabolic vasodilators.

Reactive hyperemia

A profound, transient increase in blood flow to a tissue that follows a period of reduced or absent blood flow (occlusion). During the occlusion, metabolic byproducts (e.g., CO_2, lactic acid, adenosine) accumulate, and oxygen levels drop. Once normal blood flow is restored, these accumulated vasodilators cause a pronounced vasodilation, leading to a temporary surge in blood flow well above baseline until the metabolites are washed out and oxygen debt is repaid.

Aortic valve stenosis (turbulence)

A condition where the aortic valve, which regulates blood flow from the left ventricle to the aorta, becomes narrowed, stiffened, or obstructed. This narrowing increases the velocity of blood flow through the restricted opening, leading to turbulent flow, which can produce characteristic heart murmurs audible with a stethoscope. Although flow velocity increases, the heart must work much harder (increase pressure generation) to maintain adequate cardiac output, which can lead to ventricular hypertrophy and eventual heart failure if untreated.