CV - Vasculature and Regulation of Circulation Flashcards
Describe the structure and function of arteries
Structure:
- thick tunica media
- smooth muscle layer for vasoconstriction + vasodilation
- thick elastic walls
Function:
- resist high pressure
- low compliance, high elastic recoil to maintain diastolic pressure
- low resistance to flow
- after load effect on cardiac output
- much lower pressures on right side
Describe the structure and function of arterioles:
Structure:
- muscular for their size
- Small diameter vessels
- major site of vascular resistance
- densely innervated, mostly by sympathetic noradrenergic vasoconstrictor, also sympathetic cholinergic vasodilator and parasympathetic cholinergic vasodilator
Function:
- regulate distribution of blood flow into capillary beds
- smooth muscle under sympathetic and local control adjusts their diameter
- highest resistance to flow, steepest pressure drop and smoothing of pressure
- ## tone maintains blood pressure
Describe the structure and function of capillaries:
Structure:
- single endothelial cell layer with a basement membrane
- pre-capillary sphincters
Function:
- Site of nutrient, gas, and waste exchange through diffusion, filtration, and transcytosis
- . Due to the sheer numbers of capillaries in all the systemic tissues, they offer relatively little resistance to flow
- Filtration across the capillaries depends on the balance of hydrostatic pressure within the capillary, the tissue pressure of surrounding tissue, and the colloid osmotic pressures in the vessel and in the extracellular fluid, known as Starling’s forces,
- . The vessels can become leaky to water in some situations such as inflammation, and the resulting water movement into the tissue is called oedema
Describe the structure and function of veins:
Strucutre:
- thin walls, little smooth muscle
- valves to prevent back flow of blood
- sympathetic noradrenergic venoconstriction nerves
- collapse at very low pressure
Function:
- high compliance, blood volume reservoir
- preload effect on cardiac output
- low resistance to blood flow
- skeletal muscle venous pump
- venous pressure effects on capillary pressure and fluid filtration
Describe the Gradient of blood pressure through the systemic circulation:
Blood pressure is highest in the aorta and decreases as it travels through the systemic circulation
A. Aorta and Large Arteries (High Pressure)
* Blood pressure peaks during systole (~120 mmHg) and decreases slightly during diastole (~80 mmHg).
* These vessels act as pressure reservoirs, smoothing out the heart’s pulsatile output.
B. Small Arteries and Arterioles (Sharp Pressure Drop)
* The most significant drop in blood pressure occurs in this segment, with pressures falling from ~80 mmHg to ~30-40 mmHg.
* Arterioles, with their thick muscular walls, are the primary site of resistance in the circulation.
C. Capillaries (Low and Stable Pressure)
* Blood pressure continues to decline, stabilizing around 20-30 mmHg.
* Capillaries have a high cross-sectional area, reducing velocity and pressure.
* Low pressure prevents damage to capillary walls and facilitates exchange of gases, nutrients, and waste products via diffusion.
D. Venules and Veins (Very Low Pressure)
* Blood pressure drops further in venules and near 0 mmHg as blood returns to the right atrium.
* Venules and veins act as volume reservoirs rather than pressure conduits.
Describe the innervation of blood vessels:
Sympathetic nervous system:
- primary regulator of vascular tone
- norepinephrine acts on α1-adrenergic receptors, causing vasoconstriction
- in skeletal muscle and coronary vessels, β2-adrenergic receptors mediate vasodilation
Sensory innervation:
- Baroreceptors in the carotid sinus and aortic arch sense pressure changes and mediate reflex adjustments via the autonomic system.
- Chemoreceptors detect changes in blood gases and pH, influencing vascular tone.
Describe the features of vascular smooth muscle:
Structure of Vascular Smooth Muscle:
- spindle-shaped, non-striated cells arranged in layers around the vessel wall
- found in the tunica media, controlling vessel diameter
- contract as syncytium, due to presence of gap junctions
- actin and myosin present, but not in sarcomeres
- no Z discs, but dense bodies on membrane and within cell act as anchoring points for actin
- interconnected by myosin filaments
Describe the features of vascular smooth muscle contraction:
Triggered by calcium influx (voltage-gated or ligand-gated channels)
Calcium binds to calmodulin, activating myosin light-chain kinase (MLCK)
MLCK phosphorylates myosin heads, enabling interaction with actin for contraction
Key Features of Contraction:
- sustains long-term contraction (vascular tone) with low ATP consumption
- responsive to chemical (e.g., hormones), mechanical (e.g., stretch), and electrical stimuli.
Describe the factors That Affect Arteriolar Diameter and Resistance to Blood Flow
Neural factors:
- Sympathetic activation: Vasoconstriction (via α1 receptors) or vasodilation (via β2 receptors in skeletal muscle)
Hormonal Factors:
- Vasoconstrictors: Angiotensin II, vasopressin, epinephrine (in non-skeletal tissues).
- Vasodilators: Nitric oxide, prostacyclin, and atrial natriuretic peptide (ANP)
Local (Autoregulatory) Factors:
- Metabolic: Increased CO₂, H⁺, lactate, or adenosine promotes vasodilation
- Myogenic: Increased pressure causes reflex vasoconstriction to maintain flow
Stress - Increased blood flow stimulates endothelial nitric oxide production, causing vasodilation
Describe the effect of viscosity on blood flow:
Resistance to flow increases with viscosity, described by Poiseuille’s law.
Elevated viscosity (e.g., in polycythemia) increases resistance and reduces flow.
Reduced viscosity (e.g., in anemia) decreases resistance but may impair oxygen transport
Describe the effect of Haematocrit on blood flow:
Proportion of red blood cells in blood (~45% in males, ~40% in females).
High Hct increases viscosity, raising vascular resistance and cardiac workload.
Optimal Hct balances oxygen-carrying capacity with manageable flow resistance
Blood pressure is higher in the systemic circulation compared to the pulmonary circulation – Why?
In systemic circulation blood needs to travel to the entire body meaning systemic arteries encounter high total peripheral resistance (TPR)
Pulmonary arteries encounter low vascular resistance because they supply only the lungs, where thin-walled capillaries facilitate gas exchange
Higher resistance in systemic circulation → higher blood pressure
Lower resistance in pulmonary circulation → lower blood pressure
What is the The Fahraeus-Lindqvist effect ?
Fahraeus-Lindqvist effect describes how blood viscosity decreases as blood flows through small-diameter vessels
occurs due to the non-uniform distribution of red blood cells (RBCs) within the vessel, affecting flow dynamics
In small vessels, reduced viscosity and reduced flow resistance as RBCs migrate towards centre of the vessel
In larger vessels RBCs can aggregate, increasing viscosity
What are the 3 mechanisms that initiate smooth muscle contraction ?
Agonists;
- (e.g. noradrenaline) produce 2nd messengers (e.g. IP3)
- sarcoplasmic reticulum (SR) releases Ca2+
- receptor-induced Ca2+ release from SR not reliant on depolarisation
2nd messengers bind to ion channels on membrane:
- cause depolarisation
- which then causes opening of membrane voltage-dependent Ca2+ channels
Ca2+ entry:
- after depolarization, activates SR release of Ca2+ (calcium-induced calcium release, CICR)
