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Vocabulary flashcards covering key terms and concepts from the lecture on vascular control, blood pressure regulation, and related mechanisms.
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Mean Arterial Pressure (MAP)
Average arterial pressure; MAP = Cardiac Output × Total Peripheral Resistance.
Cardiac Output (CO)
Volume of blood pumped by the heart per minute; CO = Heart Rate × Stroke Volume.
Stroke Volume
Volume of blood ejected by the ventricle with each contraction; influenced by preload, contractility, and afterload (Frank-Starling).
Arteriolar Radius
Diameter of small arteries/arterioles; changes determine local blood flow and resistance.
Total Peripheral Resistance (TPR)
Overall resistance to systemic blood flow; mainly set by arteriolar radius and blood viscosity.
Blood Viscosity
Internal friction of blood; increases with hematocrit; affects flow and pressure; non-Newtonian at low flow.
Hematocrit
Proportion of blood volume occupied by red blood cells.
Baroreceptor Reflex
Short-term BP control via stretch-sensitive receptors in carotid sinus and aortic arch; modulates sympathetic and parasympathetic activity.
Baroreceptor Resetting
Adaptation of baroreceptors over time to sustained BP changes, returning sensitivity to a new baseline.
Dynamic Baroreceptor Response
Rapid, initial response to a change in BP (phasic phase).
Static Baroreceptor Response
Sustained response to a constant BP (tonic phase).
Baroreceptor Afferent Pathways
Afferent signals from baroreceptors to the medulla to regulate autonomic outflow.
Vasomotor Centre
Brainstem region that modulates sympathetic outflow to blood vessels.
Sympathetic Vasomotor Nerves
Nerves originating in the vasomotor centre; release norepinephrine; α-receptors cause vasoconstriction; β2-receptors can cause vasodilation in select beds.
Parasympathetic Effect on Vessels
Limited direct effect on vascular resistance; mainly affects heart rate and contractility.
Alpha-adrenergic Receptors (α)
Receptors that mediate vasoconstriction when activated by norepinephrine/adrenaline.
Beta-2 Adrenergic Receptors (β2)
Receptors that mediate vasodilation in tissues with high β2 density (e.g., heart, lungs, skeletal muscle) in response to epinephrine.
Extrinsic Vasoconstrictor Control
Nervous and hormonal mechanisms (e.g., sympathetic nerves, circulating factors) that tighten vessels to raise BP.
Renin-Angiotensin-Aldosterone System (RAAS)
Hormonal cascade increasing BP via vasoconstriction (Ang II) and Na+/water retention (aldosterone).
Angiotensin II
Potent vasoconstrictor; stimulates aldosterone release; raises BP.
Aldosterone
Mineralocorticoid increasing Na+ reabsorption and water retention in the kidneys.
Renin
Kidney enzyme that begins RAAS by converting angiotensinogen to angiotensin I.
Antidiuretic Hormone (ADH/AVP)
Promotes water reabsorption; vasoconstrictor at high levels; helps regulate BP and volume.
Atrial Natriuretic Peptide (ANP)
Vasodilator that promotes natriuresis and diuresis; lowers blood volume and BP.
Bainbridge Reflex
Atrial stretch increases heart rate via atrial receptors.
Endothelin
Endothelium-derived vasoconstrictor; activity linked to local oxygen demand.
Nitric Oxide (NO)
Endothelium-derived vasodilator; increases blood flow by relaxing smooth muscle.
Reactive Hyperemia
Increased blood flow after blockage is removed; flow exceeds baseline due to accumulated metabolites.
Active Hyperemia
Increased blood flow to metabolically active tissue to meet demand.
Autoregulation
Local mechanism maintaining constant tissue perfusion despite changes in perfusion pressure.
Myogenic Mechanism
Vascular smooth muscle response to stretch; contraction reduces flow when pressure rises.
Metabolic Regulation (Autoregulation)
Vasodilation driven by metabolic byproducts (CO2, H+, K+, adenosine) and reduced O2.
Adenosine
Metabolic mediator causing vasodilation, especially in the heart.
Bradykinin
Vasodilator peptide that increases blood flow during inflammation.
Endothelin and NO Balance
Endothelin (vasoconstrictor) and NO (vasodilator) balance to match tissue oxygen needs.
Peripheral Chemoreceptors
Carotid and aortic bodies detect low PaO2, high PaCO2, H+; mainly regulate ventilation; minor BP effect.
Central Chemoreceptors
Medullary sensors detect CO2/H+; cause vasoconstriction and raise peripheral resistance.
Autoregulation and the Kidney
Renal mechanisms contribute to long-term BP control via pressure diuresis/natriuresis and RAAS interactions.
Frank-Starling Mechanism
Increased venous return increases stroke volume due to greater myocardial stretch.
Venous Return
Volume of blood returning to the heart per minute; aided by skeletal muscle pump, respiratory pump, and venous valves.
Skeletal Muscle Pump
Muscle contractions press on veins to propel blood toward the heart.
Respiratory Pump
Breathing-induced changes in thoracic pressure that aid venous return.
Blood Volume and BP Regulation
Long-term BP control via circulating volume; kidneys adjust Na+ and water balance.
EDV (End-Diastolic Volume)
Volume of blood in ventricles at end of diastole; sets preload for the next beat.
Flow–Pressure Relationship in Blood
Local flow and pressure depend on viscosity, vessel radius, and autoregulation.
EPO and Blood Viscosity
Erythropoietin raises hematocrit; increases viscosity and can affect risk of adverse events in athletes.
Long-Term BP Control Summary
MAP ≈ CO × TPR; CO = HR × stroke volume; long-term BP is governed by renal and hormonal regulation of blood volume.