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These vocabulary flashcards cover the neural, hormonal, and renal mechanisms of blood-pressure regulation, as well as related clinical conditions and blood-flow concepts discussed in the lecture notes.
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Blood Pressure (BP)
The force that blood exerts on the arterial walls, measured in millimeters of mercury (mm Hg).
Short-Term Neural Control
Rapid regulation of BP through nervous system reflexes that alter vessel diameter and cardiac output.
Vasoconstriction
Narrowing of blood vessels that increases peripheral resistance and raises blood pressure.
Vasodilation
Widening of blood vessels that decreases peripheral resistance and lowers blood pressure.
Medulla Oblongata
Brainstem region housing cardiovascular centers that integrate baroreceptor and chemoreceptor input.
Vasomotor Center
Portion of the medulla that controls blood vessel diameter via sympathetic efferent fibers.
Cardioacceleratory Center
Medullary center that increases heart rate and contractility, boosting cardiac output.
Cardioinhibitory Center
Medullary center that decreases heart rate, reducing cardiac output.
Baroreceptors
Stretch‐sensitive pressure receptors in the carotid sinuses and aortic arch that detect changes in arterial BP.
Chemoreceptors
Receptors in the aortic arch and large neck arteries that respond to high CO₂, low pH, or low O₂.
Higher Brain Centers
Hypothalamic regions that modify cardiovascular activity during exercise, temperature change, and emotions.
Peripheral Resistance (TPR)
Opposition to blood flow in the systemic circulation, chiefly influenced by arteriolar diameter.
Cardiac Output (CO)
Volume of blood the heart pumps per minute; product of heart rate × stroke volume.
Short-Term Hormonal Control
Endocrine mechanisms that quickly adjust BP by altering CO or TPR.
Adrenal Medulla Hormones
Epinephrine and norepinephrine released during stress that increase CO and produce vasoconstriction.
Epinephrine
Adrenal hormone that acts on β₁ receptors of the heart to raise heart rate and contractility.
Norepinephrine
Adrenal hormone that primarily causes α-mediated vasoconstriction of arterioles.
Angiotensin II
Potent vasoconstrictor formed in the renin-angiotensin pathway; raises BP and stimulates aldosterone.
Antidiuretic Hormone (ADH)
Posterior pituitary hormone that promotes water reabsorption; at high levels it also causes vasoconstriction.
Atrial Natriuretic Peptide (ANP)
Atrial hormone that lowers BP by promoting salt and water loss and causing vasodilation.
Long-Term Renal Regulation
Slow BP control via the kidneys by adjusting blood volume through direct and indirect mechanisms.
Direct Renal Mechanism
Kidney response that alters urine output directly to influence blood volume and BP.
Renin-Angiotensin-Aldosterone System (RAAS)
Indirect renal pathway that increases blood volume and vasoconstriction to elevate BP.
Hypertension
Chronic resting BP ≥ 140/90 mm Hg; major risk factor for cardiovascular and renal disease.
Primary Hypertension
High BP with no identifiable cause; accounts for about 90 % of cases.
Secondary Hypertension
Elevated BP due to identifiable disorders such as renal artery obstruction or endocrine disease.
Hypotension
Resting BP below 90/60 mm Hg; problematic if it leads to inadequate tissue perfusion.
Orthostatic Hypotension
Temporary BP drop and dizziness upon standing due to delayed vascular adjustment.
Circulatory Shock
Condition in which blood vessels are inadequately filled, compromising tissue perfusion.
Hypovolemic Shock
Shock resulting from large-scale blood or fluid loss.
Vascular Shock
Shock caused by extreme vasodilation and a sharp fall in peripheral resistance.
Cardiogenic Shock
Shock occurring when the heart cannot sustain adequate circulation.
Tissue Perfusion
Blood flow through body tissues, delivering oxygen/nutrients and removing wastes.
Intrinsic (Autoregulation) Control
Local adjustment of blood flow to match a tissue’s immediate metabolic needs.
Extrinsic Control
Systemic regulation of blood flow via sympathetic nerves and circulating hormones.