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Questions and Answers
What is the primary function of the kidneys in long-term blood pressure regulation?
What is the primary function of the kidneys in long-term blood pressure regulation?
According to the Guyton model, what are the two mechanisms available to move the equilibrium point for long-term arterial pressure?
According to the Guyton model, what are the two mechanisms available to move the equilibrium point for long-term arterial pressure?
What is the effect of an abrupt increase in total peripheral resistance on long-term blood pressure, assuming normal renovascular resistance and renal function?
What is the effect of an abrupt increase in total peripheral resistance on long-term blood pressure, assuming normal renovascular resistance and renal function?
What is the relationship between increased arterial pressure and renal function according to the concept of pressure diuresis?
What is the relationship between increased arterial pressure and renal function according to the concept of pressure diuresis?
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What is the purpose of the infinite feedback gain mechanism described in the Guyton model of long-term blood pressure regulation?
What is the purpose of the infinite feedback gain mechanism described in the Guyton model of long-term blood pressure regulation?
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What is the effect of a rapid infusion of 400 mL of blood on arterial pressure, cardiac output, and urine output according to the text?
What is the effect of a rapid infusion of 400 mL of blood on arterial pressure, cardiac output, and urine output according to the text?
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What is the primary cause of the increased sympathetic outflow and vasomotor center overactivity in autonomic hyperreflexia?
What is the primary cause of the increased sympathetic outflow and vasomotor center overactivity in autonomic hyperreflexia?
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What is the typical time course of the blood pressure changes in autonomic hyperreflexia?
What is the typical time course of the blood pressure changes in autonomic hyperreflexia?
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What is the primary mechanism underlying the development of primary hypertension?
What is the primary mechanism underlying the development of primary hypertension?
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Which of the following is a key characteristic of salt sensitivity in primary hypertension?
Which of the following is a key characteristic of salt sensitivity in primary hypertension?
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Which of the following drug classes is used to treat primary hypertension by blocking the renin-angiotensin system?
Which of the following drug classes is used to treat primary hypertension by blocking the renin-angiotensin system?
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Which of the following is a long-term mechanism involved in the integration of multiple systems to regulate blood pressure?
Which of the following is a long-term mechanism involved in the integration of multiple systems to regulate blood pressure?
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What is the main determinant of extracellular fluid (ECF) volume according to the text?
What is the main determinant of extracellular fluid (ECF) volume according to the text?
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In chronic hypertension, what is almost always the cause according to the text?
In chronic hypertension, what is almost always the cause according to the text?
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What is a consequence of volume-loading hypertension as described in the text?
What is a consequence of volume-loading hypertension as described in the text?
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In volume-loading hypertension, what is a result of hypertension rather than the cause?
In volume-loading hypertension, what is a result of hypertension rather than the cause?
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Which mechanism allows a small increase in cardiac output to result in a much larger increase in arterial pressure?
Which mechanism allows a small increase in cardiac output to result in a much larger increase in arterial pressure?
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What stimulates the H-P-A axis to secrete ADH according to the text?
What stimulates the H-P-A axis to secrete ADH according to the text?
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What is the primary mechanism by which inadequate dialysis leads to volume-loading hypertension?
What is the primary mechanism by which inadequate dialysis leads to volume-loading hypertension?
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What is the primary role of the renin-angiotensin-aldosterone system in regulating blood pressure?
What is the primary role of the renin-angiotensin-aldosterone system in regulating blood pressure?
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How does the renin-angiotensin-aldosterone system respond to variations in salt intake?
How does the renin-angiotensin-aldosterone system respond to variations in salt intake?
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What is the main mechanism by which coarctation of the aorta leads to hypertension?
What is the main mechanism by which coarctation of the aorta leads to hypertension?
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What is the primary mechanism by which preeclampsia leads to hypertension?
What is the primary mechanism by which preeclampsia leads to hypertension?
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How does neurogenic hypertension differ from other types of hypertension discussed?
How does neurogenic hypertension differ from other types of hypertension discussed?
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Autonomic hyperreflexia is a condition that leads to a permanent increase in blood pressure.
Autonomic hyperreflexia is a condition that leads to a permanent increase in blood pressure.
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In primary hypertension, the increased sympathetic nervous system activity is a secondary effect rather than a primary cause.
In primary hypertension, the increased sympathetic nervous system activity is a secondary effect rather than a primary cause.
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Diuretics and natriuretics are used to treat primary hypertension by directly relaxing vascular smooth muscle.
Diuretics and natriuretics are used to treat primary hypertension by directly relaxing vascular smooth muscle.
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The renin-angiotensin system is a long-term mechanism involved in the integration of multiple systems to regulate blood pressure.
The renin-angiotensin system is a long-term mechanism involved in the integration of multiple systems to regulate blood pressure.
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Increased salt sensitivity is a key characteristic of primary hypertension that often increases with age.
Increased salt sensitivity is a key characteristic of primary hypertension that often increases with age.
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The purpose of the infinite feedback gain mechanism described in the Guyton model is to move the equilibrium point for long-term arterial pressure.
The purpose of the infinite feedback gain mechanism described in the Guyton model is to move the equilibrium point for long-term arterial pressure.
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In chronic hypertension, the primary cause is almost always a decrease in total peripheral resistance.
In chronic hypertension, the primary cause is almost always a decrease in total peripheral resistance.
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Autonomic hyperreflexia is a condition that only occurs in patients with spinal cord injuries below T10.
Autonomic hyperreflexia is a condition that only occurs in patients with spinal cord injuries below T10.
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Increased physical activity is a recommended treatment for primary hypertension.
Increased physical activity is a recommended treatment for primary hypertension.
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Study Notes
Regulation of Blood Pressure
- Pressure Diuresis: mechanism by which increased arterial pressure produces increased renal water loss and salt loss
- Renal Function Curve: urinary volume increases with increasing arterial pressure, as does urine sodium output
Long-term Blood Pressure Regulation
- Primarily a function of the kidneys in regulating salt and water balance with nervous and hormonal input
- Pressure Diuresis and Pressure Natriuresis: increased arterial pressure produces increased renal water loss and salt loss
Infinite Feedback Gain Mechanism
- Based on two intersecting curves: Renal Function Curve and Salt and H2O intake curve
- Equilibrium point is where the two lines intersect
Determinants of Long-term Arterial Pressure
- Two mechanisms available to move the equilibrium point: shift the Renal Function Curve along the pressure axis or alter the salt and water intake
- Effect of Total Peripheral Resistance on Long-term Blood Pressure: abrupt increase in total peripheral resistance may produce a short-term increase in arterial pressure, but returns to normal with normal renovascular resistance and renal function
Effect of Increased Cardiac Output on Arterial Pressure
- Two mechanisms: direct effect and increased total peripheral resistance via autoregulation
- Makes it possible for a small increase in cardiac output to result in a much larger increase in arterial pressure
Importance of Salt Intake
- Salt accumulation is the main determinant of ECF volume
- Mechanisms: increased fluid osmolality stimulates the thirst center and increased osmolality stimulates the H-P-A axis to secrete ADH
Chronic Hypertension
- Almost always a result of impaired renal fluid excretion
- Main complications: excess work load on the heart, injury to vascular endothelium, neurovascular disease, and renal injury or failure
Volume-Loading Hypertension
- Hypertension resulting from excess accumulation of extracellular fluid
- Examples: decreased renal mass and increased salt, dialysis in renal failure, and aldosteronism
- Mechanism: excess fluid load leads to increased cardiac output, which increases arterial pressure, followed by increased total peripheral resistance
Renin-Angiotensin System
- Actions of Angiotensin II: vasoconstriction, decreased excretion of salt and water by kidneys, direct effect on tubular cells, renal arteriolar constriction, and stimulates aldosterone release
- Onset of action: slower in onset than nervous control, but begins to work in minutes and reaches full acute effect in ~20 minutes
- Variation in Salt Intake: negative feedback in the Renin-Angiotensin system compensates for a wide variation in salt intake
Hypertension Involving Angiotensin
- One-Kidney Goldblatt: acute renal artery constriction produces a rapid rise in renin and blood pressure due to angiotensin-induced vasoconstriction and salt and water reabsorption
- Two-Kidney Goldblatt: partial occlusion of one renal artery produces decreased perfusion pressure and release of renin, leading to increased angiotensin and aldosterone, and salt and water retention in the normally perfused kidney
Other Types of Hypertension
- Coarctation of the Aorta: constriction of the aorta distal to the branches feeding the head and neck, but proximal to the renal arteries, resulting in hypertension proximal to constriction and normotension distal
- Preeclampsia: believed to result from ischemic areas of the placenta releasing substances toxic to vascular endothelium, leading to vasoconstriction and hypertension
- Neurogenic Hypertension: following sympathetic discharge due to excitation or anxiety
- Autonomic Hyperreflexia: stimulus below level of injury, activation of spinal reflex, vasoconstriction, vasodilation, bradycardia, and baroreflexes
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