Hypertension Flashcards

1
Q

Q: What is the response of the baroreceptor reflex to high blood pressure?

A

A:

  • When the blood pressure is high, there is increased stretching of the vessel wall,
  • which leads to the activation of mechanically gated sodium (Na+) channels in the sensory nerve endings of the baroreceptors.
  • This results in an increased influx of Na+ and the generation of action potentials that travel via glossopharyngeal and vagus sensory fibers to the medulla, specifically the Nucleus Tractus Solitarius (NTS).
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2
Q

Q: What are the signals transmitted from the Nucleus Tractus Solitarius (NTS)?

A

A:

The NTS relays signals from the glossopharyngeal and vagus nerves to different centers in the medulla. These signals include:

  • NTS to the cardiac inhibitory center in the medulla, leading to a decrease in heart rate.
  • NTS to the cardioacceleratory center in the medulla, leading to a decrease in heart rate.
  • NTS to the vasomotor center in the medulla, leading to a decrease in vasomotor tone and peripheral vascular resistance.
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3
Q

Q: How does preload affect stroke volume and cardiac output?

A

A:

  • Increased preload, which refers to the volume of blood in the ventricles at the end of diastole,
  • leads to an increased stroke volume (SV) and
  • subsequently increased cardiac output (CO).
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4
Q

Q: What is the effect of afterload on stroke volume and cardiac output?

A

A:

  • Increased afterload, which refers to the resistance the heart must overcome to eject blood,
  • leads to a decreased stroke volume (SV) and
  • subsequently decreased cardiac output (CO).
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5
Q

Q: Which center is responsible for inhibiting the parasympathetic nervous system and reducing heart rate in response to high blood pressure?

A

A: The Cardio-Inhibitory Center, located in the Dorsal Nucleus Vagus (part of the parasympathetic nervous system), is responsible for this response.

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6
Q

Q: What neurotransmitter is released by the parasympathetic nervous system to decrease heart rate?

A

A: Acetylcholine (ACh) is released by the parasympathetic nervous system to decrease heart rate.

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7
Q

Q: How does acetylcholine (ACh) decrease heart rate?

A

A:

  • ACh binds to M2 receptors on nodal cells,
  • leading to a decrease in heart rate through the inhibition of adenylate cyclase (AC),
  • a decrease in cyclic adenosine monophosphate (cAMP) levels,
  • and the activation of potassium (K+) channels, resulting in hyperpolarization.
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8
Q

Q: Which center is responsible for inhibiting the sympathetic nervous system and reducing norepinephrine release in response to high blood pressure?

A

A: The Cardio-Acceleratory Center, located in the sympathetic nervous system, is inhibited in response to high blood pressure.

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9
Q

Q: What is the effect of inhibiting the sympathetic nervous system on heart rate and contractility?

A

A: Inhibiting the sympathetic nervous system decreases norepinephrine release, leading to a decrease in heart rate and contractility.

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10
Q

Q: Which center is responsible for inhibiting the sympathetic nervous system and promoting vasodilation in response to low blood pressure?

A

A: The Vasomotor Center, located in the sympathetic nervous system, is inhibited in response to low blood pressure.

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11
Q

Q: How does inhibiting the sympathetic nervous system and promoting vasodilation affect blood pressure?

A

A: Inhibiting the sympathetic nervous system and promoting vasodilation result in a decrease in resistance, an increase in vessel diameter, and a subsequent decrease in blood pressure.

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12
Q

Q: What is the direct renal mechanism of blood pressure regulation?

A

A:

  • The direct renal mechanism involves the kidneys altering blood volume independently of hormones.
  • When blood volume or pressure increases, the filtration rate in the kidney tubules speeds up,
  • leading to increased urine output and a decrease in blood volume and pressure.
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13
Q

Q: What is the renin-angiotensin-aldosterone system (RAAS)?

A

A:

  • The RAAS is an indirect renal mechanism that regulates blood pressure.
  • It involves the production of angiotensin II, a potent vasoconstrictor, through a series of steps involving renin, angiotensinogen, angiotensin I, and angiotensin-converting enzyme (ACE).
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14
Q

Q: What are the actions of angiotensin II?

A

A:

  • stimulates vasoconstriction of systemic arterioles, leading to decreased vessel diameter,
  • increased resistance, and increased blood pressure.
  • It also stimulates the release of aldosterone, which promotes sodium and water retention, further increasing blood volume and pressure.
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15
Q

Q: Which hormone, stimulated by angiotensin II, increases sodium (Na+) and water reabsorption in the distal convoluted tubules of the kidney?

A

A: Aldosterone, produced by the Zona Glomerulosa of the adrenal cortex, increases Na+ and water reabsorption in the distal convoluted tubules of the kidney.

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16
Q

Q: What is the mechanism of action of aldosterone in promoting Na+ reabsorption in the distal convoluted tubules?

A

A:

  • Aldosterone binds to intracellular receptors, activating specific genes that increase the production of proteins involved in Na+ reabsorption, such as Na+ channels, K+ channels, and the Na+/K+/ATPase pump.
17
Q

Q: Which hormone, released from the posterior pituitary gland in response to angiotensin II, promotes water reabsorption in the collecting duct of the kidneys?

A

A:
Anti-Diuretic Hormone (ADH), also known as Vasopressin,
promotes water reabsorption in the collecting duct of the kidneys.

18
Q

Q: How does ADH exert its effects on water reabsorption in the nephron?

A

A:

  • ADH binds to V2 receptors, which activate adenylate cyclase (AC),
  • leading to an increase in cyclic adenosine monophosphate (cAMP) levels.
  • This cascade of events results in the insertion of aquaporin-2 (AQ-II) water channels into the membrane of the collecting duct,
  • increasing water reabsorption.
19
Q

Q: What is the role of the thirst center in response to angiotensin II?

A

A:

  • Angiotensin II stimulates the hypothalamic thirst center,
  • leading to increased water consumption, absorption across the gastrointestinal tract,
  • and ultimately an increase in blood volume and blood pressure.
20
Q

Q: How does atrial natriuretic peptide (ANP) contribute to the regulation of blood pressure?

A

A:

In response to increased stretch on the atrium due to high blood pressure,

ANP is released.

  • ANP promotes vasodilation of systemic arterioles, decreases aldosterone production,
  • inhibits ADH release, reduces water reabsorption in the collecting duct,
  • and decreases Na+ and water reabsorption in the proximal convoluted tubules.
  • These actions collectively decrease blood volume and blood pressure.