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CardioRespiratory Year 1 > Hormonal control of blood pressure > Flashcards

Hormonal control of blood pressure Flashcards

1
Q

what are the two systems that regulate blood pressure

A
  • neuronal system - fast acting

- hormonal system - slow acting

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2
Q

what does the juxtaglomerular apparatus consist of

A

three structures

  • afferent arteriole
  • efferent arteriole
  • distal tubule
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3
Q

what lines the wall of the distal tubule

A

macula densa cells

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4
Q

what are macula densa cells

A
  • these are the sodium sensors
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5
Q

where are the juxtaglomerular cells

A

they are around the end of the proximal tubule

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6
Q

what do the juxtaglomerular cells contain

A

they contain the enzyme renin

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7
Q

what happens when the sodium concentration is too low

A
  1. the macular densa cells act via local hormones
  2. the local hormones cause the relaxation of the smooth muscle of the afferent arterioles this increases the GFR
  3. they then signal the juxtaglomerular cells which increase the release of renin into the blood stream
  4. renin released from the juxtaglomeruar cells pass into the Venus blood where it meets the globular protein angiotensinogen
  5. the renin enzyme splits of a decapeptide called angiotensin I from the angiotensinogen precursor
  6. when angiotensin I passes through the lungs it is further cleaved by endothelial bound angiotensin-converting enzymes (ACE) into an octave-tide angiotensin II
  7. angiotensin II passes into the arterial blood in the arterioles and acts on a G protein coupled receptor which activates phospholipase C and increases the cytosolic calcium concentrations which triggers the constriction of the smooth muscle of systemic arterioles therefore increasing the blood pressure
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8
Q

what secretes angiotensinogen

A

liver

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9
Q

describe the steps of the angiotensinogen pathway

A
  1. renin released from the juxtaglomeruar cells pass into the Venus blood where it meets the globular protein angiotensinogen
  2. the renin enzyme splits of a decapeptide called angiotensin I from the angiotensinogen precursor
  3. when angiotensin I passes through the lungs it is further cleaved by endothelial bound angiotensin-converting enzymes (ACE) into an octave-tide angiotensin II
  4. angiotensin II passes into the arterial blood in the arterioles and acts on a G protein coupled receptor which activates phospholipase C and increases the cytosolic calcium concentrations which triggers the constriction of the smooth muscle of systemic arterioles therefore increasing the blood pressure
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10
Q

how does renin increase blood pressure

A

renin via its product angiotensin II raises the total peripheral resistance and after load
- therefore it assumes a constant cardiac output and raises blood pressure

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11
Q

what are the ways in which renin can be released

A
  • sympathetic activation

- juxtaglomerular cells

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12
Q

How is renin released by sympathetic activation

A
  • there are sympathetic nerves to the kidney via the renal nerve (sympathetic efferent) and there are beta receptors on the juxtaglomerular cells which when stimulated causes renin release
  • this means that in addition to the vasoconstriction due to noradrenaline the sympathetic nervous system can produce further vasoconstriction via increased renin and angiotensin release
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13
Q

what receptors do the juxtaglomerular cells have

A

beta receptors

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14
Q

what type of feedback is renin angiotensin

A

negative feedback system for hormonal control of blood pressure

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15
Q

how is blood pressure controlled by GFR

A
  • a decrease in blood pressure causes a decrease in GFR which causes renin angiotensin release which raises blood pressure and restores GFR therefore in this case the renin angiotensin acts as a negative feedback loop
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16
Q

what is a problem with the theory that blood pressure is controlled by the GFR

A
  • GFR is autoregulated by the local tubulglomerular feedback
  • this means that rises in blood pressure triggered by angiotensin II do not increase GFR unless the blood pressure rise is so high that it is outside the autoregulation range
17
Q

what is a better theory than blood pressure being controlled by the GFR

A

better idea is that the renin-angiotensin system is involved in the control of blood volume

  • this is because angiotensin receptors are found on cells in the adrenal cortex as well as vascular smooth muscle
  • these cells secrete the mineralocorticoid steroid hormone aldosterone in to the blood stream
18
Q

what is the action of aldosterone

A
  • acts on the channel proteins in wall of of the distal tubule of the kidney
  • the channels when stimulated by aldosterone increase reabsorption of sodium from the tubular fluid back into the blood
  • this increases water reabsorption by osmosis
  • so the net result is a decrease in urinary loss of sodium and water and an increase in circulating blood volume
19
Q

what is the action of channel proteins in the distal tubule of the kidney

A
  • the channel proteins can take up sodium from the tubular fluids and pump it back into the blood
20
Q

what is renin release increased by

A

low sodium in the distal tubular fluid

21
Q

what causes low sodium in the distal tubular fluid

A

low sodium int he arterial blood which is called hyponatremia

22
Q

what happens if blood levels of sodium are low

A
  • the renin-angiotensin-aldosterone system acts to increase sodium reabsorption in the kidney which restores the level to normal
  • as sodium is reabsorbed water follows by osmosis and so both water and sodium are retained in the body and the blood volume increases
  • this is a negative feedback system for control of blood volume
23
Q

why does the renin angiotensin aldosterone (RAA)

A
  • if the blood pressure is too low water can move from the interstitial spaces into the blood as the blood passes through the capillaries
  • this dilutes the blood and cause hyponatremia
  • by raising the systemic blood pressure the renin-angiotensin-aldosterone system pushes the water back into the interstitial space where it belongs and restores the balance between plasma and interstitial water
24
Q

what is the overall RAA effect on sodium reabsorption

A
  • overall by mainpulating sodium reabsorption and blood pressure the RAA system keeps the interstitial fluid and circulating blood volumes at correct levels and therefore ensures adequate perfusion of all organs
25
Q

How can the RAA system malfunction

A
  • renal artery or afferent arterioles are narrowed due to atheroma formation
  • this reduces the GFR at normal blood pressure so more sodium is absorbed in the proximal tubule this leads to the reduced sodium concentration in the distal tubule
  • juxtaglomerular cells release renin, causing a chronically raised systemic blood pressure.
  • Excess aldosterone actions will cause excess sodium retention and thus excess total body water.
  • The person will have chronic hypertension and excess body water and salt.
26
Q

what are the drugs used to block hypertension If hypertension Is due to excess renin release

A
  • ACE inhibitors

- angiotensin receptor antagonists

27
Q

what is the mechanism of action of ACE inhibitors

A

eg captopril). These block angiotensin converting enzyme and thus prevent formation of Angiotensin II.

28
Q

name an example of an ACE inhibitor

A

captopril

29
Q

what is the mechanism of action of angiotensin receptor antagonists

A

These block angiotensin receptors

30
Q

name an example of an angiotensin receptor antagonists

A

losartan

31
Q

what are drugs used to reduce hypertension due to excess aldosterone levels

A

diuretics such as ..

  • thiazide derivative
  • aldosterone antagonists
  • loop diuretics
32
Q

what is the mechanism of action of Thiazide derivatives

A

eg bendroflumethiazide) these block a sodium-chloride symporter in the distal tubule (not the Enac channel)

33
Q

name an example of Thiazide derivatives

A

eg bendroflumethiazide)

34
Q

name an example of a aldosterone antagonist

A

eg spironolactone

35
Q

what are the adverse effects of ACE inhibitors

A

Bradykinin is a peptide derived from endothelium- believed to be the cause of dry cough

  • bradykinin is converted to inactive metabolites by ACE therefore inhibition of this leads to increased levels of bradykinin which causes a dry cough through bronchoconstriction
  • bradykinin may also result in angloedema, this is deem in the subcutaneous tissues
  • effect afro0caribbean patents more therefore ACE inhibitors are not the first line of defence for treating these patients

CardioRespiratory Year 1 (28 decks)

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