Central and humoral control of blood pressure (montemayor LECT) Flashcards

1
Q

what 9s the short term BP regulation mechanism

A

Neural

Effectors: Cardiac (SA node, myocardium)
Vascular smooth muscle
Adrenal medulla

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2
Q

what is the long term BP regulation mechanism

A

Endocrine/Paracrine
Effectors:
Vascular smooth muscle
Kidneys (regulation of blood volume)

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3
Q

what happens with massive sympathetic discharge on cerebral and cardiac?
what about skin, renal and splanchnic

A

Minimal effect: cerebral and cardiac resistance vessels

Significant constriction: skin, renal, and splanchnic vessels

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4
Q

what is the difference in TPR control of resting versus exercising skeletal muscle?

A

Resting skeletal muscle: neural control dominates (vasoconstrictor tone)

Exercising skeletal muscle:
intrinsic regulation dominates (vasodilation)
Local metabolic effect in active tissue overrides general sympathetic output during exercise

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5
Q

what does B1 agonist do to funny current

A

If (diastolic Na+ current)
Increases steepness of phase 4 slow depolarization

increases rate of slow depolarization

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6
Q

what does B1 agonist do to ca current

A

Increases steepness of phase 4 slow depolarization
Threshold more negative (reached sooner)

shorter diastolic duration and threshold reached more rapidly so increased HR

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7
Q

how does sympathetic input increase contractility

A

↑ Ca2+ influx via L-type DHDP channels: ↑ [Ca2+]i and ↑ Ca2+-dependent Ca2+ release from the SR

  1. ↑ sensitivity of RYR to [Ca2+]i
  2. ↑ SERCA activity (remove phospholamban inhibition), ↑ Ca2+ stores
  3. ↑ ECF Ca2+ influx, ↑ SR Ca2+ stores over time

Increase

Ca2+ –> ↑ contractile force –> ↑ SV –> ↑ CO

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8
Q

how can there be parasympathetic influence on TPR

A

postganglionic parasympathetic ACh release acts on muscarinic receptors on endothelium of vasculature. this releases NO which causes vasodilation

so this is all indirectly

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9
Q

what are the 3 currents that parasympathetic innervation influences and what does it do to these currents

A

Increased K+ conductance:
More negative maximum diastolic potential (KAch channel)

Decreased funny current:
Decreases slow depolarization rate (steepness of phase 4)

Decreased ICa:
Decreases slow depolarization rate (steepness of phase 4)
Threshold more positive (takes longer to reach)

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10
Q

what is the main integration center in the brain

A

medulla oblongata

key for regulating homeostasis of MAP

mediates sympathetic and parasympathetic effects

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11
Q

what is the bainbridge reflex

A

an increase in venous return causes increased right atrial pressure

these will cause an increase in HR to move blood through more quickly

this opposes the high pressure baroreceptor reflex

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12
Q

accumulation of too much CO2 is usually associated with

A

decreased MAP

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13
Q

what do chemoreceptors do in response to too much CO2 (decreased ph)

A

stimulates vasoconstriction leading to increased TPR

and the opposite happens for decreased CO2 (decrease vasoconstriction)

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14
Q

what happens with exercise and CO2 (peripheral)

A

there is usually normal CO2 levels b/c of hyperventilating during exercise

If PaCO2 incrases then there is going to be generalized vasoconstriction

intrinsic control of exercsiing muscle maintains vasodilation

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15
Q

what happens in cerebral ischemia

A

Local ↑ Pco2, ↑ [H+] leads to peripheral vasoconstriction

Prolonged severe ischemia leads to extreme depression of cerebral function –> MAP falls

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16
Q

what is the chemoreceptor response normally

A

↓ PO2
↑ Pco2
↓ pH,↑ [H+]
Stimulates increased ventilation
Afferents from pulmonary stretch receptors inhibit the cardioinhibitory center → ↑ HR
Increased ventilation: ↓ Pco2 (↓ [H+]) in the brain, inhibiting the cardioinhibitory center → ↑ HR

Net Physiologic Effect: ↑ Sympathetic N.S.
↑ HR
↑ TPR (↑ vasoconstriction)
↑ MAP

17
Q

what is a vasoactive substance

A

endocrine or paracrine factor that impacts vasodilation or vasoconstriction

18
Q

what are the major vasoconstrictors?

A
epinephrine
serotonin
ANG II
AVP (ADH) 
Endothelin
19
Q

what are the major vasodilators

A
Epinephrine 
histamine
ANP
Bradykinins
NO
20
Q

what causes Macula densa cells (of the renal juxtaglomuler apparatus) to secrete renin?

A

Detection of decrease Na in the distal tubule
which represents a decrease in MAP and decrease in GFR leading to increased Na reabsorption

SNS also stimulates renin release

21
Q

what happens when renin is secreted?

A

*Converts angiotensinogen –> ANG I

ACE then converts ANG I to ANG II

22
Q

what are the six effects of ANG II

A
Vasoconstriction
Stimulates adrenal gland aldosterone production
Stimulates ADH/AVP
Stimulates thirst
Stimulates renal Na+ reabsorption
Stimulates SNS activity
23
Q

what does aldosterone do and what is it secreted from?

A

Secretion by adrenal cortex triggered by ANG II

Promotes renal Na+ reabsorption

H2O follows by osmosis

↑ Effective Circulating Volume

↑ MAP