Regulation of BP Flashcards

1
Q

Resistance is equal to…

A

8nl / pi x r^4

Most effective way to alter flow in the arterial system is to increase or decrease the radius

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2
Q

2 ways the autonomic NS controls BP (short term)

A
  1. Vasoconstriction and vasodilation

2. Altering CO

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3
Q

3 prevertebral ganglia

A

Celiac
Superior mesenteric
Inferior mesenteric

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4
Q

Where is sympathetic NS mediated vasocontriction most and least powerful

A

Most: kidneys, intestine, spleen, skin
Less: skeletal muscle, myocardium, brain

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5
Q

Venoconstriction

A

Can lead to an increase in CO and then BP

Because of the increased return to the heart, leading to an increase in LVEDV

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6
Q

Post-ganglionic nerves from parasymp NS activate which receptors?

A

M2 muscarinic receptors
Decreases automaticity in the SA and AV nodes
Leads to a decrease in HR, CO, and BP

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7
Q

Baroreceptor reflex

A

Increased carotid artery and aortic pressure
Afferent sensory fibers from carotid sinus and aortic arch baroreceptors sense it
Travel via glossopharyngeal and vagus nerve to medulla and pons
Inhibitory fibers to the vasoconstrictor center, excitatory fibers to the vasodilatory center
Decrease symp outflow, increase parasymp outflow
Drops too low, and there will be a net increase in symp outflow (negative feedback)

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8
Q

How is long term regulation of BP achieved?

A

Modulation of solute and water reabsorption or excretion by the kidney

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9
Q

Renin-Angiotensin-Aldosterone System

A

JG cells on afferent arteriole make, store and release renin
Decrease afferent arteriole pressure stimulates release (also released with B1-adrenoceptor stimulation)
Macula densa cells in distal tubule sense the concentration of Na and Cl in fluid (decreased amounts stimulate renin release)
Renin cleaves angiotensinogen into angiotensin 1
A1 cleaved to A2 by ACE in pulmonary capillaries

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10
Q

5 main physiologic effects of angiotensin II

A

Systemic vasoconstriction
Enhanced Na Cl reabsorption across distal tubules (and water too)
Stimulates adrenal cortex to release aldosterone
Stimulates the posterior pituitary to release ADH (vasopressin)
Stimulates thirst centers in hypothalamus

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11
Q

Aldosterone

A

Released by the adrenal cortex

Acts on the kidneys to increase Na, Cl, and water reabsorption from the dital tubules

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12
Q

Vasopressin

A

Also called antidiuretic hormone
Released from the posterior pituitary gland
Increases water retention in the collecting ducts of the kidney

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13
Q

Natriuretic peptides

A

Counter-regulatory system to RAAS

Hormones that are synthesized by the heart, brain, etc in response to distension of the atra and ventricles

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14
Q

Physiologic effects of natriuretic peptides

A

Venodilation
Decreased central venous pressure
Decreased venous return to the right heart
Decreased CO
Dilation of arteries
Increase GFR and filtration at kidneys (Na and water excretion)

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15
Q

Nitric Oxide

A

Released from endothelial cells in response to shear stress and hormones
Activates guanylate cyclase in vascular smooth muscle cells, leading to the conversion of GTP to cGMP and activation of cGMP-dependent kinase
Ultimately causes the vascular smooth muscle to relax and blood vessels to dilate

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16
Q

2 theories behind autoregulation

A

Metabolic theory

Myogenic theory

17
Q

Metabolic theory

A

At higher BPs, increased tissue blood flow washes out the tissue factors that cause vasodilation
Leads to vasoconstriction, increased resistance, and return of blood flow to normal levels

18
Q

Myogenic theory

A

Sudden stretch of blood vessel walls as a result of increased tissue perfusion pressure causes the smooth muscle layer to contract
Leads to vasoconstriction, increased resistance, and return of blood flow to normal levels

19
Q

How does
1. The accumulation of CO2 and H+
2. The depletion of O2 and CO2
affect blood flow in the brain

A
  1. Vasodilation

2. Vasoconstriction

20
Q

3 stimuli for renin release

A

Decreased NaCl sensed by macula densa cells
Decreased perfusion pressure sensed by JG cells
B1 adrenergic stimulation