control of arterial BP Flashcards

1
Q

high pressure (arterial) baroreceptors

A

exposed nerve endings, measure stretch

carotid sinus
aortic baroreceptors

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2
Q

carotid sinus

A

loc at fork of carotid arteries
glossopharyngeal n.
cerebral blood flow
greater sensitivity = major high pressure sensor

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3
Q

aortic baroreceptors

A

arch of aorta
vagus n.
entire CV system

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4
Q

low pressure (cardiopulmonary) baroreceptors

A

cardiac atria/pulmonary artery

Sense: venous return, CVP, blood volume

Two types:

1) A - sense atrial wall tension -> HR
2) B - sense atrial stretch -> volume

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5
Q

chemoreceptors

A

carotid bodies & aortic bodies

regulation of breathing

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6
Q

baroreceptors sense

A

absolute P
rate of P change
~ inc P more sensitive to rate of change

adjustable - the thermostat -> doesn’t help w long term control

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7
Q

NTS

A

nucleus tractus soltarius
the cardiovascular center in the medulla oblongata

Inhibits; Vasomotor Center
Innervates: Cardioinhibitory center

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8
Q

Vasomotor centor

A

vasoconstrictor
pos chronotropic/iontropic response
SNS

inhibited by NTS
inc BP -> inc firing -> inc inhib of vasomotor c

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9
Q

cardioinhibitory center

A

activates vagal outputs to heart
reduce HR

excited by NTS

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10
Q

alpha1 adrenergic receptors

A

smooth mm

constriction

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11
Q

alpha2 adrenergic receptors

A

sympathetic n. endings
inhibit NE release
Autoreceptor -> neg feedback (leads to some level of vasodilation)

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12
Q

beta1 adrenergic receptors

A

cardiac myocytes

inc HR and inotropy

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13
Q

beta2 adrenergic receptors

A

vascular smooth mm beds (esp skel mm)

vasodilation

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14
Q

baroreceptor reflex

A

short term; modifies HR & TPR to control mean arterial BP

long-term, is a thermostat gets reset to the new pressure - not helpful in hypertension

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15
Q

humoral control

A

1) vasoactive - released into blood, often affect vascular smooth mm cell contraction
2) nonvasoactiv - target organs outside CV system, often modulate effective circ vol

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16
Q

biogenic amines

A

epinephrine
serotonin (5HT)
histamine

17
Q

peptides

A

angiotensin II
atrial natriuretic peptide
arginine vasopressin (AVP/ADH)
endothelins (ET)

18
Q

renin-angiotensin system, what does the final product do?

A

chronic maintenance of BP
forms Angiotensin II
- short term; potent vasocon(half life 30s
- thirst, inc ADH -> in H20 retention -> inc Blood vol -> inc PL and CO and BP
- aldosterone -> inc NACL reabsorb -> inc H2O retention

19
Q

pathway of Angiotensin II production

A

dec BP -> secretion of Renin + Angiotensinogen -> angiotensin I + angio converting enzyme (ACE) -> Angio II

20
Q

arginine vasopressin / antidiuretic hormone

A

regulates water retention in kidney
inc # of water channels

syn in paraventricular & supraoptic nuc of the hypothalamus
posterior pituitary gland
circumventricular organ - senses osmolarity
hyperosmolarity -> inc ADH secretion

atrial&pulmonary Baroreceptors also control it, when blood vol is low AVP secretion is disinhibited

21
Q

atrial natriuretic peptide

A

syn/stored by atrial myocytes
strech -> release of ANP

antagonizes effects of Ang II and dec effective blood vol
Functions:
1 - relax smooth mm (not major effect)
2 - relax arterioles to kidney to in filtration and reduce renin release
3 - inhibits aldosterone secretion by adrenal cortex
4 - inhibits Na reabsorption in Kidney
5 - inhibits secretion of ADH

22
Q

aldosterone

A

inc Na reabsorb -> inc H2O retention -> blood vol

release in resp to Angio II

23
Q

nitric oxide

A

bradykinin and Ach stim “constitutive endothelial NO synthase (ceNOS) which makes NO from arginine

NO act guanylyl cyclase, the enzyme that makes cGMP
cGMP act cGMP-dep protein kinase (PKG) that inhibits myosin light chain kinase and act SERCA Ca pump
= VASODILATION

Shear stress - stim NO synthesis
high velocity -> high sheer stress

24
Q

septic shock and NO

A

inc inducibleNOsynthase (in endothelium and smooth mm) -> massive inc in NO -> HUGE dec TPR and BP

25
Q

nitrates and angina

A

Clinical action:
nitroglycerin -> NO _> venovasodilation-> dec PL -> dec SV -> dec work of heart = reduce demand of O2 (not supply)

Normally:
NO dilates resistance vessels - dec TPR and afterload