control of arterial BP Flashcards
high pressure (arterial) baroreceptors
exposed nerve endings, measure stretch
carotid sinus
aortic baroreceptors
carotid sinus
loc at fork of carotid arteries
glossopharyngeal n.
cerebral blood flow
greater sensitivity = major high pressure sensor
aortic baroreceptors
arch of aorta
vagus n.
entire CV system
low pressure (cardiopulmonary) baroreceptors
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
chemoreceptors
carotid bodies & aortic bodies
regulation of breathing
baroreceptors sense
absolute P
rate of P change
~ inc P more sensitive to rate of change
adjustable - the thermostat -> doesn’t help w long term control
NTS
nucleus tractus soltarius
the cardiovascular center in the medulla oblongata
Inhibits; Vasomotor Center
Innervates: Cardioinhibitory center
Vasomotor centor
vasoconstrictor
pos chronotropic/iontropic response
SNS
inhibited by NTS
inc BP -> inc firing -> inc inhib of vasomotor c
cardioinhibitory center
activates vagal outputs to heart
reduce HR
excited by NTS
alpha1 adrenergic receptors
smooth mm
constriction
alpha2 adrenergic receptors
sympathetic n. endings
inhibit NE release
Autoreceptor -> neg feedback (leads to some level of vasodilation)
beta1 adrenergic receptors
cardiac myocytes
inc HR and inotropy
beta2 adrenergic receptors
vascular smooth mm beds (esp skel mm)
vasodilation
baroreceptor reflex
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
humoral control
1) vasoactive - released into blood, often affect vascular smooth mm cell contraction
2) nonvasoactiv - target organs outside CV system, often modulate effective circ vol
biogenic amines
epinephrine
serotonin (5HT)
histamine
peptides
angiotensin II
atrial natriuretic peptide
arginine vasopressin (AVP/ADH)
endothelins (ET)
renin-angiotensin system, what does the final product do?
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
pathway of Angiotensin II production
dec BP -> secretion of Renin + Angiotensinogen -> angiotensin I + angio converting enzyme (ACE) -> Angio II
arginine vasopressin / antidiuretic hormone
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
atrial natriuretic peptide
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
aldosterone
inc Na reabsorb -> inc H2O retention -> blood vol
release in resp to Angio II
nitric oxide
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
septic shock and NO
inc inducibleNOsynthase (in endothelium and smooth mm) -> massive inc in NO -> HUGE dec TPR and BP
