B4.004 Cardiovascular Control Mechanisms Flashcards
how do veins differ from arteries?
more distensible
more compliant
ability to store blood
which vessels do sympathetic axon varicosities act upon?
BOTH arterioles and venules
sympathetic action on arteries
noradrenergic- a1
decreases diameter by smooth muscle contraction
increased resistance = increased MAP
sympathetic action on veins
noradrenergic- a1
decreases diameter by smooth muscle contraction
decreased capacitance = increased venous return = increased cardiac output
which vessels do parasympathetic nitrergic axon varicosities act upon?
arterioles
parasympathetic action on arterioles
NO- guanylate cyclase -increased diameter Epinephrine- b2 (non-neural) -decreased resistance -increased flow
difference between sympathetic and parasympathetic effects on vasculature
parasympathetic = very discrete, local control mechanism within limited vessels sympathetic = overall function regulation
3 ranges for changing blood vessel diameter
- to change local blood flow
- to change total peripheral resistance (TPR)
- to change cardiac output (CO)
purpose of changing local blood flow
important for discrete reflexes (genital erection, GI vasodilation during a meal)
local resistance is decreases so local flow increases
no significant change in TPR or MAP
why does TPR need to be adjusted?
if MAP decreases (blood loss, pooling while standing, etc) this will reduce brain perfusion because the brain is at the top of the hydrostatic column
leads to syncope
compensated for by changing TPR
how is TPR determined
by arterial blood vessel diameters in vascular beds (renal, GI, skeletal)
TPR increased by arterial vascular constriction
-renal and GI by a1 receptors
-skeletal by b2 receptors
effects of TPR on MAP
increased TPR increases MAP
increased TPR normally will not significantly decrease CO
process of changing cardiac output
venules/veins store 2/3 of total blood volume
venous smooth muscle contraction forces blood back to the heart (increased venous return)
increased venous return = increased CO
increased CO = increased MAP
what is tone
level of activity of nerves and targets
high nerve discharge rate or contractile state = high tone
vascular tone
determined by balance between vasoconstrictors influences (mainly sympathetic a1) and vasodilatory factors
cardiac tone
determined by concurrent discharge of excitatory sympathetic and inhibitory parasympathetic nerves
HR increased by increasing symp or decreasing parasym discharge
describe the process of changing from supine to upright posture and the effect on MAP
increased hydrostatic pressure causes venous distention in lower body and venous pooling of about 700 mL of blood
decreased venous return > decreased CO > decreased MAP
process of increasing cardiac tone
increasing cardiac sympathetic tone and decreasing vagal parasympathetic tone increased HR and force of contraction
makes heart a more effective pump
this can help restore cardiac output
what initiated cardiovascular reflexes?
baroreceptors
- cardiopulmonary
- arterial
baroreceptors
stretch receptors located on vessel walls that tell the brain to modulate autonomic cardiovascular tone
high pressure = high firing of baroreceptor nerves
cardiopulmonary baroreceptors
measure venous return
located in right atria, vena cava, pulm vessels
stretch w more venous return
venous pressure range 0-20 mmHg
arterial baroreceptors
located on aortic arch and carotid sinus
assess blood flow to the body and brain respectively
increased pulse pressure and MAP result in increased discharge rates over 60-180 mmHg
which nerve connects the carotid sinus to the brain stem?
glossopharyngeal (9th cranial)
which nerve connects the aortic arch to the brain stem
vagus nerve (10th cranial)
which nerve connects the cardiopulmonary baroreceptors to the brain stem
vagus nerve (10th cranial)
where do the afferent axons (vagus, glossopharyngeal) fire to?
nucleus of the tractus solitaries (NTS)
what is the effect of decreased firing in the NTS (due to decrease in BP)?
decreased STIMULATION of preganglionic cardiac parasympathetic axons in dorsal motor nucleus of the vagus (DMV) and nucleus ambiguous (NA)
decreased INHIBITION of C1
action of DMV/NA
preganglionic neurons for parasympathetic cardiac fibers
decreased stim = decreased cholinergic inhibition of heart = better pumping
action of C1
sympathetic preganglionic neurons
decreased inhibition = increased firing of sympathetic nerves to heart and vasculature
summarize the action of the NTS
stimulate DMV/NA which stimulate parasympathetic system
inhibits C1 which stimulates sympathetic system
how does baroreflex selectivity influence different arteriolar beds
baroreflex activates the SNS without large effects on adrenomedullary secretion
thus…predominating vasoconstrictive effects mediated by NE (a1 with little to no b2 dilation)
most effective on renal and mesenteric arterioles
little change in cardiac and cerebral vascular beds
how are baroreceptors “buffer” nerves
if cut, more variability in BP but no change in ‘set point’
avg not changed
what are some factors that can override the baroreflex
pain
emotions
chemoreflex
involved in respiration
active when MAP falls below 60 mmHg
low blood flow detected as low O2 in carotid and aortic body chemoreceptors
central ischemic response
reduced perfusion of the medulla results in discharge of sympathetic centers (C1)
final line of defense to restore MAP and CO
cushing reaction
when intracranial pressure is abnormally high, cerebral vessels collapse, perfusion stops and the central ischemic response is initiated even though systemic arterial pressure is normal or elevated
orthostatic hypotension
inability to compensate for reduced CO associated with upright posture (autonomic failure)
3 causes of orthostatic hypotension
- baroreflex pathway diseases
- degeneration of postganglionic sympathetic neurons (autonomic failure)
- postganglionic axon degeneration (neuropathy)
carotid sinus syndrome
abnormal sensitivity of the carotid sinus receptors to touch or stretch
vasovagal syncope
abnormally robust response to emotional stimuli leading to withdrawal of vasomotor tone and vagal parasympathetic activation
“playing possum”
how does ADH exert intermediate cardiovascular control
baroreceptor mediated release
potent vasoconstrictor for both arterioles and veins
increases plasma volume by reducing urine output (long term regulatory mechanism)
how does angiotensin II exert cardiovascular control
intermediate effects via direct actions on arteriolar smooth muscle
mediates long term volume increases by directly suppressing urine formation and indirectly by causing aldosterone release from the adrenal cortex
augments NE release from sympathetic varicosities
what is renin?
converts angiotensinogen to angiotensin II
how is renin regulated
diminished renal blood flow and SNS activation increase renin
what is ANP
atrial natriuretic peptide
stored in atrial myocardial cells
what elicits ANP release
increased plasma volume and resulting atrial stretching
how does ANP work?
acts on the kidney to induce sodium excretion (and coupled water excretion)
reduces plasma volume and BP
