L28 BP reg Flashcards
SV X HR X TPR =
BP
All factors are effected physiologically
Arterial Baroreceptors - when they stretch, increases outflow to brainstem
Increase baroreceptors , reduces BP
Baroreceptors low- brainstem increases BP
Cardiopulmonary baroreceptors - sense degree of stretch but aren’t as important
Arterial chemoreceptors- secondary role in maintaining BP
MAP = CO X TPR = SV X HR X TPR
Arterial BP May be regulated via changes in CO (SV and/or HR), TPR, and/or blood volume
Perturbations to system ( BP changes or hypoxia) activate afferent pathways to brainstem nuclei which integrates these inputs
Brainstem center activates appropriate efferent pathways which adjust BP back to normal value
Some response = rapid, others take minutes, hrs, or days
Rapid controllers
Arterial baroreceptors
Peripheral chemoreceptors
Baroreceptors
Main function - short term reg of arterial BP
Minimize fluctuations in P
Located in aortic and carotid sinuses
Respond to stretch
Mean P in the aorta or carotid sinus determines baroreceptor activity
Baroreceptor neural pathways
Afferents from baroreceptors travel to brainstem via vagus and glossopharyngeal nerves
Afferent info is integrated in cardiovascular center of brainstem - nucleus tractus solitarius (NTS)
Efferent output from CNS Is via vagus or sympathetic nerves
NTS
Sensory nucleus in the dorsomedial part of brainstem
Receives most afferent info
Acts as integrator
Cardiovascular centers
Vasomotor center - regs efferent sympathetic adrenergic n activity to peripheral resistance vessels
Cardiac center- regs efferent vagal and sympathetic adrenergic n activity in the heart
Baroreceptor reflex responses to BP elevated above normal
Increase stretch of baroreceptors
Increased afferent n activity to NTS
increase PNS to SA node, decrease SNS to heart and peripheral resistance vessels, decrease HR, decrease TPR, decrease Sv, decrease CO, decrease MAP
Baroreceptor reflex responses to BP elevated below normal
Decreased stretch of baroreceptors
Decreased afferent n activity to TNS
decrease PNS to SAN, increase SNS to heart peripheral resistance vessels, increase HR, increase SV, increase CO, increase TPR, increase MAP
Peripheral chemoreceptors
In carotid and aortic bodies- receive highest blood flow per unit tissue in body
Activated by decrease in PO2 (hypoxia), increase PCO2 (hypercapnia) and decrease pH (acidosis)
Cause increase in SNS stimulation of resistance vessels (increase TPR, BP) and a transient increase in PNS outflow to heart (transient decrease HR)
Info integrated to brain stem (NTS)
Baroreceptor response is much more potent
Intermediate controllers
Capillary fluid shift
Renin-angiotebsin-aldosterone system (RAAS)
Vasopressin
Atrial natriuretic peptide
Capillary fluid shift
Arteriolar vasoconstriction - decrease Pc, favors absorption, increase intravascular volume, increase arterial pressure
And vice versa
Renin-angiotensin-aldosterone
Renin release stimulated by a decrease in BP, reduced Na flux, or sympathetic stimulation
Renin cleaves angiotensin I from angiotensinogen, a plasma globulin
Angiotensin I converted to angiotensin II by angiotensin converting enzyme (ACE) in lungs
Angiotensin II , vasoconstrictor ( increase TPR) and stimulates aldosterone release from adrenal cortex
Aldosterone, increases Na Absorption in kidney, increases intravascular volume
Antidiuretic hormone (ADH, AVP, vasopressin)
Decrease vascular V (>10%), decrease atrial stretch, increase vasopressin release from posterior pituitary, increase H2O absorption in kidney and peripheral vasoconstriction, increase MAP
Plasma conc too high, dehydrated
Low volume is hypotensive state
Atrial natriuretic peptide (ANP)
Like anti aldosterone
Increase vascular volume, increase atrial stretch, increase ANP release from atrial muscle, vasodilation and decrease reabsorption of Na/H2O by kidney, decrease MAP
Also inhibits renin, vasopressin, and aldosterone secretion
Released when vascular volumes are high, promotes fluid and Na loss by kidney
Like a natural diuretic
Released from atrium
