Cardiovascular Regulation Flashcards
Regulatory mechanisms
Pressurecontrol
Local
Nervous
Humoral
Acute control
Local
Fast blood flow changes
S-min
Vasodilation or vasoconstriction
Long term control
Local
Slow blood flow changes
Days-months
Change in size and numbers of vessels
Vasodilator theory
Increase in metabolism/O2 consumption leads to release of vasodilators that increase blood flow
Increase8 in metabolism=4 increase in acute blood flow
O2-lack theory
Low O2 in tissues leads to vasodilation and increase in local blood flow
Means that O2 keeps smooth muscles contracted, when O2 is low they dilate
25% O2 saturation=3* acute blood flow
Myogenic regulation
Not related to metabolism
Pressure stretches walls=constriction
Low stretch of walls=dilation
High AP=sudden big stretches of small vessels=vasodilation=decrease of blood flow
Low AP=little stretch of small vessels=vasodilation=increase of blood flow
Endothelial Regulation
Increased velocity leads to release of NO (inhibitory)= vasodilation=decreased velocity in blood flow
Nervous control
ANS SNS main regulator for circulation Redistribution of blood flow Regulation of heart activity Rapid control of atrial pressure
When SNS senses high AP
Arteriol and vein constriction
Increase heart rate and contractility
Vasomotortone regulated by norepinephrine
Where is cardioregulatory and vasomotorcenters located
Medulla oblongada
Excitatory effect
Alpha-adrenogenic receptors (noradrenaline+adrenaline)
Vasomotortone/vasoconstriction
Inhibitory effect
Beta-adrenergic receptors in skeletal muscle
Stimulates vasodilation by adrenaline
Parasympathetic NS
Only important in heart beat frequency
Humoral control
By sybstances set reread/absorbed in body fluids
Pressurecontrol-vasoconstriction/vasodilation
Humoral effects on vasoconstriction
Norepinephrine/epinephrine
Angiotensin II
vasopressin/ADH
Endothelin A
Humoral effects on vasodilation
Bradykinin
Histamine
Prostaglandins
Ions effecting vasodilation/constriction
Ca++- constriction K+- dilation Mg++- dilation (often inhibiting Ca++) H+- when increase=dilation, when decrease=constriction Anions- dilation CO2- dilation
Short term AP-regulation
Recovers pressure quickly
Limited time of action
ANS via baroreceptors, chemoreceptors
CNS ischemic response
Medium term AP-regulation
When AP is not recovered by short term
Endocrine/humoral mechanisms
Effective for hours
Long term AP-regulation
Can act for hours-months Renal activity (RAAS)
Baroreflex
Baroreceptors in aortic arch+carotid sinuses
Senses increase in AP-sympathetic and parasympathetic fibers-vasodilation and decreases HR
Signals also sent by SNS to adrenal medulla- releases of epinephrine+norepinephrine
Chemoreceptors reflex
Receptors in carotid body+aortic body
Senses levels of chemicals-signals to medulla oblongada
Sympathetic and parasympathetic response
CNS ischemic response/Cushing reflex
Decreased blood flow to vasomotorcenter and high CO2
Very strong sympathetic stimulation=increase in vasoconstriction and HR
emergency system
Bainbridge reflex/atrial reflex
Stretch receptors in atrial wall
Activated when preload or AP is increased
Increases HR
Opposite effect of baroreflex
Long term regulation of AP by kidneys
Control level of H2O, NaCl Controlling volume of EF and blood Control of AP When AP is high- pressure diuresis or pressure naturesis keeps AP constant Hormone based-RAAS
2 systems of kidney control
RAAS- when high blood pressure, most important hormonal cascade in control of AP, tissue perfusion, EC volume
Atrial natiuretic peptide ANP- when blood pressure decrease ANP secreted by atria=decreasing BP by stimulation Na+H2O excretion by kidneys
