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physiological factors that determine the arterial blood pressure

1. the contractile properties of the heart
2. the properties of the vasculature
3. the blood volume (ECF is in equilibrium with blood volume)
•continually regulated on a moment to moment basis by adjusting CO and TPR
•longer term basis by adjustments to blood volume


equation for MAP



cardiac output

CO = HR x SV


how is cardiac output managed

-vagus nerve
-SA node primarily: decreases rate of spontaneous depolarization of the nodal cells to threshold
-AV node: decreases nodal excitability, increasing AV nodal delay
-atria: decreases contractility
*slows HR and modestly decreases atrial contractility

-right stellate ganglion --> SA and AV nodes
-left stellate ganglion --> left ventricle
-norepinephrine ß1 adrenergic receptors
-SA node: increase in spontaneous depolarization of nodal cells
-AV node: nodal delay decreased
-ventricles: increased contractility
*increases heart rate and ventricular contractility


how is stroke volume managed

•also by ANS
•an increase in atrial contractility due to sympathetic stimulation will increase diastolic filling
•an increase in ventricular contractility due to sympathetic stimulation will increase stroke volume by increasing the volume ejected, decreasing ESV


Starling's Law of the Heart

•the ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return


how is total peripheral resistance managed

•tube length
•tube radius ***arteriole
-vasoconstriction or vasodilation = changing the degree of contraction of the smooth muscle cells that surround the vessels
-extrinsic factor: sympathetic, varies from organ to organ
alpha 1 = vasoconstriction
Beta 2 = vasodilation
-intrinsic factor: matching organ blood flow to metabolic needs of organ

•extrinsic control is primarily involved in regulation of MAP


vascular tone

the degree of smooth muscle contraction


baroreceptor reflex

•principle moment to moment controller of MAP
•feedback control system
•arch of the aorta (CN X) and carotid sinus (CN IX)(mechanoreceptors known as baroreceptors, sensitive to stretch or distension)
•afferents sent t cardiovascular control center in the reticular formation of the medulla and in the lower third of the pons --> integrated into NTS -->
1. vasoconstrictor sensor
-upper medulla and lower pons
-efferent neurons are sympathetic and synapse in spinal cord--> target organs arteriolar and venous constriction
2. cardiac accelerator center
-efferent neurons are sympathetic and synapse in spinal cord--> target organs SA node, AV node, both ventricles ( increased heart rate and weakly induces atrial contractility)
3. cardiac decelerator center
-parasympathetic fibers travel in the vagus to the heart
-increased efferent activity decreases heart rate and weakly reduces atrial contractility


increased sympathetic activity

increases both CO and SVR (TPR)


increased parasympathetic activity

decreases heart rate and atrial contractility, decreasing cardiac output



•resetting of the control point of the baroreceptor reflex (could be lesion of the receptor or receptor response to chronic increase in blood pressure)
•increased afterload on the heart
•chronic peripheral vascular changes - narrowing and rarification (vessel loss)
•vasodilators, reduction in total body fluid


ECF and blood pressure

•increased ECF tends to increase blood pressure
•blood volume is regulated by the renin-angiotensin aldosterone system, activated by a decrease in MAP
•---> 1. aldosterone in adrenal cortex to produce aldosterone which acts on the renal distal tubule and collecting duct to increase in Na+ reabsorption, increasing blood volume 2. causes arteriolar vasoconstriction 3. acts on kidney to stimulate Na+-H+ exchange in the renal proximal tube, increasing the reabsorption of Na+ and HCO3-


regulation of blood volume

- hormone produced in the pituitary gland, stimulated by increase in plasma osmolarity or decrease in blood pressure
-V1 receptors on vascular smooth muscle cells - contraction and increased SVR (TPR)
-V2 receptor on on renal collecting ducts - reabsorption of water (increasing extracellular water and dilutes the increase in osmolarity that caused V2 receptor activation)
•ANP (atrial natiuretic peptide)
-secreted by atria in response to an increase in ECF volume --> vasodilation and and increase in sodium and water excretion