Lecture 13- Blood Pressure Regulation Flashcards
blood pressure
the force exerted upon vessel walls as blood flows through
what is required to exchange substances/ fluids across capillary networks
a minimum pressure (capillary hydrostatic pressure)
formula for blood pressure
cardiac output x total peripheral resistance
what total peripheral resistance dependant on
dependant upon arteriolar radius
autoregulation of local flow is also known as
intrinsic control of blood flow
what system is responsible for short term regulation
neural/ nervous system
what system is responsible for long term regulation
endocrine system
outline intrinsic control when local blood flow in a tissue is too low
- homeostasis disturbed from physical stress (trauma, high temp etc), chemical changes (lower oxygen, lower pH, increased carbon dioxide or increased vasodilatory metabolites) or increased tissue activity (lactate)
- inadequate local blood pressure and blood flow
- autoregulation: precapillary sphincters relax and vasodilatory metabolites (nitrogen, potassium ions, hydrogen ions, carbon dioxide and lactate) enter arterioles allowing capillary regulation
4.local decrease in resistance and increase in blood flow - homeostasis returns
what occurs if blood pressure is still too low to meet demands even after autoregulation
central mechanisms are activated to increase systemic blood pressure
which branch of the autonomic nervous system is activated to restore blood pressure if intrinsic control can’t bring the body back to homeostasis
sympathetic nervous system
how does the SNS help regulate blood pressure
increases heart rate and stroke volume
enhances vasoconstriction
what centres in the CNS are activated by baroceptors
cardiovascular centres
baroreceptors
sensitive to changes in pressure and found in aorta and carotid sinus (blood flow to brain/ cerebral blood flow)
what effect does a fall in blood pressure have on baroreceptors
inhibition (less activation/ firing of the baroreceptors)
when baroreceptors are inhibited what centres are activated
cardio acceleratory centre activation and vasomotor centre activation (region in medulla)
what centre is inhibited when baroreceptors are inhibited
cardioinhibitory centre
what effect does a rise in blood pressure have on baroreceptors
baroreceptor stimulation
when baroreceptors are stimulated, what centres are inhibited
cardio acceleratory centre and vasomotor centre
when baroreceptors are stimulated, what centres are activated
cardioinhibitory centre
what occurs when blood pressure is too high
less sympathetic activity and more parasympathetic activity
reduced peripheral resistance
where are peripheral chemoreceptors found
body/ blood
why is there a fall in pH with increased CO2
co2 dissolves in the blood and forms hydrogen ions lowering the pH
what is activated by an increased respiratory rate
respiratory centre activation
what does respiratory centre activation lead to
a rise in CO2
effect of a rise in co2 on cerebral vessels
vasodilation of cerebral vessels leading to increased blood flow to the brain (must be a preserved blood flow to the brain at all times)
what receptors are found in the medulla which are sensitive to co2
central chemoreceptors
central chemoreceptors
activate the respiratory centre
why is the respiratory centre activated when there is a rise in co2
there is not enough o2 and too much co2 so there is no point increasing more blood as it won’t be able to pick up enough oxygen as not breathing fast enough so respiratory centre is activated meaning more oxygen in the lungs so the increased blood can pick up more oxygen
what centres are activated and inhibited when chemoreceptors are activated
cardio acceleratory centre activation
cardioinhibitory centre inhibition
vasomotor centre activation
what does activation of the vasomotor centre lead to
peripheral vasoconstriction
what are the three endocrine responses to a low blood pressure even after autoregulation
ADH/ vasopressin
Erythropoietin
Renin-Angiotensin-Aldosterone System (RAAS)
how does ADH regulate a low blood pressure
pituitary gland secretes ADH
ADH is a vasoconstrictor and increases fluid retention (increases thirst)
increase permeability of the csm of the collecting duct
how does erythropoietin help regulate a low blood pressure
fall in blood oxygen stimulates erythropoietin (main hormone in the formation of rbcs)
is a vasoconstrictor
more rbcs increases the blood volume
more minor compared to the others
how does Renin-Angiotensin Aldosterone System (RAAS) help regulate a low blood pressure
kidney cells have their own baroreceptors which stimulate the enzyme renin which converts angiotensinogen to angiotensin 1
angiotensin 1 is inactive but the angiotensin converting enzyme converts t into angiotensin 2 which is an active and potent vasoconstrictor (causes a greater increase in vasoconstriction and peripheral resistance)
angiotensin 2 stimulates aldosterone (increases the activity of sodium potassium ATPase pump so more sodium ions are absorbed in the distal convoluted tubule and collecting duct therefore more water is reabsorbed which increases the volume of the blood within the vascular system )
role of sensors in muscle cells of atria and ventricles
able to detect when they are being stretched too much
what is secreted when there is increased stretching of atria and ventricles when blood pressure is too high
secretion of natriuretic peptides from muscle cells
what natriuretic peptides do the atria and ventricles secrete
atria: atrial natriuretic peptides
ventricles: brain natriuretic peptides
renal effect of natriuretic peptides
act on the kidney
increased sodium loss in the urine ( inhibits sodium potassium pump therefore less sodium is reabsorbed in the kidney and more water lost in the urine)
reduced thirst (inhibit secretion of ADH)
reduce blood volume
vascular effects of natriuretic peptides
inhibition of ADH, aldosterone, NA and adrenaline release
peripheral vasodilation
reduce blood pressure
what are the 5 consequences of blood loss (severe haemorrhage)
decreased atrial pressure
altered blood gases
RAS activation
catecholamine release
vasopressin release
role of chemo and baroreceptor reflex in severe blood loss
cardiac stimulation
systemic vasoconstriction
fluid and volume redistribution
role of RAAS and ADH secretion in sever blood loss
restore blood volume, inhibit secretion of water at kidneys, recall fluid from the tissues, less ADP sceretion as want more retention of water
