Blood pressure Flashcards
What is the short-term regulation of MAP controlled by?
baroreceptors
What is the aim of negative feedback?
to minimise any disturbance to a controlled variable (MAP)
Where are the baroreceptors?
carotid sinus - base of internal carotid artery
arch of the aorta
Via which cranial nerve do each baroreceptors send signals?
carotids - CN IX (glossopharyngeal)
aortic - CN X (vagus)
What is the normal change in circulation when a healthy person stands?
venous return decrease MAP decreases (slowly) baroreceptors fire at reduced rate
What causes increased HR and SV when a healthy person stands?
reduced vagal tone to heart - sympathetic tone increases
How does postural hypotension occur?
failure of baroreceptors to respond to gravitational shifts in blood when moving from horizontal to vertical
What happens when the baroreceptors don’t respond to the gravitational shift of blood to feet?
Vagal activity increases (instead of sympathetic);
HR decreases so CO and SV does too.
Decreased sympathetic constrictor tone increases vasodilatation which reduces BP
How is BP regulated long-term?
By controlling extracellular fluid volume (ECFV)
ECFV = ?
Plasma volume (PV) + Interstitial Fluid Volume (IFV)
What happens if PV falls?
compensator mechanisms shift fluid from interstitial compartment into plasma compartment
What is the role of interstitial fluid?
bathes cells and acts as go between the blood and body cells
Which 2 basic factors affect ECFV?
Water excess / deficit
Sodium excess / deficit
Which hormones regulate ECFV by regulating the water and salt balance in our bodies?
Aldosterone (RAAS) Natriuretic peptides (NPs) Antidiuretic hormone (ADH)
What is the role of RAAS?
regulation of plasma volume and SVR and therefore, MAP
Where is renin released from?
granular cells of the juxtaglomerular apparatus
What does renin stimulate?
secretion of angiotensin I
Which plasma globulin is secreted by the liver and forms angiotensin I?
angiotensinogen
Which enzyme allows angiotensin I -> angiotensin II, and where is it produced?
ACE (angiotensin converting enzyme)
lung vascular endothelium
What does angiotensin II stimulate?
Aldosterone release
Systemic vasoconstriction - increases SVR
Thirst
ADH release
Where is aldosterone released from?
adrenal cortex
Where does aldosterone act upon? And what does it cause?
the kidneys to increase sodium and water retention -> increased plasma volume
Which physiological conditions stimulate RAAS?
Renal artery hypotension
Stimulation of renal sympathetic nerves
Decreased Na+ in renal tubular fluid
Decreased Na+ concentration in renal tubular fluid is detected by?
macula densa - specialised cells of kidney tubules
What is the juxtaglomerular apparatus?
a region comprising:
macula densa
extra-glomerular mesangial cells
granular cells
What are natriuretic peptides?
peptide hormones synthesised by heart
NPs are released in response to ?
cardiac distension or neurohormonal stimuli
How do NPs affect BP?
vasodilators - decrease SVR and BP
What are NPs in relation to RAAS?
a counter-regulatory system for RAAS
What are the 2 types of NPs released by the heart?
Brain type Natriuretic Peptide (BNP)
Atrial Natriuretic Peptide (ANP)
Which NP is released in response to hypervolaemic states?
ANP (atrial distension)
What is the role of ADH?
acts on kidney tubules to increase absorption of water (conserve water)
What stimulates the secretion of ADH?
reduced ECFV
increased ECF osmolality
What is plasma osmolality?
indicates relative solute-water balance - monitored by osmoreceptors
i.e. increased plasma osmolality = not enough water
What is the effect of ADH release?
increased reabsorption of water
concentrated urine
increased ECFV and PV
increased CO and BP
What is the effect of ADH in patients in hypovolaemic shock?
exaggerated vasoconstriction
increases SVR and BP
