blood pressure control and regulation Flashcards
Which component of the RAAS signalling pathway is synthesised in and secreted from the liver? Aldosterone Angiotensin I Angiotensin II Angiotensinogen Angiotensin Converting Enzyme
angiotensinogen is made and secreted rom the liver!
aldoserrine rom the adreneal gland
ang 1 ton ang 2 in the blood catalysed by ACE found in the lung
where are barorecpeors located
in the carotid sinus and aortic arch, they can detecth changes in blood pressure via sense/strecth receptors
also renal baroreceptors in JXG and MD
define blood pressure
difference between the pressure in the
system and the external pressure (transmural pressure)
where does blood pressure orignate from?
dynamic pressure = produced by contraction of the heart/ beat to beat changes
hydrostatic pressure = pressure exerted by the fluids in blood vvessels
how does hydrostatic rpessure change across the body
hydrotatic presure is greatest in the lower limbs than the upper limbs due to the effects of gravity
why do veins need valves? how does this relate to blood pressure?
arteries have elastic tissue to smooth out the pulsitile flow of blood from the heart so experience high pressure of 120mmHG
as we reach the capillaries the BP drops and even more so to the veins 20mmHg
so there is a very slow flow of blood so we need valves to prevent backflow
descieb how barorepceots can rgulate BP
baroreceptors are a short term acute way to respond to changes in BP
they are sensory afferent endings on cranial nerve 9 and 10 | glossopharyngeal nerve + vagus nerve
> located in carotid sinus (9) and aortic arch (10) and have mechanosentivie receport ends to sesne strect
> strech will stimutate AP to fire or be inhibited
> relay info to the CV centre at the M.oblongata and effect a response to increase or decrease BP
numbers for hyper and hypotrnsion
Like 120/80
below 90/60 mmHg is hypotension
above 140/90 mmHg is hypertension
descibe difference between A firbes and C fibres
these are types of baroreceprt
> A is quick conductance, small diameter and myelinated
Type C is unmyelineated but higher threshold
how does hormonal control of BP work # generally mechanzism
hormones will act on the kidney
> for high blood pressure they will increase water and sodium excretion
> for low blood pressure they will increase water and sodium reabsorption in the nephrons
ADH, angiotensinogen, aldosterone will retain so increase BP
and atrial natuiretic peptide will excrete so increase BP
describe the multiple ways in which renin can be released
function: converts angiotensinogen->ang1
renin is released in the KIDNEY to blood
> this whole system is for low BP
1. JXG have barorecprots which detect low BP in afferetn arteriole so release renin
2. sympathetic innervation within JGA stimultate renin release to increase BP
3. macula densa cells of DCT chemoreceotrs detect the low sodium/low osmolarity of glomerular filtrate futhur stimulating relaee of renin
> > sodium levels low as the filtrate moves slowly through the nephron so there is more time for the sodium to be reabsorbed so tubule has low sodium
how does Atrial naturetic peptide work to control BP?
released from endocrine cells of atrial tissue
> antagonises the effects of ANG2
so works to DECREASE BP in response to hypertension
> vasodilate, block ADH+aldosterone, decrease GFR, reduce CO amongst many functions!
how does the RAAS system work/what is the aim of it
Aim to increase BP
important in longer term control of BP as it takes time to convert between each molecule
end result is a balance of BP, blood volume and vascular tone
what is the equation for blood pressure
BP = CO x TPR
cardiac output is mainly controlled through renal system fluid balance and SV
and sympathetic stimulation affects heart rate and systolic pressure
total peripheral resistance is mainly controlled by renal system through changes in vascular tone affecting diastolic pressure
how can MAP/BP be affected or influenced by
CO = relates to SV and systolic pressure
TPR = diameter of arterioles and resistance to blood flow affects diastolic pressure
blood volume - fluid intake and hemorrhage/ ECF balance will contribute to MAP as it affects SV
blood distribution - diameter of veins and pooling of blood will reduce venous return. skeletal muscle and posture can also influence this
why do people who donate blood seem to look pale after donating?
donating blood reduces ECF and reduces venous return of blood to the heart = hypotension!
> to compensate you increase in SNS activity and vasoconstrict so you redistribute of blood away from peripherys to protect the central orgasn so look pale
> > blood can be directed away from the kidneys which can then stimulate the release of renin (as barorecptors of JXG detect the low BP)
why do we suggest a head down postition for a perosn feeling faint?
because person feels faint as their BP is low
so head down postition will increase venous return to heart and augment the compensationary mechanasnism associated with trying to increase the BP (increase CO, vasoconstrict)
similarly IV drips of electrolytes will help to conserve water -> increase blood volume,EDV,SV CO -> BP
similarly pharmacological interventiation such as adrenlaine will upregulate the SNS/tone response and increaing firing of baroreceptors
why is severe haemmorage so severe? # severe hypotension
markedly reduced blood flow to the heart during diastole as BP is too low so there can be cardiac depression and CNS depression. even the compensatory mechansims may not be enough to maintain blood flow to cricial organs
> eventual detriotion of myocardium so CO drops
> loss of vasomotor tone and reduced venous return
this postive feedback furthur eacerbates as time goes on
negatvie feedback mechansism fail to comepnstare and postive feedback mechansisms dominate
why can’t chronic hypertension be compensated?
normally a rise in BP will stimulate the Baroreceptor refelx to reduce the BP (e.g during exercise) so can control acute changes to BP. they will adapt to increase firing frequency but the system becomes desentitized
BUT the barorecptor reflex becomes desensitized to this persistent high BP and actually become inactive allowing BP/MAP to rise
what does chronic hyeprtenison result in / what chanllenges does it pose to cotnrilling Bp?
INTIALLY will increase the cardiac work - greater froce of contraction and hypertrophy of smooth and cardiac muscle
> educe lumen size further increasing TPR/ BP
will strain the blood vessels as they continually relax and distend so risk of rupture/haemoorage
EVENTUALLY myocardial deterioration
what is secondary hypertension
hypertension originating from a fluid volume imbalance such as from drugs, kidney damage or endocrine causes // other underlying health conditions
accounts for 2-10% of all hypertension cases
there are different types of barorecrotrs -A and C how do they function
A firbres/neeve type = are myelinated, fast conduction switiched on during normal pulsatile changesd in BP (20-120)
C fibres are unmyelinares so slower connuction but sticth on in higher pressures = 100-200mmHg so have more dynamic control of BP
genrally rhe carotid sinus has lower threshold and sortic arch barorecpotrs has higher pressure threshold
why does a giraffe have high bp?
needs to voercome and counteract the high hydrostatic pressure to drive blood to the head/brain
apart from giraffe, why is blood pressure consereved acrooss animal kingdom of 120/80 mmHg?
this BP maintains blood flow to the kidnet so the glomerular filtration rate to remains at 120mL/min which is essentila for its funtion. kindey uses around 25% of CO to function
describe the consequences of hypertension
INITIALLY increased cardiac work so greater force of contraction = muscle hypertrophy which will reduce lumen size, increasing TRP further increasing BP /// Positive feedback
PROGRESSES risk of vessel rupture and hemorrhage as blood vessels continually distend and relax
The barorecptors get desentised and there can be CNS depression and CV deterioration
what is primary hypertension?
i guess its ideopathic, majority of people have
changes to TPR and fluid imbalance (increased BV, increased BP)
originate from genetic or lifestyle factors including age,diet,microbiota
