Hypertension Flashcards
formula for hBP treatment
- BP = CO x TPR (increasing TPR ^ CO wc BP)
- BP = SV x HR x TPR (since co = sv x hr)
4 main neurohumeral systems
renin-angiotensin-aldosterone system SMP ADH partial natriuretic peptide (ANP)
Atrial natriuretic peptides
- promotes Na+ excretion
- stored and synthesised In arterial myocyte
- respond to stretching
- c vasodilation -
high-up c its release and c vasodilaton of afferent arteriole so more Na+ (natriuresis removed from the body so water follows it and overall v BV and v BP
how do adrenal causes result in secondry hypertension
Conn’s syndrome= (hyperaldsteronism ) ^ aldosterone
Cushing’s syndrome = at high levels cortsiol can act on aldosterone receptors
Phaechromocytoma = adrnealine and noradrenaline
diuretics
–thiazide diuretics; used to increase NA+ and water excretion
- inhibit NA/CL channels on apical tubule of DCT so na+ can be removed and not reabsorbed so water can follow bv decreased and with it bp
- spironolactone (aldosterone antagonist) ; decreased bp - block aldosterone
NOT COMMONLY USED FOR HYPERTENSION
- use beta blockers to slow down HR and SV b1 (only if MI)
bradykinin
- present in lungs
- bradykinin is broken down into peptide proteins using ACE
- using ace inhibitors causes bradykinin to build up and hence why you can get a dry cough
- RAAS allows inhibition of the breakdown of bradykinin the
treatment for HP
- ACe inhibitor
- AN2 inhibitor /antagonist
- L-type ca2+ channel blockers (verapamil, nifedipine) c less CA2+ entry so smooth muscles don’t contract as much so vasodilation
- a1 receptor blockers (doxazosin) since they c vasoconstriction of smooth msucle b you can get postural hypotension hypotension
aldosterone
- acts on the principle cells of collecting such
c Na+/K+ channels c na+ absorption (and k+ excretion) and therefore c water to reabsorbed
- it also acts on apical na+ channels ENaC (epithelial Na channels)
renovascular disease
- occlusion of the renal artery c decreased perfusion pressure in the kidney
- so v bp in the kidney so renin released c effects (activation of the RAAS/vasoconstriction/aldosterone)
- b stenosis still present its continuously activated
renal parenchymal disease
- disease wehre damage to the cells involved in filtrationof blood
- in early stages you lose vasodilator substances
- later stages NA+ and water retention inadequate glomerular filtration (volume-dependent hypertesion)
why is it important to treat high bp and whats the effects of intervention
c death like MI
every 10mmHg reduction in blood pressure results in;
- 17% decrease of coronary heart disease
- 27%decrease of stroke
- 28% decrease if heart failure
- 13% decrease in all -cause mortality
describe the short term regulation of blood pressure
- baroreceptors located on the carotid sinus and aortic arch
- detect changes in b presure (as the receptor fibres are strecthed with ^ BP) and send this info. to the medulla of the brain wc then works to decrease bp
angiotensin
Renin released from glandular cells of just angiotensinogen made in the liver need enzyme in lung to convert it into angiotensin 1 then need renin to convert it into angiotensin 2 giving angiotensin 1 enzyme inhibitor can cause cough because that enzyme also work on brdyc
name the neurohumeral system
- RAAS
- SNS
- ADH
- ANP
ace inhibitors
preventing convention of AT1 to AT2 to deal with ^bp
what does the SNS do
- ^ Renin release from the juxtaglomerular apparatus ‘s glandular cells
- activates apical Na\H exchange system and also basolateral NA/K ATPase inPCT
- vasoconstriction
how does decreasing circulating volume stimulate renin release
drop in BP in afferent arteriole bp and blood volume ,
since b is moving slowly through the PCT etc there’s moreNA+ being reabsorbed
so by the time you reach DCT there’ll be less NA+
this c release are RENIN too.
this is detected by macular dense cells in the DCT,
they are chemoreceptors and measure conc of NA+
- innervation of the SMP b we want to ^ bp so we can deliver more b to muscles
what type of angiotensin 2 receptors are there?
describe these receptors
- 2 AT1 and AT2
- main actions usually via AT2
- G-protein coupled receptor
classficiatio
STAGE 1;
- BP = >140/90mmHg
- ABPM / HBPM (ambulatory/house b p measure) >135/85
STAGE 2;
- BP = >160/100
- ABPM/HBPM >150/95
STAGE 3:
- >180/110 OR >110 diastolic
dopamine
- can be formed locally in the kidneys from circulating L-DOPA
- dopamine receptors can be located in the renal b vessels of the PCT and TAL
- c vasodilation and increases renal b flow
- reduces reabsorption of NAcl by inhibiting Na/K ATPA and NHX in the principal cells of the TAL and PCT
hypertension
^ afterlod so LV works harder and undergoes hypertrophy LV then fail c HF ^ demand for O2 so arterial damage
what does ADH do
- vasoconstriction
- increases water reabsorption to increase blood volume and so blood pressure
what does AT2 do
- vasoconstrictor (general) c ^ BP
- c smooth muscles of the efferent arteriole to constrict increasing filtration rate as b backs up, ^ glomerular filtration rate this c less Na+ to be reabsorbed in CT AND CD, so overall more NA+ at DCT
- c adrenal cortex to release aldosterone wc c distal DCT to remove Na+ back into body c water to follow c ^ Bv and ^ BP
- hypothalamus c ADH released from PPG wc goes to DCT and CD to reabsorb water back into body to ^BV and therefore ^ BP
what released renin
what c renin release
there are specialised cells on the afferent arteriole = granular cells ofthe juxtaglomerular apparatus JGA
- reduced nacl dleivery to macula densa cells of the distal tubule
- reduced renal perfusion
- sympathetic nervous system stimualtesthe JGA
normal b
90/60 and 120/80
how is blood pressure regulated? what’s the formula
- mean ABP= CO X TPR
CO = SV X HR
- baroreceptors short term and then medium/long term regulation = neurohumeral and sodium balance
c of hypertension
95% primary
5% secondary d CHAPS ( cushing’s sydnrome, Hyperaldosteronism (conn’s syndrome) , Aortic Coarctation, Phaechromocytoma, Stenosis of the renal arteries)
prostaglandins
local mediators and can act as vasodilators
- they enhance glomerular filtration to reduce NA+ reabsorption
- act as a buffer d ^ SNS and RAAS system c too much vasoconstriction
- important when levels of A2 are high
what does renin do briefly
renin causes angiotensiosngen to AN 1 , ACE made my lung converted A1 to A2 and A2 c vasoconstriction, stimulates Na+ reabsorption to increase perfusion and c aldosterone release from the adrenal cortex
medium and longer term control of blood pressure
- neurohumoral responses
- RAAS
- SYMPATHETIC NERVOUS SYSTEM
- ADH
- ANP (atrial natriuretic peptide)
- direct control of sodium levels (sodium balance
hypertension
sustained high b pressure
upon renin release what happens
- goes into systemic circulation
- liver produced and stores ANGIOTENSINOGEN, wc is inactive and released into b stream.
- meets R w enzyme and activates it creating AT1
- gets to lungs where there’s ACE (angiotensin converting enzyme)
- ACE converts A1 to A2
