Session 5- Control of blood pressure Flashcards
what is hypertension
sustained increase in blood pressure
what is the normal range for blood pressure
90/60 mmHg and 120/80mmHg
what does hypertension lead to
afterload…
increased after load
-left ventricular hypertrophy - >heart failure
increased after load
-increased myocardial oxygen demand -> myocardial ischaemia and MI
what does hypertension lead to
arterial damage ….
arterial damage
leads to atherosclerosis and weakened vessels - MI
both lead to cerebro-vascular disease stroke, aneurysm, nephro-sclerosis and renal failure, retinopathy
why isnt the baroreceptor reflex long term
it works for acute changes
the threshold rests after a while
how does fuild volume affect blood pressure
if fluid volume increases, stroke volume increases therefore there is more fluid for heart to pump
therefore BP increases
what stimulates renin release
- reduced NaCl delivery to distal tube
- reduced perfusion pressure in the kidney causes the -release of renin- detected by baroreceptors in afferent arteriole
- sympathetic stimulation of JGA increases release of renin
where is renin released
juxtaglomerular apparatus JGA in the afferent arteriole to kidney
renin-angiotensin-aldosterone system
angiotensinogen is converted to angiotensin I by renin
angiotensin I converted into angiotensin II by angiotensin converting enzyme
angiontensin II causes vasoconstriction, stimulates Na+ resorpton at kidney and stimulates aldosterone from adrenal cortex
action of aldosterone on kidney
AngII receptors stimulates aldosterone release from the adrenal cortex
- acts on principal cells of collecting ducts
- stimulates Na+ and therefore water resorption
- activates apical Na+ channel (Epithelial Na channel and apical K+ channel)
- also increases basolateral Na+ extrusion via Na/K/ATPase
ACE effect on bradykinin
ACE causes the breakdown of bradykinin it reduces the vasodilation properties of Bradykinin
what effect do ACE inhibitors have
they allow bradykinin to build up and inhibit ACE
role of ADH
main role is formation of concentration urine by retaining water to control plasma osmolarity
-increases water reabsorption in distal nephron
- stimulates Na+ reabsorption
- acts on thick ascending limb
- stimulates apical Na/K/Cl co-transporter
what stimulates ADH release
increase in plasma osmolarity or severe hypovolaemia
Natriuretic peptides
ANP promotes Na + excretion
released from atrial cells in response to stretch
low pressure volume sensors in the atria
reduced effective circulating volume inhibits the release of ANP to support BP
-reduced filling of the heart-less stretch- less ANP released
where are natrieuretic peptides synthesised and stored
atrial myocytes
actions of ANP
causes vasodilation of the afferent arteriole
increased blood flow increases GFR
inhibits Na+ reabsorption along the nephron
acts in opposite direction to the other neurohumoral regulators
-causes natriuresis
if circulating volume is low ANP release is inhibited- supports BP
prostaglandins
vasodilators
more important clinically than physiologically
locally acting prostaglandins enhance glomerular filtration and reduce Na+ reabsorption
act as a buffer to excessive vasoconstriction produced by SNS and RAA system
dopamine
dopamine is formed locally in the kidney from circulation L-DOPA
dopamine receptors are present on renal blood vessels and cells of PCT and TAL
DA cause vasodilation and increase renal blood flow
DA reduces reabsorption of NaCl
-inhibits NH exchanger and Na/K ATPase in principal cells of PCT
renovascular disease
occlusion of the renal artery causes a fall in perfusion pressure in that kidney
decreased perfusion pressure leads to increased renin production
activation of renin-angiotensin-aldosterone system
vasoconstriction and Na+ retention
renal parenchymal disease
earlier stage may be a loss of vasodilator substances
in later stage Na+ and water retention due to inadequate glomerular filtration
-volume-dependant hypertension
Conn’s syndrome
aldosterone secreting adenoma
-hypertension and hypokalaemia
Cushings syndrome
excess secretion of glucorticoid cortisol
-at high concentration acts on aldosterone receptors- Na+ and water retention
phaechromocytoma
tumour of the adrenal medulla
- secretes catecholamines (adrenaline and noradrenaline)
- over production of catecholamines can stimulate sympathetic NS
