Session 5- Control of blood pressure

Question 1

what is hypertension

Answer 1

sustained increase in blood pressure

Question 2

what is the normal range for blood pressure

Answer 2

90/60 mmHg and 120/80mmHg

Question 3

what does hypertension lead to

afterload…

Answer 3

increased after load
-left ventricular hypertrophy - >heart failure

increased after load
-increased myocardial oxygen demand -> myocardial ischaemia and MI

Question 4

what does hypertension lead to

arterial damage ….

Answer 4

arterial damage
leads to atherosclerosis and weakened vessels - MI

both lead to cerebro-vascular disease stroke, aneurysm, nephro-sclerosis and renal failure, retinopathy

Question 5

why isnt the baroreceptor reflex long term

Answer 5

it works for acute changes

the threshold rests after a while

Question 6

how does fuild volume affect blood pressure

Answer 6

if fluid volume increases, stroke volume increases therefore there is more fluid for heart to pump
therefore BP increases

Question 7

what stimulates renin release

Answer 7

• 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

Question 8

where is renin released

Answer 8

juxtaglomerular apparatus JGA in the afferent arteriole to kidney

Question 9

renin-angiotensin-aldosterone system

Answer 9

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

Question 10

action of aldosterone on kidney

Answer 10

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

Question 11

ACE effect on bradykinin

Answer 11

ACE causes the breakdown of bradykinin it reduces the vasodilation properties of Bradykinin

Question 12

what effect do ACE inhibitors have

Answer 12

they allow bradykinin to build up and inhibit ACE

Question 13

role of ADH

Answer 13

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

Question 14

what stimulates ADH release

Answer 14

increase in plasma osmolarity or severe hypovolaemia

Question 15

Natriuretic peptides

Answer 15

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

Question 16

where are natrieuretic peptides synthesised and stored

Answer 16

atrial myocytes

Question 17

actions of ANP

Answer 17

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

Question 18

prostaglandins

Answer 18

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

Question 19

dopamine

Answer 19

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

Question 20

renovascular disease

Answer 20

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

Question 21

renal parenchymal disease

Answer 21

earlier stage may be a loss of vasodilator substances
in later stage Na+ and water retention due to inadequate glomerular filtration
-volume-dependant hypertension

Question 22

Conn’s syndrome

Answer 22

aldosterone secreting adenoma

-hypertension and hypokalaemia

Question 23

Cushings syndrome

Answer 23

excess secretion of glucorticoid cortisol

-at high concentration acts on aldosterone receptors- Na+ and water retention

Question 24

phaechromocytoma

Answer 24

tumour of the adrenal medulla

• secretes catecholamines (adrenaline and noradrenaline)
• over production of catecholamines can stimulate sympathetic NS

Question 25

non pharmacological approaches

Answer 25

exercise
diet
reduced Na+ intake
reduced alcohol intake
lifestyle changes above can have limited effect
failure of implement lifestyle changes could limit the effectiveness of antihypertensive therapy

Question 26

vasodilators

Answer 26

l-type Ca channel blockers

• reduce calcium entry to vascular smooth muscle cells
• relaxation of vascular smooth muscle

alpha 1 receptor blockers
-reduce sympathetic tone
can cause postural hypotension

Question 27

diuretics

Answer 27

Thiazide diuretics

inhibit Na/Cl co-transporter on apical membrane of cells in distal tubule

Question 28

beta blockers

Answer 28

less commonly used
blocking b1 receptors in the heart will reduce effects of sympathetic output
-reduce HR and contractility
not used in hypertension alone

only used if there are other indicators such as previous MI