Flashcards in CVS - Hypertension Deck (35):
How do baroreceptors reduce high blood pressure?
Nerve endings in the carotid sinus and aortic arch are stretched due to increased arterial pressure. They send an impulse via afferent pathways to the medulla oblongata, which sends an impulse causing bradycardia and vasodilation.
Why does the baroreceptors reflex not work against long-term blood pressure increase?
The threshold for baroreceptor firing resets after a short period of time
What are the four parallel neurohumoral pathways that control circulating volume and hence blood pressure?
- renin-angiotensin-aldosterone system
- sympathetic nervous system
- antidiuretic hormone
- atrial natriuretic peptide
Where is renin released from?
The granular cells of the juxtaglomerular apparatus in the kidney
Give some factors that stimulate renin release
- reduced NaCl delivery to distal tubule
- reduced perfusion pressure in the kidney
- sympathetic stimulation to juxtaglomerular apparatus
What is the juxtaglomerular apparatus made up of?
Macula densa cells, granular cells and surrounding mesangial cells
Summarise the mechanism of the RAAS
- Angiotensinogen is converted to angiotensin I by renin.
- angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE).
- angiotensin II stimulates aldosterone, which stimulates Na+ reabsorption at the kidney
- angiotensin II also stimulates vasoconstriction
What type of receptor are AT1 and AT2 (angiotensin II receptors)?
What is the action of angiotensin on the arterioles?
What is the action of angiotensin on the kidney?
Stimulates Na+ reabsorption
What is the action of angiotensin on the sympathetic nervous system?
Increased release of noradrenaline
What is the action of angiotensin on the adrenal cortex?
Stimulates release of aldosterone
What is the action of angiotensin on the hypothalamus?
Increases thirst sensation by stimulating ADH release
What are the actions of aldosterone?
- acts on principal cells of collecting ducts
- stimulates Na+ and therefore water reabsorption
- activates apical Na+ channel and apical K+ channel
- increases basolateral Na+ extrusion via Na/K/ATPase
What is the role of ACE and bradykinin in the RAAS?
They further augment the system - bradykinin has vasodilator actions, but it is broken down by ACE to form peptide fragments.
How does sympathetic nervous system stimulation regulation blood pressure?
- renal blood flow is reduced due to vasoconstriction of arterioles
- apical Na/H+ exchanger and basolateral Na/K ATPase in PCT are activated
- this stimulates renin release from cells
What are the main roles of antidiuretic hormone?
Formation of concentrated urine by retaining water to control plasma osmolarity. It retains water by stimulating Na+ resorption in the kidney.
What stimulates ADH release?
Increases in plasma osmolarity and severe hypovolaemia
How does atrial natriuretic peptide work?
It is synthesised and stored in the atrial myocytes, from which it is released in response to stretch, it promotes Na+ excretion, meaning that more water is lost and blood pressure is reduced. It also causes vasodilation of afferent arteriole to increase filtration rate of the blood.
What are the functions of prostaglandins?
- Act as vasodilators
- enhance glomerular filtration
- reduce Na+ resorption
- act as a buffer to prevent excessive vasoconstriction caused by SNS and RAAS
What does dopamine cause?
- increased renal blood flow
- reduces resorption of NaCl
What is hypertension?
A sustained increase in blood pressure. There are three stages - stage one (over 140/90), stage two (over 160/100) and severe (over 180 systolic or over 110 diastolic)
What is the difference between primary and secondary hypertension?
Primary - cause is unknown (95% of cases)
Secondary - cause can be defined, primary disease must be treated first
How does renovascular disease lead to secondary hypertension?
- occlusion of renal artery causes fall in perfusion pressure in the kidney
- decreased perfusion pressure leads to increased renin production
- activation of RAAS
- vasoconstriction and Na+ retention at other kidney
How does renal parenchymal disease lead to secondary hypertension?
Na+ and water retention due to inadequate glomerular filtration
Give some adrenal causes of secondary hypertension
- Conn's syndrome (aldosterone secreting adenoma)
- Cushing's syndrome (excess secretion of glucocorticoid cortisol)
- tumour of adrenal medulla (secretes catecholamines)
Why is it important to treat hypertension even if it's asymptomatic?
Can have unseen damaging effects on heart and vasculature, potentially leading to heart failure, MI, stroke, renal failure and retinopathy
Give some consequences of arterial damage
Atherosclerosis and weakened vessels leading to:
- cerebrovascular disease/stroke
- nephrosclerosis and renal failure
- myocardial ischaemia and MI
Hypertension causes increased afterload. Give some consequences of this.
Left ventricular hypertrophy, increased myocardial oxygen demand, heart failure, myocardial ischaemia and MI
Which organs are most likely to be damaged by hypertension?
Brain, eyes, heart, arteries, kidneys
Give some non-pharmacological approaches to treating hypertension
- reduced Na+ intake
- reduced alcohol intake
How can the RAA system be targeted when treating hypertension?
- use of ACE inhibitors
- Ang II receptor antagonists (this leads to NaCl and H2O retention)
How can vasodilators be used to treat hypertension?
- L-type Ca2+ channel blockers reduce entry of Ca2+ to vascular smooth muscle cells and cause relaxation
- alpha-1 receptor blockers reduce sympathetic tone and cause relaxation of vascular smooth muscle, but also cause postural hypotension
How can diuretics be used to treat hypertension?
Thiazides diuretics inhibit the Na/Cl co-transporter on apical membrane of cells distal tubule. This leads to a reduction in circulating volume.