control of blood pressure Flashcards
what is normal BP
between 90/60mmHg and 120/80mmHg
what are the 3 classifications of hypertension
stage 1 hypertension - more than 140/90 mmHg
stage 2- more than 160/100 mmHg
severe hypertension- more than 180 systolic or more than 110 diastolic
what causes hypertension
primary hypertension- when the cause is unknown
secondary- when the cause can be defined e.g renovascular disease, chronic renal disease, hyperaldosteronism, Cushing’s syndrome.
what organs does hypertension damage and should be examined
eyes - hypertensive retinopathy brain heart arteries- listen for bruit kidneys - may be enlarged , listen for bruit , urine test
how is blood pressure regulated short term
baroreceptor reflex - nerve endings in the carotid sinus and aortic arch are sensitive to stretch so can detect BP.
adjust sympathetic and parasympathetic inputs to the heart to alter cardiac output.
adjust sympathetic input to peripheral input to peripheral resistance vessels to alter TPR
how is blood pressure regulated medium and longterm
complex interaction of neurohumoral responses
directed at controlling sodium balance and thus extracellular fluid volume
-control of extracellular fluid vol controls plasma vol
water follows Na+ therefore controlling total body Na+ levels controls plasma vol
what are the four parallel neurohumeral pathways that control circulating volume and hence BP
- renin-angiotensin-aldosterone system
- sympathetic nervous system
- antidiuretic hormone
- atrial natriuretic peptide
factors stimulating renin release
reduced NaCl delivery to detail tubule of kidney
reduced perfusion pressure( sensing low BP/less blood supply) in the kidney detected by baroreceptors in afferent arteriole
sympathetic stimulation in JGA increases release of renin
what are the types of angiotensin ii receptors
AT1 and AT2
main actions via AT1 receptor
g-protein coupled receptor
what do angiotensin ii receptors on these sites cause : arterioles , kidney, sympathetic NS, adrenal cortex, hypothalamus
arterioles- vasoconstriction
kidney - stimulates Na+ reabsorption at the kidney raising plasma vol
sympathetic NS- increased release of NA
adrenal cortex- stimulates release of aldosterone
Hypothalamus -increases thirst sensation (stimulates ADH release)
action of aldosterone on the kidney
acts on principal cells of collecting ducts
stimulates Na+ and therefore water reabsorption
activates apical Na+ channel (ENaC) and apical k+ channel
also increases basolateral Na+ extrusion via Na/K/ATPase
what is the issue with angiotensin converting enzyme (ACE)
has vasodilator actions
as it is also the enzyme that breaks down bradykinin into peptide fragments
this causes dry cough as some is found in the lungs
how SNS regulates BP
high levels of sympathetic stimulation reduce renal blood flow by vasoconstriction of arterioles and also by decreasing GFR which decreases Na+ secretion. this stimulates renin release leading to increased Ang II levels leading to increased aldosterone production causing increased Na+ reabsorption.
how antidiuretic hormone reduces BP
main role is formation of a concentrated urine by retaining water to control plasma osmolarity
ADH release is stimulated by plasma osmolarity/ severe hypovolaemia
stimulates Na+ reabsorption
and cause some vasoconstriction
how natriuretic peptides reduce blood pressure
atrial natriuretic peptide (ANP) promotes Na+ excretion
ANP is made and stored in atrial myocytes and is released in response to stretch.
ANP causes vasodilation of the afferent arteriole which increases blood flow increasing GFR.
inhibits Na+ reabsorption along the nephron.
ANP is inhibited if there is low circulating vol
role of prostaglandins
act as vasodilators
reduces BP
reduces Na+ reabsorption
important when levels of Ang II is high
role of dopamine in terms of BP
found locally in kidney from circulating L-DOPA
causes vasodilation and increases renal flow
reduces reabsorption of NaCl
how renovascular disease causes hypertension
occlusion of renal artery causes fall in perfusion pressure in that kidney leading to increased renin production.
this activates the renin-angiotensin-alsosterone system and causes vasoconstriction and Na+ retention at the other kidney
how Cushing’s syndrome can accuse hypertension
excess secretion of cortisol which at high conc can act o aldosterone receptors causing retention of Na+ and water.
non pharmacological way to treat hypertension
exercise
diet
reduce Na+ intake
reduce alcohol
pharmacologically treating hypertension
ACE inhibitors- e.g captopril, lisinopril, perindopril, enalapril. prevent production of Ang II and Ang I.
Ang II receptor antagonists-losartan, valsartan, temisartan.
L type Ca channel blockers - reduce Ca2+ entry to vascular smooth muscle cells causing relation of muscle (vasodilation).
a1 receptor blockers- reduce sympathetic tone causing vasodilation.
thiazide diuretics- reduce circulating vol. inhibit Na/Cl co-trransporter on apical membrane of cells in distal tubule.
