Differentiate between neuronal and hormonal control of blood pressure.
Neuronal: fast acting, moment-to-moment regulation, imp for postural hypotension and BP maintenance after hemorrhage
Hormonal: slower, sensor in juxtaglomerular apparatus of DCT, regulates GFR by tubuloglomerular feedback and also regulates BP
What are the 3 components of the juxtaglomerular apparatus?
1. Macula densa cells
2. Extraglomerular mesangial cells in between efferent and afferent arteriole
3. Juxtaglomerular/granular cells around afferent and efferent arteriole walls
A: Extraglomerular mesangial cells
B: Macula densa cells
C: Granular cells
D: juxtaglomerular apparatus
What happens if the conc of Na+ in DCT fluid is too low (= low GFR)?
Persistant low Na+ in DCT -> macula densa signals to juxtaglomerular cells -> release renin to efferent arterioles -> cleaves angiotensinogen from liver to angiotensin I (10aa) -> lungs -> cleaved by angiotensin-convertin-enzyme (ACE) to angiotensin II (8aa) = constrictor of SM of systemic arterioles, thus increasing BP -> raises GFR and afterload.
Angiotensin II also constricts SM in efferent arteriole (increases filtration pressure in glomerulus)
Angiotensin also stimulates secretion of steroid hormone aldosterone from adrenal glands atop kidney -> acts on receptors in DCT and stimulates Na+ reabsorption -> increases H2O absorption -> decreased loss in urine and increase in blood volume, BP and preload.
ADH is also released
How does aldosterone act in DCT?
Apart from the RAA system, how can renin also be released?
Increases ENaC channel expression and Na/K pump expression
Sympathetic stim - sympathetic nerves to kidney, and beta receptors on cells of JGA. Possibility of +ve fb.
Where are angiotensin II receptors found?
Describe the 2 types of angiotensin II receptors.
On luminal surface of endothelium lining BVs.
1) AT1: GPCR, directly increases BP by increasing Ca2+ entry into underlying SM = constrict. Indirectly increases BP by stimulating NA release from sympathetic nerve terminals. AT1 may cause hypertrophy irt systemic hypertension. AT1 also on adrenal cortex.
2) AT2: Actions in CNS, maybe involved in nueron apoptosis, growth and development
How do the AT1 receptors in adrenal cortex act?
The action of this is opposite to what hormone?
Secrete mineralcorticoid steroid hormone aldosterone, acts on receptors in DCT - stimulates Na+ reabsoprtion -> increases H2O reabsorption so increase in blood vol and BP
How does renin affect the blood volume and blood pressure control system?
What happenes to the blood pressure if there is an atheroma in the renal artery?
Affects BP system via affect of angiotensin II on systemic arteriolees, and blood vol system via effect of aldosterone on kidney tubules
Decreased blood flow to kidney -> decreased GFR -> more Na+ reabsorbed -> decreased Na+ in DCT -> JGA releasese renin -> BP increases
Describe the 5 drugs used to decrease hypertension (with 1 and 2 being the main ones). What is the first line treatment?
Give SEs, and examples for the first two.
1. ACE inhibitors: block ACE = prevent angiotensin II formation, SE: cough, decreased BP, captopril
2. Angiotensin receptor angtagonists: block AT1 receptors, SE: dereased BP, losartan
3. Ca2+ antagonists: vasodilate (1st line for high BP), SE: flushing, oedema
4. Thiazides: Salt/H2O loss (decreases Na+ reabsorption in DCT)/vasodilation, SE: impotence, low K+
5. Beta-blockers: slow heart rate, decrease renin secretion, SE: lethargy, bronchospasm
NB: drugs do not cure primary problem (poss. poor renal perfusion), and kidney may respond to ACE inhibitors by increasing renin output and have to then give greater drug doses.
What 3 things happen to control BP and blood volume after blood loss via hemorrhage?
1. H2O moves into blood (osmosis) = increased volume but more dilute, Na+ conc decreases, hyponatraemia occurs (plasma Na+ = 140mmol/L normally but becomes <135mmol/L)
2. Sympathetic NA constricts veins (where 3/4 circulating blood is = venous return to heart and cardiac vol almost unchanged)
3. Na+ conc decreases in DCT b/c blood diluted even though GFR normal -> renin release -> angiotensin -> aldosterone -> increased Na+ reabsorption in DCT
This ensures a small vol of hemorrhage does not affect BP
Label A and B