RAAS Flashcards
what is the main role of RAAS
regulate volume and pressure
what is the first thing that happens during acute bleeds
decreased renal perfusion which stimulates the kidney to release renin into the veins of the kidneys.
afferent vs efferent
afferent brings blood to nephrons
what is the BP monitoring mechanism of the nephrons
Each nephron their own monitoring system. As afferent aterioles approach the glomerulus the normal smooth muscle cells that make the outer lining are altered and are called baroreceptors. The bundle of baroreceptors on a single afferent arteriole are known as a pokisin. These baroreceptors also have a second function which is to release renin.
describe the normal process of filtration in the kidneys
normally as blood passes through the afferent arterioles some of it gets filtered mainly sodium passes through into the nephron where 90%(most at the proximal convoluted tubule and the rest at the ascending loop of henley) is reabsorbed before reaching the distal convoluted tubule. At the junction of the distal convoluted tubule and the ascending loop of henley you have chemo receptors which like to monitor the salt levels. These chemo receptors are connected to the baroreceptors(pokinsin) with a layer of connective tissue. the bundle of chemo receptors here are known as the macula densa (b/c this part appears darker)
what is the juxtaglomerular apparatus
the pokisin + the macula densa apparatus together.
describe what happens to the filtrate as pressure drops
less filtrate is able to pass through into the lumen of the nephron causing the fluid the move slower through the nephron. Since the fluid is moving slower the proximal convoluted tubule and the ascending loop are able to reabsorb more sodium. This causes less sodium to reach the macula densa which causes it to activate. this causes it to release prostaglandins and nitric oxid these activate pokisin cells causing increase in renin. THEREFORE sodium changes and pressure changes can both cause a release in renin.
where else are baroreceptors located
carotid sinus (neck) which sends signals to the brain when it senses decrease in BP stem via the glossopharyngeal nerve(#9) the brain then stimulates sympathic nerves of the juxtaglomerular apparatus. the sympathic nerves release epinephrine which can bind to the b1 receptors on the JGA
what is renin
an enzyme that converts angiotensinogen to angiotensin 1 which is then converted to angiotensin 2 in the lungs (pulmonary capillaries endothelium) via angiotensin converting enzyme (ACE). ACE also breaks down bradykinin (vasodilator).
what is the main anabolic job of the liver
protein synthesis (e.g albumin, angiotensinogen)
what does angiotensin 2 do
- acts on and venous smooth muscle(the venous part of the capillary beds) this increases venous pressure increasing preload, increasing SV, increasing CO, increasing systolic BP(mainly determined by CO)
- acts on the arteriole smooth muscle. This causes vasoconstriction of the arterioles of the capillary bed. leading to increase in diastolic BP because less blood is able to get into the capillary bed and the pressure builds up.
- acts on the zona glomerulosa located on the outer cortex of the kidney. These cells have angiotensin 2 receptors. causing them to release aldosterone into circulation
- there are angiotensin 2 receptors in the hypothalamus also. stimulating the release of ADH making the last part of the nephron more permeaable to water.
- it also stimulates the SNS to release more norepi and also reuptake less of it
- there are angiotensin 2 receptors in the thrist region increasing thrist
how does aldosterone work
it works on the principle cells located at the end of the distal convoluted tuble and the collecting ducts. aldosterone enters the P cell and binds to the aldosterone receptors located on the nuclear membrane acting as the key to the cells genes. This starts the transcription of proteins that get placed into the basil layer of the plasma membrane of the p cell. These proteins are sodium/potassium ATPases. This casuses the cell to release sodium from the cytoplasm into the blood and start collecting potassium.
- Aldosterone receptors also activate a second gene which transcribe sodium channel proteins which connect the p cell to the lumen of the distal convoluted tubule. Since the sodium concentration is low in the cytoplasm the sodium will move into the p cells and then be released back into the blood stream via the sodium ATPases. Also remember that water follows sodium therefore water will also be reabsorbed
- a third gene which creates potassium channels that connect the p cell with the nephrone lumen. Since there is a bunch of potassium build up in the cytoplasm, potassium will start moving into the distal convoluted tubule where it will excreted in urine.
what can cause chronic elevation in RAAS and whats it lead to
low perfusion to kidney such as in CHF leading to chronic SNS activation leading to cardiomegaly
