RAAS system Flashcards
What is Renin?
An enzyme released by the JGA. which results in the
formation of angiotensin II.
What is the Juxtaglomerular apparatus (J GA)?
The combination of the tubular cells of the macula densa, granular afferent arteriolar cells that secrete renin, and extraglomerular mesangial cells.
What are the Macula densa?
A patch of columnar tubular epithelial cells
that forms part of the JGA and may sense tubular ion
concentration. It is situated at the junction of the thick
ascending limb of the loop of Henle and the early distal
tubule.
The Systemic Blood pressure can vary from 80-180 mm Hg systolic? What is a healthy reference range?
- 120 mm Hg is reference
What does RAAS stand for?
Renin-Angiotensin-Aldosterone System.
RAAS is an important hormone axis effecting the kidney.
What can activate the RAAS system?
The system can be activated when there is a:
- loss of blood volumeor a drop inblood pressure(such as inhemorrhageordehydration). This loss of pressure is interpreted bybaroreceptorsin thecarotid sinus.
- A decrease in the filtrate NaCl concentration and/or decreased filtrate flow rate will stimulate themacula densato signal thejuxtaglomerular cellsto release renin.
What are the four stages of RAAS system action?
- If perfusion at juxtaglomerular apparatusin the kidney’smacula densadecreases, the juxtaglomerular cells (granular cells, modified pericytes in the glomerular capillary) release theenzymerenin.
- Renin cleaves a decapeptide from a plasmaα-2-globulincalledangiotensinogen. The 10 amino acid long peptide is known asangiotensin I.
- Angiotensin I is then converted toangiotensin IIbyangiotensin-converting enzyme(ACE), found in lung cells and endothelial cells.
- Angiotensin II is the major bioactive product of the renin-angiotensin system, binding to receptors onintraglomerular mesangial cells, causing these cells to contract along with systemic blood vessels. Angiotensin II is a potent vasoconstrictor, 40X more potent than epinephrine. Angiotensin II also acts on theadrenal cortexculminating in the release ofaldosteronefrom thezona glomerulosa. Angiotensin II acts as anendocrine,autocrine/paracrine, andintracrinehormone.
What does aldosterone do?
Aldosterone, is a steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland. It is essential for sodium conservation in the kidney, salivary glands, sweat glands and colon. It plays a central role in the regulation of the plasma sodium (Na+), the extracellular potassium (K+) and arterial blood pressure.
It does so mainly by acting on the mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron.
It influences the reabsorption of sodium and excretion of potassium (from and into the tubular fluids, respectively) of the kidney, thereby indirectly influencing water retention or loss, blood pressure and blood volume.
How does Myogenic feedback work during High BP?
HIGH BP —»increased RenaI BIood FIow —»stretches Vascular Smooth Muscle in AFFERENT arteriole—»leads to automatic constriction of afferent =reduces flow to glomerulus = - GFR to minimise damage to renal tissue during high BP.
How does the Myogenic feedback work during Low BP?
Low BP -»reduced RBF —»> relaxes Vascular Smooth Msucle in AFFERENT arteriole —»> leads to automatic vasodilatation of afferent = increased flow to glomerulus.
What are the extrinsic mechanisms that kick in when low BP happens?
— Extrinsic mechanisms kick in
. Sympathetic Nervous System (vasoconstriction)
. Angiotensin II
. Endothelin to some extent (vasoconstriction)
. Prostaglandins (vasodilate afferent)
. Nitric Oxide (vasodilate afferent)
The JGA releases renin in response to a drop in:
- afferent arteriolar pressure.
- a fall in tubular flow rate,
- or a fall in tubular sodium and chloride concentration at the macula densa
- Other stimuli include sympathetic nerve stimulation of beta 1-adrenergic receptors.
ReniN promotes production of Angiotensin II which acts via AT1 (type 1 angiotensin II receptors) to vasoconstrict afferent and efferent arterioles. What is the dominant effect of this?
Dominant effect is on efferent arteriolar constriction. so the GFR is increased during low BP.
What does the RAAS enable after a meal?
The RAAS enables variable salt intake, whilst
maintaining ECF volume and thus arterial pressure
i.e. 50-fold increase in salt intake —only moves pressure by 5-6mmHg. Without the RAAS, pressure may go up 50-6OmmHg!
Angiotensin II also induces ……………. in aid of the rapid response of the RAAS to restore Na content in body and thus blood volume/BP.
Insertion of Na channels in : *renal tubules via AT1 *In the Proximal tubule *In the Thick ascending limb *In the Collecting duct — via Epithelial Na channel (ENaC)
