#Renin #AldosteroneSystem #DrNajeeb

Renin Angiotensin Aldosterone System | RAAS👨‍⚕️

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▬▬▬▬▬▬▬▬▬▬ Contents of this video ▬▬▬▬▬▬▬▬▬▬

00:00:00 Explanation of RAAS with the help of a case of haemorrhage
00:03:42 Renin production in detail
00:13:53 Low Renal Perfusion leads to low Glomerular Filtration
00:17:05 External or Systemic Mechanism of Renin Production
00:22:02 Function of Renin
00:31:30 Actions of Angiotensin II
00:39:34 Action of Aldosterone
00:46:19 Angiotensin II action in CNS
00:53:21 Pathological functions of RAAS

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Explaining RAAS with the help of a case of hemorrhage; Low Renal Perfusion leading to Renin release from kidney.

Renin production in detail;
Low blood flow in Afferent arterioles; Polkissen are the modified afferent arteriolar smooth muscles that are able to measure blood flow to nephrons.
Low blood flow to nephrons; Polkissen releases Renin into the blood.
Second mechanism of Renin production: Na-sensing device in DCT; Macula Densa.
Polkissen measures blood flow/pressure and is derived from afferent arterioles; while Macula Densa is a Na-measuring device derived from nephrons in the kidney.
Polkissen and Macula Densa are held together by connective tissues; as a complex; known as Juxta Glomerular Apparatus (JGA).

Low Renal Perfusion leads to low Glomerular Filtration; slow movement of filtrate through nephrons; leads to increased Na+ reabsorption and ultimately decreased amount of Na+ reaching the Macula Densa of JG apparatus.
Polkissen of JG apparatus receive that message; and increases production of Renin.
Both are Intrarenal Mechanisms of Renin Production.

Extrarenal or Systemic Mechanism of Renin Production:
Baroreceptors in Carotid Sinus; Low blood flow activates them; message to CNS; Vasomotor Center (in Medulla) activated; stimulates the Sympathetic Outflow.
Sympathetic fibers in JG apparatus release Norepinephrine (NE) to act on Beta1-adrenergic receptors in JG apparatus; leading to increased production of Renin by JG apparatus.

Function of Renin: will go into systemic circulation through the renal vein.
Angiotensinogen (ATG); produced by the liver. Renin; (which is an enzyme) will act on ATG and convert ATG into Angiotensin-1(AT-1).
AT-1 gets converted into AT-2; enzyme in the lung (on the surface of endothelial cells) responsible for this conversion = Angiotensin Converting Enzyme (ACE).
ACE inhibitors (Captopril, Enalapril).
Bradykinin (a vasoconstrictor); is also broken down/inactivated by ACE; thus, doubly ensuring vasodilation.
Recap.

Actions of AT-2: AT-2 receptors are present in venous smooth muscles; AT-2 acts on them to cause venoconstriction; which increases Venous Return; increased Stroke Volume; increased Cardiac Output; increase in Systolic Blood Pressure (SBP).
AT-2 will also cause arteriolar vasoconstriction; results in blood retained in arterial tree during diastole; increased blood pressure during diastole = Increased Diastolic Blood Pressure (DBP).
AT-2’s action on Zona Glomerulosa (ZG) in Adrenal Cortex; releases Aldosterone.

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