Renin Angiotensin Aldosterone System (RAAS)

HOW RENIN IS RELEASED FROM KIDNEY DURING LOW BP TO MAINTAIN BP INTO NORMAL SET POINT:

Decreased blood pressure cause decreased renal perfusion via Afferent artery, theses afferent artery is interconnected with Juxtaglomerular apparatus (artery has specialized Smooth cells called POLKISON CELLS and Macula densa on PCT is interconnected with Lasix cells. These 3 things makes a group of cells called Juxtaglomerular apparatus) which acts as baroreceptor of kidney.*RAAS system 

Juxtaglomerular apparatus is stimulated by

1) Decreased BP so called decreased renal perfusion/flow and Juxtaglomerular apparatus is less stretched which releases Renin and flow towards venous system via Efferent artery.

2) Decreased NA+ ions in blood during low BP. Juxtaglomerular apparatus is near to Bowman's capsule and Glomerular filtration rate is decreased and Movements of NA+ ions in lumen decreased and increase Reabsorption affinity and Reabsorbed back to the blood thus increases blood pressure.

3) During Vasomotor stimulation by baroceptors to adrenal medulla. releases NE/Epi which Stimulates Juxtaglomerular apparatus via B1 receptor and releases Renin and flow into systemic circulation via efferent artery thus increases BP.*RAAS system 

SUMMARY :-

1) Decreased renal perfusion during low bp releases renin from Juxtaglomerular apparatus and increases BP.

2) Stimulation of juxta medullary apparatus by B1 releases renin and increases BP

3) Decreased NA+ ion in the blood stimulates Bowman's capsule to slow GMR by which retention of Na+ ions occurs and increases BP

The released Renin enters the systematic Circulation.

Mechanism of RAAS :-

From Liver Angiotensinogen ( inactivated deca peptide) is released and Coverts into Angiotensin-I by renin (From systemic circulation) by removing 2 peptides (Still inactive) which converted into Angiotensin-II by A.C.E which is found in Microvascular Endothelial cells of Pulmonary system and Activated ANG-II which binds to AT-1 receptors located specifically all over the body.* RAAS

Location and Function of ANG-II receptor "AT1":

1-Vessles (Veins + Arteries) and vasoconstriction

General Mechanism:

ANG-II is Gq coupled which increase PLC and Breaks PIP2 into  DAG and IP3, IP3 releases Ca+ from endoplasmic reticulum of the SM cell cause Contraction and increases BP.

(I) Vein dilation due to ANG-II  increase Venous return , increase Afterload ,increase Stroke volume , increase Cardiac output, and increase Systolic Blood pressure.

(II) Arteriolodilation due to ANG-II increase  Total peripheral resistance (TPR) and increase Diastolic Blood pressure.*RAAS system 

2-Hypothalamus

ANG-II acts on Hypothalamus ,increase  Thirst increase Water intake which in turn increse Blood volume ,increase Venous return , increase Afterload, increase Stroke volume, increase Cardiac output and finally increase Systolic Blood pressure.

3- Sympathetic post nerves endings

AT1 also present on Sympathetic outflow, increase stimulation of sympathetic outflow by releasing the increase Nor eepinephrine cause Cardio stimulation + adrenal gland +Juxtaglomerular apparatus stimulation and increases Systolic+ Diastolic BP.*RAAS system 

4- Adrenal gland

Zona Glomerular release Aldosterone and Steroid lipid soluble hormone which distributes in All tissues including kidney , Collecting duct cause Stimulation of Aldosterone receptors in Principal cell of Collecting duct cause Formation of the following Genes

 Na+ channels-Luminal membrane , Na+ comes in from Lumen into principal cells cause Na+ Retention.

 K+ channels -Luminal membrane, K+ Comes out  from the Principal cells into the lumen --cause K+ loss.

Na/K ATPase antipork channel - Formation of these channels in basoliteral membrane of principal cells then more Na+ retention into the principal cells and more K+ excretion to the cells

above all have significant High blood pressure effect.*RAAS

Pharmacology of RAAS:

Renin Inhibitors:

Aliskirin

ACE inhibitors

Captopril

Lisinopril

Enalapril

Quinapril

Benzapril

Ramipril

AT1 blockers:

Telmisartan

Losartan

Valsartan

Candesartan

Ibrasartan

Olmesartan

Note :-

ACE also breaks bradykinin ,by blocking ACE, no breakdown of Bradykinin hence vasodilatory and antihypertensive affect is achieved but causes dry cough and oedema due to vasodilation because it increases permeability of the cells causes leakage of fluid into tissues causes dry cough and oedema.* RAAS system 

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