Renin Angiotensin System

 
 

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Renin Angiotensin Aldosterone System is one of the most important physiological systems which does a lot of functions but its most important function is blood pressure regulation. For instance, if a patient has hemorrhage, this system gets activated and helps maintain blood pressure and blood volume.


Renin

Renin is an enzyme produced by kidney, (juxtaglomerular apparatus) in response to poor blood flow and decreased blood pressure. Its release is influenced by pressure change and Na+ change.


Polkissen

Polkissen is a special apparatus which is made of modified afferent arteriolar smooth muscles. This apparatus has the ability to measure blood flow when blood flow to nephron is decreased. If the blood flow is decreased this apparatus starts releasing renin. Since every nephron has its own Polkissen apparatus its like every nephron has a small endocrine system with it. This apparatus helps measure blood pressure and act as baroreceptors.


Macula Densa

There are some modified tall and dark cells present at the end of the thick part of ascending limb of loop of henle and distal convoluted tubule. These cells form macula densa and are sensitive to sodium. These are sodium sensors and act as chemoreceptors.


Juxtaglomerular Apparatus

Glomerular apparatus and macula densa are held together by lacis cells and collectively form Juxtaglomerular apparatus. If there is decreased blood volume and blood pressure, there will be decreased glomerular filtration resulting in decreased glomerular filtrate. This filtrate moves slowly in the lumen of the nephron and facilitiates reabsorption of sodium. The decreased amount of sodium in the lumen activates the macula densa and it releases nitric oxide and prostaglandins. Nitric oxide and prostaglandins further stimulate Polkissen cells resulting in further release of renin.


Carotid Sinus

There is another place where baroreceptors are present, this is bifurcation of carotid artery where blood pressure can be measured. When blood pressure decreases it gets activated and reports to CNS. It also stimulates sympathetic outflow through vasomotor center in medulla.From medulla this sympathetic outflow reaches to juxtaglomerular apparatus and there post ganglionic sympathetic nerve endings will release nor-epinephrine. This nor-epinephrine will stimulate (Beta 1) adrenergic receptors present in Juxtaglomerular apparatus and more renin will be released.


Renin Releasing Mechanisms:

Intra-renal

*Decreased blood pressure in afferent arteriole.

*Decreased sodium concentration in macula densa.

Extra-renal

*Sympathetic fibers connected with juxtaglomerular apparatus.

Renin will go to general circulation through renal vein.


Role of Angiotensinogen.

Angiotensinogen is produced by hepatocytes and renin converts this angiotensinogen into angiotensin-I (deca-peptide). When angiotensin-I passes through the lungs, it is converted into angiotensin-II (Octa-peptide) by angiotensin converting enzyme. This enzyme is present on surface of endothelial lining of pulmonary capillaries, for this reason it is also known as an Ecto-enzyme. This enzyme also causes breakdown of bradykinin. Bradykinin is a vasodilator however angiotensin-II is a vasoconstrictor. Breaking down of bradykinin causes decreased vasodilation and due to increased concentration of angiotensin-II results in vasoconstriction hence resulting in increased blood pressure.


Functions and Actions of Angiotensin-II.

Venular Constriction.

Angiotensin-II acts on receptors of venular smooth muscle, leading to venular constriction hence increasing venous return, which results in increased cardiac output ultimately increasing systolic blood pressure.


Arteriolar Constriction.

Angiotensin-II also acts on cells of arteriolar smooth muscle and causes arteriolar constriction. This will result in retention of blood on the arterial side, the pressure will also increase in the arterial tree during diastole resulting in increased diastolic blood pressure.


Release of Aldosterone in Renin Angiotensin Aldosterone System.

Angiotensin-II also acts on the cells of Zona glomerulosa (adrenal cortex) and causes release of aldosterone. Aldosterone acts on the principal cells (p-cells) which are present at last part of distal convoluted tubules and collecting tubules. On activation of receptor it stimulates different genes. Gene-I makes special type of protein known as Na+/K+ ATPase (Na+/K+ pump) planted in baso-lateral membrane of P-cells. It throws Na+ out of the cell and K+ starts accumulating into the cell. Gene-II produces special proteins, known as Na-channels, planted in luminal membrane of P-cells, through these channels, Na+ moves from distal convoluted tubules and collecting tubules to the P-cells. Along Na+, water is also absorbed. Gene-III produces proteins known as K-channels, planted in luminal membrane of P-cells. Through these channels K+ leaks out into lumen (urine). Under influence of aldosterone, reabsorption of Na+ and water increases resulting in increased blood volume, increased venous return and eventually increased systolic blood pressure.


Release of ADH.

Angiotensin-II acts on its receptors in hypothalamus which results in production of ADH from posterior pituitary gland. This ADH will make last part of nephron more permeable to water and more reabsorption of water takes place.


Super stimulation of sympathetic nervous system.

Angiotensin-II increases central sympathetic outflow and in post-ganglionic sympathetic nerve endings it will increase nor-epinephrine secretion and decrease its reuptake, so this causes increase response of target tissue and also increases adrenergic receptors of target tissue.


Stimulation of Thirst Center.

Angiotensin-II stimulates thirst center in CNS and increases water intake.


Cardiac Remodeling.

In congestive cardiac failure, blood flow to kidney decreases leading to chronic activation of renin angiotensin aldosterone system and chronic sympathetic activation. Consequently, proto-oncogenes in myocardium will be stimulated leading to pathological hypertrophy of the heart, at the sometime extra production of connective tissue takes place. Resulting in progressive alteration of geometry of heart, this phenomena is called cardiac remodeling.


Vascular Pathology.

Chronically elevated angiotensin-II also work on smooth muscles of vessels and produce vascular pathologies.


Angiotensin converting enzyme Inhibitors (ACE-1).

This group of drugs inhibits angiotensin-I converting enzyme, and decreases angiotensin II resulting in prevention of cardiac remodeling. We hope you liked this article on Renin Angiotensin Aldosterone System.


 

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