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Raas System

The Renin-Angiotensin System (RAS) is a hormone system that regulates blood pressure and fluid balance by releasing renin in response to low blood pressure or volume. This initiates a cascade resulting in the formation of angiotensin II, which causes vasoconstriction, stimulates aldosterone and ADH release, and promotes sodium and water retention. Dysregulation of the RAS can lead to hypertension and other health issues, making it a target for various medications.

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6 views2 pages

Raas System

The Renin-Angiotensin System (RAS) is a hormone system that regulates blood pressure and fluid balance by releasing renin in response to low blood pressure or volume. This initiates a cascade resulting in the formation of angiotensin II, which causes vasoconstriction, stimulates aldosterone and ADH release, and promotes sodium and water retention. Dysregulation of the RAS can lead to hypertension and other health issues, making it a target for various medications.

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fredrick ciira
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The Renin-Angiotensin System (RAS), also known as the Renin-Angiotensin-Aldosterone

System (RAAS), is a crucial hormone system that regulates blood pressure, fluid balance, and
electrolyte balance in the body. It's a complex cascade of reactions involving several key
components. Here's a step-by-step breakdown:

1. Stimulus for Renin Release:

The RAS is activated when there's a decrease in blood pressure or blood volume. This can be
detected by three main mechanisms:

 Juxtaglomerular (JG) cells in the kidneys: These cells, located in the walls of the
afferent arterioles (blood vessels entering the glomerulus), act as baroreceptors. When
they sense a decrease in blood pressure, they release renin.
 Macula densa in the kidneys: These specialized cells in the distal tubule monitor the
sodium and chloride concentration in the tubular fluid. If the concentration is low
(indicating low blood flow and filtration), they signal the JG cells to release renin.
 Sympathetic nervous system: Activation of the sympathetic nervous system (e.g.,
during stress or exercise) stimulates beta-1 adrenergic receptors on the JG cells, leading
to renin release.

2. Renin Action:

 Renin is an enzyme released into the bloodstream by the JG cells.


 It acts on a large protein produced by the liver called angiotensinogen, converting it into
angiotensin I. Angiotensin I is relatively inactive.

3. Conversion of Angiotensin I to Angiotensin II:

 Angiotensin I travels in the blood, primarily to the lungs.


 In the lungs (and also in the kidneys and vascular endothelium), an enzyme called
angiotensin-converting enzyme (ACE) converts angiotensin I into angiotensin II.
 Angiotensin II is the primary active hormone of the RAS.

4. Effects of Angiotensin II:

Angiotensin II has a wide range of powerful effects on the body, all aimed at increasing blood
pressure and blood volume:

 Vasoconstriction: Angiotensin II is a potent vasoconstrictor, causing the smooth muscles


in the walls of blood vessels to narrow. This increases peripheral resistance and directly
raises blood pressure. It preferentially constricts the efferent arterioles in the kidneys,
which helps maintain glomerular filtration rate (GFR) even when overall kidney blood
flow is reduced.
 Aldosterone Release: Angiotensin II stimulates the adrenal cortex (outer layer of the
adrenal glands) to release aldosterone. Aldosterone acts on the distal tubules and
collecting ducts of the kidneys to increase the reabsorption of sodium and water into the
blood, while promoting the excretion of potassium. This increases blood volume and
consequently blood pressure.
 Antidiuretic Hormone (ADH) Release: Angiotensin II stimulates the posterior pituitary
gland to release antidiuretic hormone (ADH), also known as vasopressin. ADH
increases water reabsorption in the collecting ducts of the kidneys, further increasing
blood volume and blood pressure. It also causes vasoconstriction.
 Thirst Stimulation: Angiotensin II acts on the hypothalamus in the brain to increase the
sensation of thirst, leading to increased fluid intake and thus increased blood volume.
 Sodium Reabsorption in the Kidneys: Angiotensin II directly stimulates sodium
reabsorption in the proximal tubules of the kidneys, further contributing to increased
blood volume.
 Increased Sympathetic Activity: Angiotensin II can increase the release of
norepinephrine from sympathetic nerve endings and inhibit its reuptake, enhancing
sympathetic nervous system activity, which also leads to vasoconstriction and increased
heart rate.

5. Regulation of the RAS:

The RAS is a tightly regulated system. As blood pressure and volume increase due to the actions
of angiotensin II and aldosterone, the initial stimuli for renin release are reduced, leading to a
negative feedback loop that prevents excessive increases in blood pressure. Other hormones,
such as atrial natriuretic peptide (ANP), also act to counter the effects of the RAS.

In summary, the Renin-Angiotensin System is a vital hormonal mechanism that the body
uses to maintain blood pressure and fluid balance. When blood pressure drops, the kidneys
release renin, initiating a cascade that leads to the production of angiotensin II and
aldosterone, ultimately causing vasoconstriction, increased sodium and water retention,
and increased blood volume, thereby raising blood pressure back to normal.

Dysregulation of the RAS can contribute to conditions like hypertension, heart failure, and
kidney disease, which is why many medications target different components of this system to
manage these conditions.

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