Renin–angiotensin system: Difference between revisions
Created page with "{{Short description|Hormone system}} thumb|250px|Anatomical diagram of RAS The '''renin–angiotensin system''' ('''RAS'''), or '''renin–angiotensin–aldosterone system''' ('''RAAS'''), is a hormone system that regulates blood pressure, fluid and electrolyte balance, and systemic vascular resistance. When renal blood flow is reduced, juxtag..." |
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{{Short description|Hormone system}} | {{Short description|Hormone system}} | ||
[[File:Renin-angiotensin system in man shadow.svg|thumb|250px|Anatomical diagram of RAS]] | [[File:Renin-angiotensin system in man shadow.svg|thumb|250px|Anatomical diagram of RAS]] | ||
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[[File:RenalHormoneRegulation.png|thumb|350px |Renal hormone regulation schematic]] | [[File:RenalHormoneRegulation.png|thumb|350px |Renal hormone regulation schematic]] | ||
Angiotensin I may have some minor activity, but angiotensin II is the major bio-active product. Angiotensin II has a variety of effects on the body: | Angiotensin I may have some minor activity, but angiotensin II is the major bio-active product. Angiotensin II has a variety of effects on the body: | ||
* Throughout the body, angiotensin II is a potent [[vasoconstrictor]] of [[arteriole]]s. | * Throughout the body, angiotensin II is a potent [[vasoconstrictor]] of [[arteriole]]s. | ||
* In the kidneys, angiotensin II constricts [[Glomerulus (kidney)|glomerular]] arterioles, having a greater effect on [[efferent arterioles]] than afferent. As with most other capillary beds in the body, the constriction of [[afferent arterioles]] increases the arteriolar resistance, raising [[systemic circulation|systemic]] [[arterial blood pressure]] and decreasing the blood flow. However, the kidneys must continue to filter enough blood despite this drop in blood flow, necessitating mechanisms to keep glomerular blood pressure up. To do this, angiotensin II constricts efferent arterioles, which forces blood to build up in the glomerulus, increasing glomerular pressure. The [[glomerular filtration rate]] (GFR) is thus maintained, and blood filtration can continue despite lowered overall kidney blood flow. Because the filtration fraction, which is the ratio of the glomerular filtration rate (GFR) to the renal plasma flow (RPF), has increased, there is less plasma fluid in the downstream peritubular capillaries. This in turn leads to a decreased [[hydrostatic pressure]] and increased [[oncotic pressure]] (due to unfiltered [[plasma proteins]]) in the peritubular capillaries. The effect of decreased hydrostatic pressure and increased oncotic pressure in the peritubular capillaries will facilitate increased reabsorption of tubular fluid. | * In the kidneys, angiotensin II constricts [[Glomerulus (kidney)|glomerular]] arterioles, having a greater effect on [[efferent arterioles]] than afferent. As with most other capillary beds in the body, the constriction of [[afferent arterioles]] increases the arteriolar resistance, raising [[systemic circulation|systemic]] [[arterial blood pressure]] and decreasing the blood flow. However, the kidneys must continue to filter enough blood despite this drop in blood flow, necessitating mechanisms to keep glomerular blood pressure up. To do this, angiotensin II constricts efferent arterioles, which forces blood to build up in the glomerulus, increasing glomerular pressure. The [[glomerular filtration rate]] (GFR) is thus maintained, and blood filtration can continue despite lowered overall kidney blood flow. Because the filtration fraction, which is the ratio of the glomerular filtration rate (GFR) to the renal plasma flow (RPF), has increased, there is less plasma fluid in the downstream peritubular capillaries. This in turn leads to a decreased [[hydrostatic pressure]] and increased [[oncotic pressure]] (due to unfiltered [[plasma proteins]]) in the peritubular capillaries. The effect of decreased hydrostatic pressure and increased oncotic pressure in the peritubular capillaries will facilitate increased reabsorption of tubular fluid. | ||
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==Fetal renin–angiotensin system== | ==Fetal renin–angiotensin system== | ||
In the [[fetus]], the renin–angiotensin system is predominantly a sodium-losing system, | In the [[fetus]], the renin–angiotensin system is predominantly a sodium-losing system, as angiotensin II has little or no effect on aldosterone levels. Renin levels are high in the fetus, while angiotensin II levels are significantly lower; this is due to the limited pulmonary blood flow, preventing ACE (found predominantly in the pulmonary circulation) from having its maximum effect. | ||
==Clinical significance== | ==Clinical significance== | ||
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[[Category:Cardiovascular physiology]] | [[Category:Cardiovascular physiology]] | ||
[[Category:Endocrinology]] | [[Category:Endocrinology]] | ||
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