Help with RAAS Physiology - Anatomy

Aldosterone is a steroid hormone that is released from the adrenal cortex. The function of aldosterone is to increase reabsorption of sodium ions from the distal tubule. Increased sodium ion concentration in the blood then causes the diffusion of water from the nephron into the circulatory system, preventing water loss due to excretion and increasing blood pressure and volume)

Release of aldosterone is mediated by the renin-angiotensin system (RAS). When juxtaglomerular cells detect low blood pressure, they release renin. Renin travels to the liver, where there angiotensinogen is produced, and cleaves angiotensinogen to produce angiotensin I. Angiotensin I then travels to the lungs, where angiotensin converting enzyme (ACE) cleaves it to produce angiotensin II. Angiotensin II then travels to the adrenal cortex to stimulate release of aldosterone into the blood.

Adrenocorticotropic hormone is secreted by the anterior pituitary and acts on the adrenal cortex to stimulate release of cortisol and cortisone, but does not affect aldosterone release. Vasopressin is released by the posterior pituitary and helps the body to retain water; it is not related to aldosterone release.

Renin is a hormone released by granular cells in the juxtaglomerular apparatus, near the nephron glomerulus. These cells monitor the pressure of the filtrate in the distal convoluted tubule. The release of renin will stimulate a cascade of angiotensin I and II. Angiotensin II will ultimately stimulate the adrenal cortex to release aldosterone and increase sodium reabsorption and potassium excretion from the filtrate, leading to water retention.

Angiotensin II is a major influence on the kidney's function when the body needs to retain fluid - it works in tandem with antidiuretic hormone and aldosterone to accomplish this. Angiotensin II will also act upon the afferent and efferent arterioles in order to control the glomerular filtration rate and stimulates reabsorption to ensure that the body is keeping necessary solutes/molecules. Diluting the filtrate in the nephron is the opposite effect that angiotensin has on the kidney.

Angiotensin II (part of the RAAS) works in the body to cause vasoconstriction in an effort to raise blood pressure. Too much of this substance will cause hypertension, another name for elevated blood pressure. Nitric oxide and prostacyclin work to vasodilate and lower blood pressure. Atrial natriuretic peptide and brain natriuretic peptide are released by the body to lower blood pressure in volume overloaded states.

Aldosterone is a steroid hormone that is released from the adrenal cortex. The function of aldosterone is to increase reabsorption of sodium ions from the distal tubule. Increased sodium ion concentration in the blood then causes the diffusion of water from the nephron into the circulatory system, preventing water loss due to excretion and increasing blood pressure and volume)

Release of aldosterone is mediated by the renin-angiotensin system (RAS). When juxtaglomerular cells detect low blood pressure, they release renin. Renin travels to the liver, where there angiotensinogen is produced, and cleaves angiotensinogen to produce angiotensin I. Angiotensin I then travels to the lungs, where angiotensin converting enzyme (ACE) cleaves it to produce angiotensin II. Angiotensin II then travels to the adrenal cortex to stimulate release of aldosterone into the blood.

Adrenocorticotropic hormone is secreted by the anterior pituitary and acts on the adrenal cortex to stimulate release of cortisol and cortisone, but does not affect aldosterone release. Vasopressin is released by the posterior pituitary and helps the body to retain water; it is not related to aldosterone release.

Renin is a hormone released by granular cells in the juxtaglomerular apparatus, near the nephron glomerulus. These cells monitor the pressure of the filtrate in the distal convoluted tubule. The release of renin will stimulate a cascade of angiotensin I and II. Angiotensin II will ultimately stimulate the adrenal cortex to release aldosterone and increase sodium reabsorption and potassium excretion from the filtrate, leading to water retention.

Angiotensin II is a major influence on the kidney's function when the body needs to retain fluid - it works in tandem with antidiuretic hormone and aldosterone to accomplish this. Angiotensin II will also act upon the afferent and efferent arterioles in order to control the glomerular filtration rate and stimulates reabsorption to ensure that the body is keeping necessary solutes/molecules. Diluting the filtrate in the nephron is the opposite effect that angiotensin has on the kidney.

Angiotensin II (part of the RAAS) works in the body to cause vasoconstriction in an effort to raise blood pressure. Too much of this substance will cause hypertension, another name for elevated blood pressure. Nitric oxide and prostacyclin work to vasodilate and lower blood pressure. Atrial natriuretic peptide and brain natriuretic peptide are released by the body to lower blood pressure in volume overloaded states.

Aldosterone is a steroid hormone that is released from the adrenal cortex. The function of aldosterone is to increase reabsorption of sodium ions from the distal tubule. Increased sodium ion concentration in the blood then causes the diffusion of water from the nephron into the circulatory system, preventing water loss due to excretion and increasing blood pressure and volume)

Release of aldosterone is mediated by the renin-angiotensin system (RAS). When juxtaglomerular cells detect low blood pressure, they release renin. Renin travels to the liver, where there angiotensinogen is produced, and cleaves angiotensinogen to produce angiotensin I. Angiotensin I then travels to the lungs, where angiotensin converting enzyme (ACE) cleaves it to produce angiotensin II. Angiotensin II then travels to the adrenal cortex to stimulate release of aldosterone into the blood.

Adrenocorticotropic hormone is secreted by the anterior pituitary and acts on the adrenal cortex to stimulate release of cortisol and cortisone, but does not affect aldosterone release. Vasopressin is released by the posterior pituitary and helps the body to retain water; it is not related to aldosterone release.

Renin is a hormone released by granular cells in the juxtaglomerular apparatus, near the nephron glomerulus. These cells monitor the pressure of the filtrate in the distal convoluted tubule. The release of renin will stimulate a cascade of angiotensin I and II. Angiotensin II will ultimately stimulate the adrenal cortex to release aldosterone and increase sodium reabsorption and potassium excretion from the filtrate, leading to water retention.

Angiotensin II is a major influence on the kidney's function when the body needs to retain fluid - it works in tandem with antidiuretic hormone and aldosterone to accomplish this. Angiotensin II will also act upon the afferent and efferent arterioles in order to control the glomerular filtration rate and stimulates reabsorption to ensure that the body is keeping necessary solutes/molecules. Diluting the filtrate in the nephron is the opposite effect that angiotensin has on the kidney.

Angiotensin II (part of the RAAS) works in the body to cause vasoconstriction in an effort to raise blood pressure. Too much of this substance will cause hypertension, another name for elevated blood pressure. Nitric oxide and prostacyclin work to vasodilate and lower blood pressure. Atrial natriuretic peptide and brain natriuretic peptide are released by the body to lower blood pressure in volume overloaded states.

Aldosterone is a steroid hormone that is released from the adrenal cortex. The function of aldosterone is to increase reabsorption of sodium ions from the distal tubule. Increased sodium ion concentration in the blood then causes the diffusion of water from the nephron into the circulatory system, preventing water loss due to excretion and increasing blood pressure and volume)

Release of aldosterone is mediated by the renin-angiotensin system (RAS). When juxtaglomerular cells detect low blood pressure, they release renin. Renin travels to the liver, where there angiotensinogen is produced, and cleaves angiotensinogen to produce angiotensin I. Angiotensin I then travels to the lungs, where angiotensin converting enzyme (ACE) cleaves it to produce angiotensin II. Angiotensin II then travels to the adrenal cortex to stimulate release of aldosterone into the blood.

Adrenocorticotropic hormone is secreted by the anterior pituitary and acts on the adrenal cortex to stimulate release of cortisol and cortisone, but does not affect aldosterone release. Vasopressin is released by the posterior pituitary and helps the body to retain water; it is not related to aldosterone release.

Renin is a hormone released by granular cells in the juxtaglomerular apparatus, near the nephron glomerulus. These cells monitor the pressure of the filtrate in the distal convoluted tubule. The release of renin will stimulate a cascade of angiotensin I and II. Angiotensin II will ultimately stimulate the adrenal cortex to release aldosterone and increase sodium reabsorption and potassium excretion from the filtrate, leading to water retention.

Angiotensin II is a major influence on the kidney's function when the body needs to retain fluid - it works in tandem with antidiuretic hormone and aldosterone to accomplish this. Angiotensin II will also act upon the afferent and efferent arterioles in order to control the glomerular filtration rate and stimulates reabsorption to ensure that the body is keeping necessary solutes/molecules. Diluting the filtrate in the nephron is the opposite effect that angiotensin has on the kidney.

Angiotensin II (part of the RAAS) works in the body to cause vasoconstriction in an effort to raise blood pressure. Too much of this substance will cause hypertension, another name for elevated blood pressure. Nitric oxide and prostacyclin work to vasodilate and lower blood pressure. Atrial natriuretic peptide and brain natriuretic peptide are released by the body to lower blood pressure in volume overloaded states.