Angiotensin II: role in controlling renal excretion
When sodium falls below normal, Angiotensin II levels increase, causing sodium and water retention, and also counteract a drop in arterial blood pressure if not.
One of the most powerful control of sodium excretion by the body is Angiotensin II. Changes in sodium and fluid intake are associated with mutual changes in the formation of Angiotensin II, and this contributes largely to maintaining the balance of sodium and fluids in the body. That is, when sodium intake is higher than normal, renin secretion decreases, causing a decrease in Angiotensin II formation. Since Angiotensin II has a number of important effects to increase renal tubular sodium reabsorption, a decrease in Angiotensin II levels decreases renal tubular water and sodium reabsorption, thereby increasing renal excretion of sodium and water. The net result is a reduction in extracellular fluid volume and arterial pressure that would otherwise occur as sodium intake is increased.
Conversely, when sodium levels drop below normal, Angiotensin II levels increase, causing sodium and water retention, and also counteract a drop in arterial blood pressure if not occurring. Therefore, the changes in the activity of the renin-angiotensin system act as a powerful amplifier of the pressure sodium diuretic mechanism to maintain stable blood pressure and body fluid volume.
The importance of changes in Angiotensin II in changing urine pressure
The importance of Angiotensin II in making the pressure sodium diuretic mechanism more effective. Note that when angiotensin is fully active sodium diuretic control, the steep pressure sodium diuretic curve (normal curve), indicates that a change in blood pressure is necessary to increase sodium excretion as sodium intake increases. .
Figure. Effects of excessive angiotensin II (Ang II) formation or inhibition of Angiotensin II formation on the renal diuretic-pressure curve.
Note that the formation of high-level Angiotensin II reduces the slope of the pressure sodium diuresis, making blood pressure very sensitive to changes in sodium intake. The blockade of the Angiotensin II formation alters the pressure sodium diuretics to reduce blood pressure. Conversely, when angiotensin levels cannot be reduced in response to an increase in sodium intake (high angiotensin II curve), as occurs in some hypertensive patients there is a potential to decrease renin secretion and formation. With Angiotensin II, the urinary sodium pressure curve is not nearly steep. Therefore, as sodium intake increases, more arterial pressure is needed to increase sodium excretion and maintain sodium balance. For example, in most people, a 10-fold increase in sodium only increases arterial pressure by a few millimetres of mercury, While in subjects that we're unable to properly inhibit Angiotensin II formation in response to excess sodium, sodium intake also similarly increased, causing blood pressure to rise up to 50 mm Hg. Therefore, the inability to inhibit angiotensin II formation in the presence of excess sodium reduces the slope of the pressurized sodium diuresis and makes arterial pressure very salt sensitive.
The use of drugs to suppress the effects of Angiotensin II has been shown to be clinically important to improve the kidneys' ability to excrete salt and water. When Angiotensin II formation is blocked with an ACE inhibitor or an Angiotensin II receptor antagonist, the renal pressure-induced urinary sodium excretion curve changes to a lower pressure, which indicates the potential for sodium excretion. is strengthened by the kidneys. because normal sodium excretion can now be maintained at reduced arterial pressure. This change in pressurized sodium diuretics forms the basis for the chronic hypotensive effects of ACE inhibitors and Angiotensin II receptor antagonists in hypertensive patients.
An excess of angiotensin II usually does not cause a large increase in extracellular fluid volume because an increase in pressure of the Angiotensin II counterpart artery holds sodium mediated.
Although Angiotensin II is one of the most powerful sodium and water retention hormones in the body, reducing or increasing Angiotensin II in circulation does not have a major effect on the extracellular fluid volume or blood volume as long as heart failure or kidney failure. not occur. The reason for this phenomenon is that when Angiotensin II levels rise greatly, as occurs with renin secreting tumours of the kidneys, high Angiotensin II levels initially cause the kidneys to retain sodium and water and slightly increase extracellular fluid volume. This also causes an increase in arterial pressure, which rapidly increases the sodium and water intake of the kidneys, thereby overcoming the water and sodium retention effects of Angiotensin II and re-establishing the balance between sodium intake and head. out at higher blood pressure. Conversely, after blocking the formation of Angiotensin II, as occurs with an ACE inhibitor, it reduces sodium and water initially,
If the heart has a failure or latent heart disease, the heart's ability to pump blood may not be large enough to increase the arterial pressure enough to overcome the sodium retention effect when Angiotensin II levels are high; In these cases, Angiotensin II can cause retention of large amounts of sodium and water which can lead to congestive heart failure. In these cases, blocking the formation of Angiotensin II may decrease sodium and water retention, while also reducing the extracellular fluid volume associated with heart failure.