Normal arterial blood pressure: Role of Renin-angiotensin system
The renin-angiotensin system is perhaps the body's most powerful system, making small changes in arterial blood pressure in response to large fluctuations in salt intake.
In addition to the kidney's ability to control blood pressure through changes in extracellular fluid volume, the kidney also has a powerful mechanism for blood pressure control: the renin-angiotensin system.
Renin is a protein enzyme released by the kidneys when arterial blood pressure falls too low. In turn, it increases arterial blood pressure in several ways, thereby helping to correct the drop in blood pressure.
One of the most important functions of the renin-angiotensin system is to allow a person to ingest very small or very large amounts of salt without causing major changes in extracellular fluid volume or blood pressure. This function is explained by the diagrams in the figure, which show that the initial effect of increased salt intake is an increase in extracellular fluid volume, followed by an increase in arterial blood pressure. Subsequently, hypertension increases renal blood flow, as well as other effects, in which decreased renin secretion causes the kidneys to reduce salt and water retention, return the extracellular fluid volume to near-normal, and, ultimately Eventually, blood pressure returned to almost normal. As such, the renin-angiotensin system is an automatic feedback mechanism that helps maintain blood pressure at or near-normal levels even when salt intake is increased. When salt intake falls below normal,
Figure. A series of problems in which increased salt intake increases arterial pressure, but the hypoactive renin-angiotensin system returns arterial pressures to near-normal levels.
To emphasize the effectiveness of the renin-angiotensin system in controlling blood pressure, when systemic functions are normal, blood pressure increases by no more than 4-6 mm Hg in response to a 100-fold increase in salt intake. In contrast, when the renin-angiotensin system is blocked and normally prevents angiotensin formation, the same increase in salt intake sometimes causes blood pressure to rise by 50-60 mm Hg, more than 10 times the normal increase. When salt intake falls to as low as 1/10 of normal, arterial blood pressure remains largely unchanged if renin-angiotensin system functions are normal. However, when angiotensin II formation is blocked by an angiotensin-converting enzyme inhibitor, blood pressure is markedly reduced as salt intake is reduced. As such, the renin-angiotensin system is perhaps the most powerful system in the body,
Figure. Changes in mean arterial pressure during chronic changes in sodium intake in normal control dogs and in dogs treated with angiotensin-converting enzyme (ACE) inhibitors to block angiotensin II formation ( Ang II) or infusion of Ang II to prevent Ang II from being inhibited. Sodium intake was increased in steps from a low of 5 mmol/day to 80, 240 and 500 mmol/day for 8 days at each level.