regulation of systemic arterial blood pressure by circulatory renin-angiotensin

Definition

Target type: biologicalprocess

The process in which angiotensinogen metabolites in the bloodstream modulate the force with which blood passes through the circulatory system. The process begins when renin is released and cleaves angiotensinogen. [ISBN:0721643949]

The renin-angiotensin system (RAS) plays a crucial role in regulating systemic arterial blood pressure. This complex system involves a cascade of enzymatic reactions that ultimately lead to the production of angiotensin II, a potent vasoconstrictor.

The process begins in the kidneys, specifically in the juxtaglomerular cells located near the glomeruli. These cells sense changes in blood pressure, sodium levels, and blood flow. When blood pressure drops, the juxtaglomerular cells release renin, an enzyme that converts angiotensinogen, a protein produced in the liver, into angiotensin I.

Angiotensin I then travels through the bloodstream and reaches the lungs, where it encounters angiotensin-converting enzyme (ACE). ACE, an enzyme found primarily in the lungs, converts angiotensin I into angiotensin II.

Angiotensin II acts as a powerful vasoconstrictor, causing blood vessels to narrow, thereby increasing peripheral resistance and blood pressure. It also stimulates the release of aldosterone from the adrenal glands, a hormone that promotes sodium retention by the kidneys, further contributing to increased blood volume and blood pressure.

In addition to its direct effects on blood pressure, angiotensin II also activates various signaling pathways that affect other organs, including the heart, brain, and kidneys. It can cause hypertrophy (enlargement) of the heart, promote atherosclerosis (hardening of the arteries), and contribute to the development of kidney disease.

The RAS is finely regulated by various feedback mechanisms. For example, increased blood pressure inhibits the release of renin from the kidneys, reducing the production of angiotensin II. Additionally, angiotensin II itself can inhibit its own production by suppressing renin release and downregulating ACE expression.

The regulation of systemic arterial blood pressure by the RAS is essential for maintaining cardiovascular homeostasis. Disruptions to this system, such as overactivation of the RAS, can lead to hypertension (high blood pressure) and other cardiovascular diseases. Therefore, understanding the complex mechanisms involved in RAS regulation is crucial for developing effective treatments for these conditions.'
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