What Factors Affect Renin Levels?

Renin, also known as angiotensinogen enzyme, is a proteolytic enzyme released by the juxtaglomerular apparatus (also known as juxtaglomerular complex) of juxtaglomerular granule cells. It is a renin-angiotensin Components of the system. Renin was first discovered, described, and named in 1898 by Robert Tigerstedt, a professor of physiology at the Caroline College in Stockholm, Sweden. Renin is secreted by the cells near the glomerulus, and its secretion is affected by factors such as renal arterial pressure and the amount of sodium flowing through the dense urine. Renin acts on angiotensinogen in plasma to produce inactive angiotensin I. Angiotensin I is hydrolyzed into active angiotensin II by the action of angiotensin converting enzyme. Angiotensin can cause arteriolar vasoconstriction, promote adrenal cortex synthesis and secrete aldosterone ^[1] .

Renin is

Renin precursors by 406

Renin is secreted by the granulocytes of the juxtaglomerular apparatus by the following stimuli:

Reduced blood pressure Reduced sodium chloride concentration in nephron ultrafiltrate (raw urine) Sympathetic nerve excitement

Human renin is secreted by at least two cellular pathways: a structural pathway that secretes prorenin and a mediation pathway that secretes mature renin.

Renin produces angiotensin I by shearing angiotensinogen synthesized by the liver. Angiotensin I can be further sheared into angiotensin II by Angiotensin Converting Enzyme (ACE).

Angiotensin II can effectively constrict blood vessels, increase secretion of aldosterone and antidiuretic hormone, stimulate hypothalamus to produce thirst, and eventually increase hypertension.

Renin-secreting granulocytes receive

The renin-angiotensin system (abbreviated as RAS) or the renin-angiotensin-aldosterone system (RAAS) is a hormone system. When massive blood loss or blood pressure drops, this system is activated to help regulate long-term blood pressure and extracellular fluid volume (body fluid balance) in the body.

When blood pressure drops, the kidneys secrete renin. Renin catalyzes angiotensinogen hydrolysis to produce angiotensin I. Angiotensin I basically has no biological activity, but angiotensin II is formed by angiotensin converting enzyme (Angiotensin Converting Emzyme, ACE) cutting two amino acid residues at the C-terminus. Angiotensin II has a highly effective vasoconstrictive effect, which increases blood pressure; angiotensin II can also stimulate the adrenal cortex to secrete aldosterone. Aldosterone can promote reabsorption of water and sodium ions by the kidneys, which in turn increases fluid volume and raises blood pressure.

The excessive activation of the renin-angiotensin-aldosterone system is one of the causes of hypertension. The following classes of drugs can be used to inhibit the renin-angiotensin system:

1. angiotensin converting enzyme inhibitor;

2. Angiotensin II receptor antagonist;

3. Renin inhibitors ^[2] .