Why Does the Body Produce Renin?

The main function of the Renin-Angiotensin-System (RAS) is to regulate human blood pressure, moisture, electrolytes and maintain the stability of the human body environment. The renin-angiotensin system exists in both the circulatory system and the vascular wall, heart, center, kidney, and adrenal glands, and participates in the regulation of target organs.

Renin-angiotensin system

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The main function of the Renin-Angiotensin-System (RAS) is to regulate human blood pressure, moisture,

Renin in the blood circulation mainly comes from the kidney. It can convert angiotensinogen, which is mainly from the liver, to angiotensin I, which is then converted to angiotensin II (AngII) by the action of angiotensin converting enzyme, and then passes through tissues. Angiotensin II receptor. Local RAS exists in many tissues, and plays an important role in the function regulation of corresponding organs, tissues and cells. RAS is similar to a chain, interlocking with each other, and finally generates AngII. Any link is blocked, which can inhibit the effect of RAS.

Damage of RAS to blood vessel wall: Angiotensin II produced by RAS in circulation and in vascular smooth muscle cells and endothelial cells acts on itself or adjacent smooth muscle cells to cause vasoconstriction. It can also act on sympathetic nerve endings and adrenals to promote the release of catecholamines. , Which in turn causes vasoconstriction, leading to increased blood pressure. Angiotensin II can directly stimulate the proliferation and hypertrophy of vascular smooth muscle cells or induce the expression of proto-oncogenes as an autocrine growth factor, increase the protein synthesis of smooth muscle cells, extracellular interstitial proliferation, and thicken blood vessel walls, small arterial walls and small An increase in the arterial lumen ratio leads to an increase in vascular resistance, leading to an increase in blood pressure. It also causes stenosis or occlusion of small arteries throughout the body, leading to damage to organ function, such as retinal arteriosclerosis, bleeding, retinal detachment and even blindness; the occurrence and development of peripheral large atherosclerosis, and even large arterial occlusion, causing intermittent claudication when walking Renal arteries and glomerular arteriosclerosis and stenosis, leading to glomerular atrophy and renal function damage, which in turn causes renal hypertension, which in turn aggravates vascular sclerosis and renal damage, forming a vicious cycle.

Damage of RAS to the heart: In addition to causing local contraction of coronary arteries, RAS can also promote the release of calcium ions from cardiac muscle cells from the sarcoplasmic reticulum and change the permeability of slow calcium channels on the cell membrane, increase the influx of calcium ions, and make Increased calcium ions in myocardial cells increase myocardial contractility; RAS also acts on the cardiac conduction system, slowing heart rate and reducing cardiac output; RAS can promote myocardial protein synthesis, promote myocardial cell proliferation, hypertrophy, and increase ventricular walls Thick, the lumen shrinks and affects the diastolic function of the heart; during myocardial ischemia / infarction, DNA synthesis increases, collagen produced by fibroblasts increases, often causes ventricular fibrosis; affects myocardial metabolism and ischemia and reperfusion The stability of cardiac electrical activity, aggravates myocardial damage during ischemia and triggers ventricular arrhythmias. RAS increases blood volume and returning blood volume through water and sodium retention and vasoconstriction, which greatly increases the preload of the heart and aggravates heart failure. At the same time, heart failure activates RAS and forms a vicious cycle, which eventually leads to whole heart enlargement and end-stage damage.

The effects of RAS on the central nervous system: RAS can increase the excitability of sympathetic nerves, stimulate the sympathetic ganglia to increase the release of neurotransmitters in preganglionic neurons; reduce the uptake of transmitters by the presynaptic membrane, and promote the synthesis of peripheral noradrenaline ; Promote the release of catecholamines from the adrenal medulla, thereby increasing peripheral vascular resistance; inhibit the vagus afferent nerves of the heart, increase cardiac output; increase thirst, stimulate drinking, and promote water absorption, eventually leading to increased blood pressure.

RAS promotes sustained aldosterone release and causes sodium retention; intrarenal RAS participates in regulating glomerular-tubular balance in the kidney, resulting in reduced blood vessel blood flow and sodium reabsorption; reduced glomerular filtration pressure; thereby increasing blood volume , Resulting in increased blood pressure. (Excerpt)