Most people are familiar with aldosterone. The main function of aldosterone is to regulate the kidney's absorption of sodium to maintain water balance. To put it simply, aldosterone is used to regulate kidney function. If aldosterone is too high, it is necessary to see if the kidney function is not good. Too high aldosterone can cause kidney deficiency and edema, which seriously affects people's daily life and work. Therefore, everyone can exercise and enhance the body's resistance. Effects of aldosterone: Aldosterone is a mineralocorticoid hormone secreted by the zona glomerulosa of the adrenal cortex. Medicine | Education Network. The main function of aldosterone is to promote the active reabsorption of Na+ by the distal convoluted tubule and collecting duct of the kidney, and at the same time promote the excretion of K+ and H+ through the exchange of Na+, K+ and Na+-H. Therefore, aldosterone has the functions of excreting potassium, excreting hydrogen and retaining sodium. As the active reabsorption of Na+ increases, the reabsorption of Cl- and water also increases, which shows that aldosterone also has a water-retaining effect. The secretion of aldosterone is mainly regulated by the renin-angiotensin system and plasma Na+ and K+ concentrations. When blood volume decreases and arterial blood pressure drops due to blood loss or other reasons, the stretch receptors in the wall of the renal afferent arterioles are stimulated by the drop in afferent arteriole blood pressure and the decrease in blood volume, and the secretion of renin by the juxtaglomerular cells increases. At the same time, since the glomerular filtration rate is also reduced accordingly, the Na+ flowing through the macula densa is also reduced, which can also increase the secretion of renin by the juxtaglomerular cells. (Another completely opposite view is that the increase in Na+ concentration in the tubular fluid at the beginning of the distal convoluted tubule can stimulate the macula densa and increase the secretion of renin by the juxtaglomerular cells. At present, these two views have not been unified.) After the increase of renin, angiotensin I, II, and III will increase successively. Angiotensin II and III can stimulate the zona glomerulosa of the adrenal cortex to increase the synthesis and secretion of aldosterone. In addition, the small arteries near the glomerular cells are innervated by sympathetic nerve endings, and when the renal sympathetic nerves are excited, the release of renin can be increased. Epinephrine and norepinephrine can also directly stimulate juxtaglomerular cells, increasing the release of renin. Aldosterone is a mineralocorticoid hormone secreted by the zona glomerulosa of the adrenal cortex. The main function of aldosterone is to promote the active reabsorption of Na+ by the distal convoluted tubule and collecting duct of the kidney, and at the same time promote the excretion of K+ and H+ through the exchange of Na+, -K+ and Na+-H. Therefore, aldosterone has the functions of excreting potassium, excreting hydrogen and retaining sodium. As the active reabsorption of Na+ increases, the reabsorption of Cl- and water also increases, which shows that aldosterone also has a water-retaining effect (Figure 5-2). The secretion of aldosterone is mainly regulated by the renin-angiotensin system and plasma Na+ and K+ concentrations. When blood volume decreases and arterial blood pressure drops due to blood loss or other reasons, the stretch receptors in the wall of the renal afferent arterioles are stimulated by the drop in afferent arteriole blood pressure and the decrease in blood volume, and the secretion of renin by the juxtaglomerular cells increases. At the same time, since the glomerular filtration rate is also reduced accordingly, the Na+ flowing through the macula densa is also reduced, which can also increase the secretion of renin by the juxtaglomerular cells. (Another completely opposite view is that the increase in Na+ concentration in the tubular fluid at the beginning of the distal convoluted tubule can stimulate the macula densa and increase the secretion of renin by the juxtaglomerular cells. At present, these two views have not been unified.) After the increase of renin, angiotensin I, II, and III will increase successively. Angiotensin II and III can stimulate the zona glomerulosa of the adrenal cortex to increase the synthesis and secretion of aldosterone. In addition, the small arteries near the glomerular cells are innervated by sympathetic nerve endings, and when the renal sympathetic nerves are excited, the release of renin can be increased. Epinephrine and norepinephrine can also directly stimulate juxtaglomerular cells, increasing the release of renin. An increase in plasma K+ concentration or a decrease in Na+ concentration can directly stimulate the zona glomerulosa of the adrenal cortex to increase the secretion of aldosterone; conversely, when the plasma K+ concentration decreases or the Na+ concentration increases, the secretion of aldosterone decreases. |
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