Page created on December 14, 2018. Last updated on January 4, 2019 at 22:51
Kidney’s role in blood pressure regulation
The kidney has two ways to influence the blood pressure – it has one system to increase it (the pressor system, RAAS) and one system to decrease it (the depressor system)
The kidney pressor system is activated by low intrarenal blood pressure, which occurs when the RBF is decreased or when the systemic blood pressure is low. This enhances renin secretion by juxtaglomerular cells. Renin will cleave angiotensinogen (produced by the liver) into angiotensin I, which will be cleaved into angiotensin II by angiotensin converting enzyme. Angiotensin II activates aldosterone production, but angiotensin is a vasoconstrictor by itself as well. Aldosterone increase the circulating plasma volume by increased salt and water retention.
The kidney depressor system is activated by high blood pressure. The renal parenchyme produces prostaglandins, kinins and medullary lipids. They cause systemic vasodilation and inhibit tubular sodium reabsorption, which decreases plasma volume.
Erythropoietin secretion is enhanced by hypoxia of the renal tissue. Cells in the juxta-tubular interstitium produce it. EPO secretion isn’t enhanced by moderate changes in RBF but it does occur in hypoxaemic hypoxia, anaemic hypoxia and stagnation (extreme congestion). Except for in anaemic hypoxia can polyglobulia develop.
EPO production is also stimulated by glucocorticoids and androgens.
Chronic renal failure causes decreased EPO production with resulting extreme anaemia.
Vitamin D and calcium metabolism
The last step in the formation of 1,25-dihydroxy-cholecalciferol, also known as vitamin D, takes place in the kidney. This last step requires the presence of PTH. PTH increases serum calcium by two ways:
- Increasing calcium mobilization from bone
- Activates vitamin D formation in the kidney
Vitamin D enhances calcium absorption from the gut and calcium reabsorption from tubules.
In chronic renal disease do both calcium loss and phosphate retention occur, which stimulate PTH secretion. This secondary hyperparathyroidism leads to severe bone deformities. Simultaneously will the sick kidney have problems with converting 25-dihydroxy-cholecalciferol into vitamin D, meaning there will be vitamin D deficiency and the following symptoms, such as weak bone.
The kidneys have multiple metabolic functions, like:
- Producing ammonia to regulate pH
- Use renal glycogen to replenish low blood glucose
- Break down and excrete insulin