To combat these adverse effects, drugs such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are used in the clinic, although these do have side effects and can lead to excessive retention of potassium hyperkalaemia. Control of plasma sodium and potassium concentrations, and the regulation of blood volume and pressure, are all hormonal mechanisms that are impaired by low angiotensin levels.
Absence of angiotensin can be associated with retention of potassium, loss of sodium, decreased fluid retention increased urine output and low blood pressure.
About Contact Events News. Search Search. You and Your Hormones. Students Teachers Patients Browse. Human body. Home Hormones Angiotensin. Angiotensin Angiotensin is a protein hormone that causes blood vessels to become narrower. It helps to maintain blood pressure and fluid balance in the body. Alternative names for angiotensin The different forms of angiotensin are denoted by Roman numerals, angiotensin I—IV.
What is angiotensin? Angiotensin II has effects on: Blood vessels — it increases blood pressure by causing constriction narrowing of the blood vessels Nerves: it increases the sensation of thirst, the desire for salt, encourages the release of other hormones that are involved in fluid retention.
How is angiotensin controlled? What happens if I have too much angiotensin? What happens if I have too little angiotensin? Renin, which is released primarily by the kidneys, stimulates the formation of angiotensin in blood and tissues, which in turn stimulates the release of aldosterone from the adrenal cortex. Renin is a proteolytic enzyme that is released into the circulation by the kidneys. Its release is stimulated by:. Juxtaglomerular JG cells associated with the afferent arteriole entering the renal glomerulus are the primary site of renin storage and release.
A reduction in afferent arteriole pressure causes the release of renin from the JG cells, whereas increased pressure inhibits renin release. Beta 1 -adrenoceptors located on the JG cells respond to sympathetic nerve stimulation by releasing renin.
Specialized cells macula densa of distal tubules lie adjacent to the JG cells of the afferent arteriole. The macula densa senses the concentration of sodium and chloride ions in the tubular fluid. When NaCl is elevated in the tubular fluid, renin release is inhibited.
In contrast, a reduction in tubular NaCl stimulates renin release by the JG cells. When afferent arteriole pressure is reduced, glomerular filtration decreases, and this reduces NaCl in the distal tubule.
This serves as an important mechanism contributing to the release of renin when there is afferent arteriole hypotension, which can be caused by systemic hypotension or narrowing stenosis of the renal artery that supplies blood flow to the kidney.
When renin is released into the blood, it acts upon a circulating substrate, angiotensinogen , that undergoes proteolytic cleavage to form the decapeptide angiotensin I.
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