Its role may be to provide “fine tuning” for the regulation of blood pressure. It has a 10-fold lower affinity for its receptor, so its effects are less than those of ANH. There is also B-type natriuretic peptide (BNP) of 32 amino acids produced in the ventricles of the heart. It also decreases sodium reabsorption in the DCT. These events lead to an increased loss of water and sodium in the forming urine. It increases GFR through concurrent vasodilation of the afferent arteriole and vasoconstriction of the efferent arteriole. The over-stretching occurs in persons with elevated blood pressure or heart failure. One example from this family of hormones is atrial natriuretic hormone (ANH), a 28-amino acid peptide produced by heart atria in response to over-stretching of the atrial wall. Therefore, natriuretic peptides inhibit both Na + and water recovery. Natriuretic hormones also inhibit ADH release, which of course will result in less water recovery. If Na + remains in the forming urine, its osmotic force will cause a concurrent loss of water. Natriuretic hormones act by inhibiting aldosterone release and therefore inhibiting Na + recovery in the collecting ducts. Natriuretic hormones are peptides that stimulate the kidneys to excrete sodium-an effect opposite that of aldosterone. It may cause increased retention of water during some periods of the menstrual cycle in women when progesterone levels increase. This process is unimportant in men due to low levels of circulating progesterone. It binds to the aldosterone receptor and weakly stimulates Na + reabsorption and increased water recovery. Progesterone is a steroid that is structurally similar to aldosterone. At the same time that aldosterone causes increased recovery of Na +, it also causes greater loss of K +. (This dual effect on two minerals and its origin in the adrenal cortex explains its designation as a mineralocorticoid.) As a result, renin has an immediate effect on blood pressure due to angiotensin II–stimulated vasoconstriction and a prolonged effect through Na + recovery due to aldosterone. It is also important in regulating K +, promoting its excretion. It promotes Na + reabsorption by the nephron, promoting the retention of water. Its release is usually stimulated by decreases in blood pressure, and so the preservation of adequate blood pressure is its primary role.Īldosterone, often called the “salt-retaining hormone,” is released from the adrenal cortex in response to angiotensin II or directly in response to increased plasma K +. In instances of blood loss or dehydration, it reduces both GFR and renal blood flow, thereby limiting fluid loss and preserving blood volume. It acts systemically to cause vasoconstriction as well as constriction of both the afferent and efferent arterioles of the glomerulus. People with high blood pressure are sometimes prescribed ACE inhibitors to lower their blood pressure.Īngiotensin II is a potent vasoconstrictor that plays an immediate role in the regulation of blood pressure. ACE is important in raising blood pressure. It enzymatically converts inactive angiotensin I into active angiotensin II. It is produced in the lungs but binds to the surfaces of endothelial cells in the afferent arterioles and glomerulus. Its release is stimulated by prostaglandins and NO from the JGA in response to decreased extracellular fluid volume.ĪCE is not a hormone but it is functionally important in regulating systemic blood pressure and kidney function. It enzymatically converts angiotensinogen (made by the liver, freely circulating) into angiotensin I. Renin is an enzyme that is produced by the granular cells of the afferent arteriole at the JGA.
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