6 Hormonal Regulation
Hormones also regulate GFR. One such mechanism is activated when juxtaglomerular (JG) (or granular) cells are stimulated to secrete the enzyme renin. This enzyme begins a process that results in the production of angiotensin II, a powerful systemic vasoconstrictor that also constricts the afferent and efferent arterioles. Angiotensin II also stimulated the contraction of mesangial cells resulting in a decrease in the surface area of the glomerulus. Because renin is released when blood pressure is low, the resulting constriction of the efferent arteriole helps maintain net filtration pressure in the glomerular capillary and consequently, GFR. Another hormone, atrial natriuretic peptide (ANP) increases GFR. ANP is released when the atria of the heart is stretched, for example, in heart failure when blood volume increases due to sodium and water retention. ANP relaxes the mesangial cells of the glomerulus, making more surface area available for filtration. This increases GFR.
Glomerular Filtration Regulation
| Regulation | Primary Stimulus | Mechanism/Activity Site | Effect |
|---|---|---|---|
| Renal autoregulation | Systemic rising or falling of arterial blood pressure | Adjusts resistance to the flow of blood, when systemic arterial blood pressure rises or falls | Prevents significant fluctuations in GFR |
| Myogenic mechanism | Smooth muscle fibers in walls of afferent arteriole are stretched when blood pressure increases | Contraction of smooth muscle fibers narrows lumen of afferent arterioles | GFR decrease |
| Tubuloglomerular feedback | Increased delivery of sodium ions and chloride ions to the macula densa when blood pressure increases | Constriction of afferent arterioles due to the release of adenosine by macula densa cells | GFR decrease |
| Vasoconstrictor adenosine | Decreased delivery of sodium ions and to the macula densa when blood pressure drops | Dilation of afferent arterioles due to inhibition of adenosine release by macula densa cells | GFR increase |
| Neural regulation | Release of norepinephrine due to increased activity of renal sympathetic nerves | Constriction of afferent arterioles due to activation of alpha-adrenergic receptors and renin release | GFR decrease |
| Hormone regulation | Stimuli cause juxtaglomerular cells to secrete renin. | Once juxtaglomerular cells secrete renin, angiotensin II is produced. | Maintains GFR |
| Angiotensin II | Production of angiotensin II due to decreased blood volume or blood pressure | Constriction of afferent arteriole and contraction of mesangial cells | GFR decrease |
| ANP | Secretion of ANP due to stretching of atria of heart | Capillary surface area available for filtration increased due to relaxation of mesangial cells in glomerulus | GFR increase |
Hormonal Regulation of Reabsorption and Secretion
Five hormones control the absorption of water, and sodium, chloride, and calcium ions: angiotensin II, aldosterone, antidiuretic hormone, atrial natriuretic peptide, and parathyroid hormone.
Let’s look at each:
Angiotensin II
The renin-angiotensin-aldosterone system is stimulated when blood volume and blood pressure decrease. A decrease in blood pressure reduces the amount of stretch in afferent arteriole walls and stimulates juxtaglomerular cells to release renin into the blood. Renin release is also stimulated directly by sympathetic nerve fiber activity. Renin sets in motion a cascade of events that leads to the production of the hormone angiotensin II.
Angiotensin II plays three primary roles. First, it constricts afferent arterioles, resulting in a reduction in GFR. Second, it stimulates an exchange mechanism. This leads to an increase in the reabsorption of water, sodium ions, and chloride ions. Finally, the hormone prompts the adrenal cortex to secrete the hormone aldosterone.
Aldosterone
The release of aldosterone from the adrenal cortex is stimulated by the presence of angiotensin II as well as an increased concentration of potassium ions. Aldosterone stimulates the insertion of sodium channels in the apical membrane and sodium/potassium pumps in the basolateral membranes of the principal cells of the distal convoluted tubules and the collecting ducts. The result is an increase in the reabsorption of sodium ions. Aldosterone also increases the secretion of potassium ions by principal cells in the collecting duct. Because of the increased reabsorption of sodium ions, more water is reabsorbed and blood volume is effectively increased.
Antidiuretic Hormone (ADH)
Antidiuretic hormone (ADH)acts to decrease urine production by increasing the permeability of principal cells in the late distal convoluted tubule and the collecting duct, thus increasing facultative water reabsorption. Without ADH, the apical membranes of principal cells are relatively water-impermeable. ADH also stimulates the insertion of aquaporins in the apical membrane, allowing water molecules to move more quickly from tubular fluid into the cells and then through the always fairly permeable basolateral membrane and into the blood. When you are dehydrated, ADH is released, and the kidneys conserve water by producing a small volume of very concentrated urine. ADH secretion is controlled by a negative feedback system. When the water concentration of plasma and interstitial fluid decreases (i.e., when osmolarity increases), more ADH is secreted into the blood, making principal cells more water-permeable. This restores plasma osmolarity towards normal.
Atrial Natriuretic Peptide
Atrial natriuretic peptide is released from the heart in response to large increases in blood volume. This hormone inhibits the reabsorption of water and sodium ions in the proximal convoluted tubule and collecting duct. It also inhibits aldosterone and ADH secretion. The resulting increased sodium ion excretion in urine and the increased urine output lower blood volume and pressure.
Parathyroid Hormone (PTH)
Parathyroid hormone (PTH) affects calcium and phosphate ion reabsorption. It is released by the parathyroid glands in response to a reduced concentration of calcium ions in the blood. PTH stimulates increased reabsorption of calcium ions in the early distal convoluted tubule. PTH also inhibits the reabsorption of phosphate ions in the proximal convoluted tubule, prompting the excretion of phosphate ions in the urine.
| Hormone | Stimulus for Release | Result |
|---|---|---|
| Aldosterone | Increased levels of angiotensin II and plasma potassium ion (K+) | Increased secretion of K+ and reabsorption of sodium ions (Na+) and chloride ions; increased water reabsorption, leading to increased blood volume |
| Angiotensin II | Reduced blood volume or reduced blood pressure | Increased reabsorption of solutes (including Na+) and water, leading to increased blood volume |
| Antidiuretic hormone | Increased osmolarity of extracellular fluid or decreased blood volume | Increased facultative reabsorption of water, leading to reduced osmolarity of body fluids |
| Atrial natriuretic peptide | Stretching of atria of heart | Increased excretion of Na+ in urine; increased urine output reduces blood volume |
| Parathyroid hormone | Decreased plasma calcium ion (Ca2+) level | Increased Ca2+ reabsorption, leading to decreased reabsorption of phosphate ions in the proximal convoluted tubule and increased excretion of phosphate ions in urine |
