Active reabsorption of sodium in the proximal tubule increases the hydrostatic pressure gradient and facilitates the passive reabsorption of bicarbonate.
The regulated movement of molecules in the nephron involves the renal corpuscle, distal convoluted tubule, and collecting duct.
The renal corpuscle regulates filtration.
The distal convoluted tubule is involved in regulated reabsorption.
The collecting duct is part of the nephron and is involved in regulated reabsorption.
The site of urine volume production in the nephron is the renal corpuscle.
The renal corpuscle has two types of regulation: intrinsic regulation and regulation of filtration.
Intrinsic regulation in the renal corpuscle alters the glomerular filtration rate.
Inherent to the structure of the glomerular capillaries and glomerular/bowman's capsule are sensors that respond to changes in blood pressure.
A decrease in blood pressure results in dilation of the afferent arteriole, increased blood flow into the glomerular capillary, and decreased glomerular filtration.
An increase in blood pressure increases GFR, causing the afferent arteriole to constrict and decrease the flow of blood into the glomerular capillaries, resulting in a decreased GFR.
Exercise increases GFR, causing the afferent arteriole to constrict and decrease the flow of blood into the glomerular capillaries, resulting in a decreased GFR.
Extrinsic regulation of the nephron involves the autonomic nervous system, specifically the sympathetic division.
Dropped blood pressure or increased blood pressure (exercise) results in increased sympathetic stimulation, increased cardiac output, and increased mean arterial pressure, which drives glomerular filtration rate up.
Autoregulatory mechanisms in the nephron counter increased blood pressure with exercise, preventing increased urinary output.
Vasoconstriction of afferent arterioles, induced by sympathetic stimulation, drives GFR down.
Exercise causes the body to conserve blood volume by preserving blood volume.
The juxtaglomerular apparatus consists of cells found at the interface between the afferent arteriole and the ascending limb of the loop of henle.
There are two cell types in the juxtaglomerular apparatus: granular cells and macula densa cells.
The location of the juxtaglomerular apparatus includes the afferent arteriole, which enters into the renal corpuscle, and the ascending limb of the loop of henle.
The juxtaglomerular apparatus consists of two populations of cells: granular juxtaglomerular cells, which are sensitive to volume changes, and sympathetic (beta adrenergic) + macula densa, which are minor pathways.
Granular juxtaglomerular cells respond to changes in blood volume.
A drop in blood volume stimulates granular juxtaglomerular cells, leading to the secretion of renin.
Renin is an enzyme, not a hormone, and the amount of enzyme determines the impact on reaction rate.
The reaction catalyzed by renin is plasma protein, angiotensinogen, which converts into angiotensinogen I.
Increased renin levels increase the conversion into angiotensin I.
ACE, or angiotensin converting enzyme, is responsible for converting angiotensin I into angiotensin II.
More angiotensin I increases the conversion into angiotensin II.
Aldosterone is a hormone responding to increased angiotensin II.
Aldosterone acts on the distal convoluted tubule and collecting duct of the kidney, targeting sodium transport.
Increased sodium reabsorption leads to increased water reabsorption, decreased volume, and decreased urination.
Potassium is detrimental to cardiac function if too high.
More sodium reabsorption removes excess potassium, a process that also increases water reabsorption and decreases volume and urination.
Mineralocorticoid is a hormone that acts on the distal convoluted tubule and collecting duct of the kidney, targeting sodium transport.
Elevated potassium stimulates the adrenal cortex, leading to increased aldosterone and increased water reabsorption.
Less aldosterone in the distal convoluted tubule/collecting duct slows down or stops reabsorbing sodium, leading to less water reabsorption and increased water in the filtrate, larger urine volume, and increased urination.
The third regulatory hormone pathway is atrial natriuretic factor (HORMONE) (SODIUM → NATRIUM) → new 30-50 years.
Atrial natriuretic factor (ANH) acts on the posterior pituitary to inhibit ADH production, leading to lower urine production.
Atrial natriuretic factor (ANH) acts on the adrenal gland to inhibit aldosterone production, leading to lower urine production.
Inhibiting both hormones increases urine production.