Angiotensin II has three main methods affecting on renal physiology. First, it decreases GFR by causing vasoconstriction of the afferent arterioles. Second, it enhances reabsorption of Na+, CL-, and water in the proximal convoluted tubule by stimulating the activity of Na+/H+ antiporters. Last, it stimulates the adrenal cortex to release aldosterone, a hormone that in turn stimulates principal cells in the collecting ducts to reabsorb more Na+ and Cl- and secrete more K+.
The posterior pituitary releases Antidiuretic Hormone (ADH) which regulates facultative water reabsorption by increasing the water permeability of principal cells in the last part of the distal convoluted tubule and the collecting duct. ADH stimulates insertion of aquaporins (water channel proteins) into their apical membranes then the principal cell’s apical membrane of the water permeability increases. Water molecules move more rapidly from the tubular fluid into the cells. ADH regulates facultative water reabsorption through a negative feedback system.
Atrial Natriuretic Peptide is released by the blood volume increasing. This hormone inhibits reabsorption of Na+ and water in …show more content…
Therefore the urinary system eliminates or keeps the excess or shortage solutes or water. When water intake is not enough, blood volume decreases, blood pressure goes down, and this leads the renin secretion which promotes releasing of angiotensin II for increasing osmotic pressure to stimulate hypothalamus. Also water loss is regulated by ADH with water reabsorption mechanism. When osmotic pressure increased ADH also secreted to promotes absorbing water from the collecting ducts causing the produce of concentrated