Changes

                                       Renin                                      ACE                                Action on adrenal cortex  

                                       Renin                                      ACE                                Action on adrenal cortex  

The action of angiotensin II is not restricted to just the kidney. Amongst other effects, Ang II causes the secretion of AVP from the supraoptic region (found in mammalian brains) of the hypothalamus; is a potent dipsogen (stimulates the sensation of thirst) in an attempt to increase fluid volume; and results in the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland. ACTH also induces an increase in aldosterone levels in the blood by direct action on glomerulosa cells . These mechanisms are designed to increase the fluid volume of the plasma in order to return blood pressure to normal levels. An understanding of the renin-angiotensin system has clear clinical significance. For example, the use of ACE inhibitors, such as Captopril, and of direct renin inhibitors, such as aliskiren, which obviates the binding of angiotensinogen to renin , are important ways in which hypertension can be treated.  

The action of angiotensin II is not restricted to just the kidney. Amongst other effects, Ang II causes the secretion of AVP from the supraoptic region (found in mammalian brains) of the hypothalamus; is a potent dipsogen (stimulates the sensation of thirst) in an attempt to increase fluid volume; and results in the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland. ACTH also induces an increase in aldosterone levels in the blood by direct action on glomerulosa cells . These mechanisms are designed to increase the fluid volume of the plasma in order to return blood pressure to normal levels. An understanding of the renin-angiotensin system has clear clinical significance. For example, the use of ACE inhibitors, such as Captopril, and of direct renin inhibitors, such as aliskiren, which obviates the binding of angiotensinogen to renin , are important ways in which hypertension can be treated.  

The nephron itself has a nominal role to play in glucose homeostasis. The efficiency with which glucose is reabsorbed in the proximal tubule is an essential way to prevent hypoglycaemia. When hyperglycaemia occurs, however, any excess glucose that cannot be reabsorbed is excreted in the urine. This occurs on account of the fact that the protein transport mechanisms have a maximum rate at which it can facilitate transepithelial movement, which is indeed the limiting factor in glucose reabsorption. When the glucose concentration reaches a threshold value, which is determined to be approximately 180-200 mg/dL in humans , the apical sodium-glucose symporters become “saturated”. The rate at which the substrates of the symporter can bind onto their respective domains on the protein is at a maximum, meaning that if glucose concentration is augmented above the threshold value, the excess glucose is simply excreted from the body.

The nephron itself has a nominal role to play in glucose homeostasis. The efficiency with which glucose is reabsorbed in the proximal tubule is an essential way to prevent hypoglycaemia. When hyperglycaemia occurs, however, any excess glucose that cannot be reabsorbed is excreted in the urine. This occurs on account of the fact that the protein transport mechanisms have a maximum rate at which it can facilitate transepithelial movement, which is indeed the limiting factor in glucose reabsorption. When the glucose concentration reaches a threshold value, which is determined to be approximately 180-200 mg/dL in humans , the apical sodium-glucose symporters become “saturated”. The rate at which the substrates of the symporter can bind onto their respective domains on the protein is at a maximum, meaning that if glucose concentration is augmented above the threshold value, the excess glucose is simply excreted from the body.