Answer:
Acting on the mineralocorticoid (MR) receptors of the main cells in the distal convoluted tubule, which increases the permeability in its luminal apical membrane to potassium and sodium and activates the basolateral Na + / K + pumps, stimulating the hydrolysis of ATP that leads to phosphorylation of the pump, causing a conformational change in this membrane protein. The phosphorylated form of the pump has a low affinity for Na + ions, thereby expelling them into the extracellular space between each epithelial cell in the tubule. This will lead to reabsorption of these ions (and the water they carry) into the adjacent blood capillaries, thus concentrating the concentration of Na + in the blood. Similarly, the concentration of K + (potassium) ions in the extracellular space (which is precisely one of the signals collected by Aldosterone secretion); This means an intracellular K + increase, for which potassium channels are opened mainly in the apical region of the cell membrane, excreting this ion towards the luminal area of the tubule, where it will be incorporated into the urine. (Chloride anions are also reabsorbed in conjunction with sodium cations to maintain the electrochemical balance of the system.)
Aldosterone stimulates H + secretion by cells interspersed in the collecting tubule, regulating plasma levels of bicarbonate (HCO3−) and its acid-base balance.
Explanation:
Aldosterone is one of the most important pillars of the renin angiotensin aldosterone system, in this way we are saying that it is part of one of the regulators of blood pressure.
When blood pressure decreases, the blood vessel proprioceptors capture the drop in pressure and thereby activate the presence of aldosterone in the body.
Aldosterone is a mineralocorticoid that generates an increase in sodium in the lumen of vessels by dragging masses of water. By dragging water due to a difference in concentrations of said ion, the blood vessel volume increases.
By increasing the blood volume of the vessel, it generates more pressure on the walls and therefore increases the blood pressure, compensating for the hypovolemia for which this route began.
