The effects of ADH, Aldosterone, and Angiotensin II all increase blood pressure. AntiDiuretic Hormone (ADH) increases reabsorption of water, plasma volume, and cardiac output e.g. EDV and therefore blood pressure increases. In the Distal convoluted tubule, aldosterone determines the final rate of sodium reabsorption and therefore adjusts the sodium concentration in the bloodstream It’s a hormone so it’s regulated by the endocrine system. Aldosterone is secreted by the adrenal cortex of the kidney. High aldosterone means increased sodium reabsorption. Because water follows solutes, if we increase sodium reabsorption, water reabsorption also occurs. Though, this ultimately depends on expression of ADH, which we will get into...but for now, just assume if everything else is “normal,” increased aldosterone release increases sodium reabsorption and water as well. The increased sodium reabsorption would increase blood volume, blood pressure, cardiac output, increases EDV, and increases SV. It is important to know that blood pressure increases in response to more reabsorption of fluid, and the reabsorption of fluid is driven by the reabsorption of sodium.
In the collecting duct, we know that final reabsorption of water occurs here and is dependent on ADH. ADH adjusts the osmolarity of the extracellular fluid by reabsorbing water, and is secreted by the pituitary gland of the hypothalamus. If ADH is secreted, this will signal the insertion of aquaporins, which are the channels that allow water to pass and be reabsorbed in the medulla when it follows down its concentration gradient. Side note - but remember that the gradient water follows is basically anything with a lot of salt. Deep in the medulla, as discussed, is a highly concentrated area. So water follows salt as it reaches down there when its traveling in the collecting duct, and gets reabsorbed into the blood. But like I said, this is only if ADH is secreted and signals aquaporin insertion.
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