Maintaining fluid homeostasis and blood pressure is essential for the body. To achieve this, the volume of the extra cellular matrix (and therefore blood pressure) must be kept relatively constant, and the relative concentrations of necessary ions must be corrected to within acceptable levels. These factors are important to control perfusion pressure of necessary substances from the blood plasma into the tissues.
Here is a list of some of the major mediators involved in the maintenance of blood pressure and Ca/Phosphate concentrations, including where they are produced, the factors that cause their release, and the effect they have:
Anti-Diuretic Hormone (ADH, Vasopressin): Released by the Posterior Pituitary following the formation of Angiotensin II as a result of a drop in blood pressure and therefore a decrease in the stretch of the kidney's afferent (incoming) arteriole). AHD acts on V2 receptors in the kidney (collecting and connecting ducts) to cause aquaporin insertion. There aquaporins absorb water and sodium cations from the filtrate (urine') back into the body. This increases the blood volume and therefore increases blood pressure.
Aldosterone: Also released following Angiotensin II formation as a result of decreased blood pressure. It is released from the Zona Glomerulosa in the adrenal cortex. It results in greater Na+ (and therefore water through osmosis) absorption into the body from the filtered urine. It achieves this by enhancing the gene expression of three key channels: Epithelian Sodium Channels which reabsorb sodium, the Na-K ATPase which pumps Na from the kidney cell the to blood stream, and the ROM K1 channel which pumps potassium into the urine and therefore helps the Na-K ATPase continue to do its job. Because its K-eliminating function, aldosterone may also be secreted as a result of hyperkalaemia (excessive K in the blood).
Several other factors can also come into play when the blood pressure is low to cause vasoconstriction (constriction of blood vessels) and an increase in cardiac output.
When the blood pressure is too high, however, mediators must come into play to stop it causing capillary damage or oedema (leakage of blood plasma into tissues).
Adenosine: Released by the kidney's Macula Densa cells following a rise in blood pressure and therefore more Cl ions passing through the distal convoluted tubule. Adenosine stops the action of Aldosterone and Angiontensin II, causing loss of sodium in the urine (termed natriuresis) and therefore a decrease in blood volume, resulting in a decrease in blood pressure.
Atrial Natriuretic Peptide (ANP. BNP may also be involved): released form the heart's right atrium following an increase in atrial stretch (due to high blood pressure). This causes natriuresis and therefore decreases blood pressure.
Other factors which cause natriuresis include the Endogenous digitalis-like factor which inhibits the Na-K ATPase (which Aldosterone increases).
The maintenance of ion concentrations is also critical. For example, if the concentration of Ca is too high in the body muscle (including cardiac muscle) function is impaired. Ca is regulated together with PO4.
Para Thyroid Hormone (PTH): Released from the Parathyroid gland following in a drop in calcium availability. It promoted the excretion of Phosphate (PO4) so that this does not complex (form compounds with) Ca, making more Ca freely available. It causes greater reabsorption of Ca by the kidneys by increasing the maximum transport capacity for Ca from the filtrate into the body. It also causes the release of Ca and PO4 from bones, which will be returned from dietary calcium when the hypocalcaemia (low Ca levels in the blood) is fixed. Finally it causes the formation of Calcitriol
Calcitriol: Formed by the kidney from Vitamin D3 following PTH secretion. It causes greater Ca absorption from food, thus making more Ca available to be returned to bone. It may also inhibit PO4 reabsorption, with PTH.
Once the hypocalcaemia is overcompensated and hypercalcaemia (excessive blood Ca) occurs Calcitonin is released, which decreases the reabsorption of Ca by the kidneys