Renin-Angiotensin-Aldosterone-System (RAAS) and Release of Anti-Diuretic Hormone (ADH)

Sodium in the human body is of critical importance as it accounts for about 90% of the extracellular fluids cations (ECF) which are positively charged ions. As the single most abundant ECF cations in the body in combination to the constituents' anions of chloride and bicarbonates which are negatively charged ions, sodium is in a position to regulate the body's extracellular osmotic forces and as a consequence regulating the body water balance (Weinberg, Weinberg, & Zappe, 2015). Other essential functions of sodium in our bodies include:

• Aiding in nerve impulses through the maintenance of neuromuscular irritability (this happens in conjunction with potassium and calcium).
• Regulating the levels of acid and base in the body (this happens through sodium phosphate and sodium bicarbonate).
• It participates in the chemical cell reactions.
• Helps in the transportation of substances across the cellular membrane

Aldosterone is responsible for the hormonal regulation of sodium balance. Aldosterone is a mineral corticoid or steroid that is synthesized by the adrenal cortex and is secreted as the end product of the renin-angiotensin-aldosterone system. Renin is released by the juxtaglomerular cells of the kidney in case there is a reduction in the fluid blood pressure, the reduction of renal blood flow or decrease in the concentration of serum sodium. Renin that is secreted in effect stimulates the formation of angiotensin I which is converted by the Angiotensin-converting enzyme (ACE) found in the pulmonary vessels to angiotensin II (Weinberg, Weinberg, & Zappe, 2015).

Anti-diuretic hormone (ADH) is a peptide hormone secreted by the neurons in the hypothalamus, and it controls the direct excretion of water in the kidney. ADH is released from the posterior pituitaries in the kidney in case of hyper-tonicity and causes the re-absorption of water and in the process reduces the urine volume. When ADH is released in very high concentrations, it may cause the blood pressure to rise, cause a variety of neurological effects on the brain and affect pair-bonding in voles (Puri, 2017). The secretion of ADH is influenced by:

• Neurons in the hypothalamus that detect an increase in plasma osmolarity thus stimulating ADH secretion
• Stretch receptors in atria of the heart that are sensitive when large volumes of blood than normal flow to the heart and in turn inhibit ADH secretion
• Stretch receptors in some arteries that detect fall in blood pressure and stimulate ADH secretion to maintain a higher volume to increase blood pressure to take blood to all body parts.

When a patient experiences heart failure or a patient experiences a hypovolemic state from severe blood loss, the loss of sodium and water is proportionate, and the body should conserve their loss. The kidney is in a position to sense low blood pressure due to the low rate of filtration and low pressure through the tubule. In response, this will trigger a complex response to raise the blood pressure or conserve the blood volumes in case of severe blood loss. Juxtaglomerular cells produce renin that initiates a hormonal cascade to generate angiotensin II. Inside the body, Angiotensin II has two leading roles. The first role is causing vasoconstriction which as a consequence elevates the body blood pressure and thus stimulating the secretion of aldosterone. When aldosterone is secreted, it prompts the re-absorption of sodium and water by the proximal tubules of the kidneys which has the total effect of conserving sodium in the body, maintains the blood volumes and thus regulating the blood pressure (Motwani, 2012). Aldosterone is also responsible for stimulating secretion and as a result the excretion of potassium which through the distal tubule of the kidney and thus reducing its concentration in the ECF. When the average levels of sodium, blood volumes, and renal perfusions are attained, then the further release of renin is inhibited.

References

Motwani, J. G. (2012). Review: Combining renin-angiotensin-aldosterone system blockade with diuretic therapy for treatment of hypertension. Journal of the Renin-Angiotensin-Aldosterone System, 3(2), 72-78. doi:10.3317/jraas.2002.021

Puri, V. (2017). Urinary anti diuretic hormone level in essential hypertension. Pharmacological Research Communications, 19(1), 53-58. doi:10.1016/0031-6989(87)90032-4

Weinberg, M. S., Weinberg, A. J., & Zappe, D. H. (2015). Effectively targetting the renin-angiotensin-aldosterone system in cardiovascular and renal disease: rationale for using angiotensin II receptor blockers in combination with angiotensin-converting enzyme inhibitors. Journal of the Renin-Angiotensin-Aldosterone System, 1(3), 217-233. doi:10.3317/jraas.2000.034