Renin Angiotensin System and Antidiuretic Hormone

The human body’s Renin-Angiotensin Aldosterone System (RAAS) regulates blood pressure and fluid balances. When a person’s blood pressure or water levels drop, the body’s baroreceptors identify the drop, as do cells in the kidneys, which are responsible for releasing rennin into the body. In the case of a decline in blood pressure, the enzyme Renin transforms angiotensinogen to angiotensin I. Angiotensinogen is a protein in the liver, and, essentially, a chain-reaction process gets under way in which the body’s RAAS acts like a line of dominoes responding to the drop in low blood pressure: the kidney gets the chain reaction underway first, by releasing Renin. Renin converts the protein in the liver to the hormone angiotensin I. Angiotensin I is then converted by an enzyme in the lungs, which is called the angiotensin-converting enzyme (Angiotensin I is transformed into Angiotensin II). So kidneys, liver and lungs all work together in the initial stages of the body’s response to a drop in blood pressure. Angiotensin II raises the blood pressure in the body to counteract the drop and it does so by tightening the blood vessels. The narrower the blood vessels become, the greater the pressure on the blood stream grows. By constricting the blood vessels, the body is able to elevate the blood pressure back up to where it should be (Wasilewski, Myers, Recchia, Feldman & Tilley, 2016).
For fluid balance, the same functions and mechanisms are involved. The amount of water in the body has to be regulated. When the balanced fluid levels drop, the kidney responds by activating the RAAS. In the case of restoring fluid balance, the RAAS is triggered by the juxtaglomerular apparatus. The renal tubules begin to take in water and salt via the body’s urine supply, and potassium is traded for sodium. Aldosterone is released by the adrenal cortex, activated by the RAAS, and the aldosterone assists in the body’s absorption of sodium ions. In order to facilitate water absorption, the body releases the anti-diuretic hormone vasopressin, which assists in opening aquaporin channels. Recent studies have shown that the anti-diuretic hormone “can be synthesized in the heart to act locally in a cardiac paracrine [anti-diuretic] system prior to release into effluent vessels, where it is predicted to act systemically” (Wasilewski et al., 2016, p. 226).
When a patient experiences heart failure, the body does not receive the needed oxygen in the blood as blood pressure drops: heart failure thus triggers the RAAS system. However, in chronic cases, this triggering can damage the heart. The anti-diuretic hormone may exacerbate the heart failure though it is needed by the RAAS to assist in the process of raising the body’s blood pressure (Wasilewski et al., 2016). The anti-diuretic stimulates the renal tubules and the collecting ducts where aquaporin channels can be created. While this is necessary too for the boosting and balancing of water levels, there can be adverse effects in the case of chronic heart failure, as it can lead to hypnotremia. Moreover, the heart can suffer from an afterload effect following the constriction of blood vessels throughout the RAAS process of boosting blood pressure. A negative feedback loop can persist in the sense that while the RAAS is necessary for drops in blood pressure and to balance fluid levels on occasion, in the case of heart failure the system is not engaging in a one-time fix and as a result triggers the body into what amounts to the central nervous system changing the way the baroreceptors act: the effect is that “increase cardiac hypertrophy and dilation and fibrosis” occur for someone suffering from heart failure (Wasilewski et al., 2016).
References
Wasilewski, M. A., Myers, V. D., Recchia, F. A., Feldman, A. M., & Tilley, D. G.
(2016). Arginine vasopressin receptor signaling and functional outcomes in heart failure. Cellular Signalling, 28(3), 224-233.