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The angiotension renal system adjusts blood circulating volume and pressure during hypertension management. It activates when the blood pressure declines to increase electrolyte and water reabsorption in the kidney (Foundation & Lappin, 2017). Angiotensin II and aldosterone in the brain elevate sympathetic outflow, leading to hypertension. The system balances electrolyte and fluid levels and manages vascular resistance and tones (Takahashi et al., 2011). In this regard, it promotes oxidative stress in the brain, which activates sympathetic outflow.
Hypertension can lead to chronic renal failure, which makes arteries surrounding the kidenys weaken, narrow, or harden. Therefore, the affected arteries deliver insufficient blood to kidney tissues because the nephrons have inadequate oxygen and nutrient (Pugh et al., 2019). When the kidneys are affected, they cannot filter blood properly or control BP.
References:
Fountain, J. H., & Lappin, S. L. (2017). Physiology, renin-angiotensin system.
Pugh, D., Gallacher, P. J., & Dhaun, N. (2019). Management of hypertension in chronic kidney disease. Drugs, 79(4), 365-379.
Takahashi, H., Yoshika, M., Komiyama, Y., & Nishimura, M. (2011). The central mechanism underlying hypertension: a review of the roles of sodium ions, epithelial sodium channels, the renin-angiotensin-aldosterone system, oxidative stress, and endogenous digitalis in the brain. Hypertension Research, 34(11), 1147-1160.
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