Many mechanisms have been proposed to account for the rise in peripheral resistance in hypertension. Most evidence implicates either disturbances in the kidneys' salt and water handling (particularly abnormalities in the intrarenal renin–angiotensin system)[61] or abnormalities of the sympathetic nervous system.[62] These mechanisms are not mutually exclusive and it is likely that both contribute to some extent in most cases of essential hypertension. It has also been suggested that endothelial dysfunction and vascular inflammation may also contribute to increased peripheral resistance and vascular damage in hypertension.[63][64] Interleukin 17 has garnered interest for its role in increasing the production of several other immune system chemical signals thought to be involved in hypertension such as tumor necrosis factor alpha, interleukin 1, interleukin 6, and interleukin 8.[65]
Unlike high blood pressure symptoms, which are poorly defined and often totally absent, low blood pressure symptoms tend to be more upfront and easily recognizable. The development of symptoms is often a warning sign of a potentially serious underlying disorder. Generally speaking, your blood pressure would need to fall pretty dramatically before symptoms develop.