Experimental data is presented to show that hypertension occurs when angiotensin II levels are inappropriate high to the amount of sodium intake. Normal levels of sodium intake can induce hypertension when plasma angiotensin II concentration are inappropriately elevated. Similarly, very small doses of Ang II (2-3 ng/kg/min) increase arterial pressure (AP) when sodium intake is enhanced (300-500 mEq/day). Nitric oxide (NO) also plays a role in minimizing the effect of Ang II and sodium. NO synthesis inhibition accentuates hypertensive effects of both Ang II and sodium intake.

Ang II stimulates superoxide in a biphasic response. A fast response (30 seconds) is accounted for by the stimulation of NADPH through protein kinase C after binding to AT1 receptor. A second and more delayed response of O₂ production (peak 30 minutes) is produced by a series of intracellular signaling factor, mainly Src protein and epidermal growth factor (EGRF), phosphatidyl inositol, Rac GDP-GTP. The production of oxygen from these reactions are important because it feeds forward by stimulating again Src and epidermal growth factor. This creates an autostimulated cycle that explains why OXST is sustained with such small doses of Ang II. The importance of this cycle is stressed because inhibition of EPFR by AG1478 blocked the vasoconstriction induced by angiotensin II or phenylephrine.

These results indicate that OXST is a major mechanism underlying hypertension which can be induced by a disparity between the level of angiotensin and sodium intake. Stimulation of Src protein and EGFR are important to sustain OXST and hypertension.