A study was conducted to determine the pressor response to angiotensin II (A-II) in young primigravid women throughout pregnancy. The study aimed to identify when resistance to A-II pressor effects develops, define the physiological sequence of events leading to this resistance, and determine if sensitivity to infused A-II could be detected before clinical signs of pregnancy-induced hypertension (PIH) appear. The study included 192 patients, with 120 remaining normotensive and 72 developing PIH. Vascular resistance to A-II was observed as early as the 10th week of pregnancy. In normotensive women, maximum vascular resistance occurred at 18–30 weeks, while in those who developed PIH, it occurred at 18 weeks. By 22 weeks, a clear separation between the two groups was evident, with those destined to develop PIH requiring lower doses of A-II. By 23–26 weeks, the difference became statistically significant (P < 0.01). Among patients requiring more than 8 ng/kg/min of A-II on one or more tests between weeks 28–32, 91% remained normotensive, while 90% of those requiring less than 8 ng/kg/min developed PIH. The study confirmed that normal pregnant women are resistant to A-II pressor effects, while those with PIH are highly sensitive. Resistance to A-II develops early in pregnancy and is maintained throughout. However, in normotensive women, resistance slightly decreases by 30 weeks. In those who develop PIH, resistance decreases earlier, up to 12–14 weeks before clinical signs of PIH appear. The study also found that sensitivity to A-II in those destined to develop PIH was not preceded by significant increases in blood pressure. The results suggest that A-II pressor response testing could be used as a predictive tool for PIH. The study highlights the importance of early detection and monitoring of A-II sensitivity in pregnant women to identify those at risk of developing PIH. The findings have implications for the management of pregnancy and the prevention of complications associated with PIH.A study was conducted to determine the pressor response to angiotensin II (A-II) in young primigravid women throughout pregnancy. The study aimed to identify when resistance to A-II pressor effects develops, define the physiological sequence of events leading to this resistance, and determine if sensitivity to infused A-II could be detected before clinical signs of pregnancy-induced hypertension (PIH) appear. The study included 192 patients, with 120 remaining normotensive and 72 developing PIH. Vascular resistance to A-II was observed as early as the 10th week of pregnancy. In normotensive women, maximum vascular resistance occurred at 18–30 weeks, while in those who developed PIH, it occurred at 18 weeks. By 22 weeks, a clear separation between the two groups was evident, with those destined to develop PIH requiring lower doses of A-II. By 23–26 weeks, the difference became statistically significant (P < 0.01). Among patients requiring more than 8 ng/kg/min of A-II on one or more tests between weeks 28–32, 91% remained normotensive, while 90% of those requiring less than 8 ng/kg/min developed PIH. The study confirmed that normal pregnant women are resistant to A-II pressor effects, while those with PIH are highly sensitive. Resistance to A-II develops early in pregnancy and is maintained throughout. However, in normotensive women, resistance slightly decreases by 30 weeks. In those who develop PIH, resistance decreases earlier, up to 12–14 weeks before clinical signs of PIH appear. The study also found that sensitivity to A-II in those destined to develop PIH was not preceded by significant increases in blood pressure. The results suggest that A-II pressor response testing could be used as a predictive tool for PIH. The study highlights the importance of early detection and monitoring of A-II sensitivity in pregnant women to identify those at risk of developing PIH. The findings have implications for the management of pregnancy and the prevention of complications associated with PIH.