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Abstract Preeclampsia remains one of the leading causes of maternal and fetal morbidity and mortality. Despite extensive researches, our knowledge of the aetiology and pathophysiology of the preeclampsia is still limited. Current therapy remains impiric, based on earl\ delivery with attendant risks of operative delivery and iatrogemc prematunu Recently there has been interest in the role of hypeniisulinemia in the pathogenesis of preeclampsia. There are several reasons why hyperinsulinemia may be considered a pathogenic mediator of hypertension in insulin resistant resistant status especially in cases with preeclampsia. 1- Insulin is known to promote sodium retention by the kuun.-} 2- Insulin is known to stimulate sympathetic nervous system activity. 3- There is some evidence that insulin has direct and indirect effects on a variety of membrane cation transport systems. 4- Insulin can stimulate the release of vasopressoi substances, as it stimulates production of endothelin-1 from endothehai ells Endothelin-1 is now considered the most potem vasoconstrictor recently discovered and it is well established thai maternal plasma endothelin-1 level increases in preeclampsia.Thus, one of the objectives of this study was o investigate the pathophysiological role of hyperinsulinemia (in pregnancies complicated |