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Abstract Introduction Despite inten ive re earch, mo t theories on the cnu arion of pregnancyinduced hypertension have been either dismissed or unproven and the disease process remained uncertain, TI,e aetiology of eclampsia, the most severe form of the disease. has not yet been ettled (Z/lspan,] 9 7). The endogenou opiates probably originate from pituitary gland and are ecreted in parallel with adrenocorticotropic hormone (A TH) in respoll e to c rticorropin relea ing It rmone (Hung, 1987). s- endorphin i 1’1 natural! occurring brain peptide having opiate like propertie . It nO\.\1appears to pia an important central nervous system regulatory function involving ardiovascular regulatory function. neuroendocrin and eizure threshold r gulation (Morley, J 983. B- endorphin has a depres, or role Oil the cardiovascular sy tern while other neuropeptides I1a\e a pre sor one (De JOl1g a M, ,1983). Speroff et al. (1989 believed thai 111 pregnancy the intermediate lobe of maternal pituitary gland is a major source of progre sively increa ing opiates e pecially B- endorphin and enkephalins. The authors added that, the function ofndog nous opiat in pregnancy may b r lat d to str ss, inhibition of oxytocin, va opr in, well a gonadorrophines, promotion of prolactin s cretion and of course maternal analgesic action during labour and delivery. Bend rphin levels were reported to iucreas sis~nifican I).; in preg~nancyJinduced hyperI 11 ion being roo rt significant in vere preeclamptic toxaemia Attie/” and Fayed, 1991 . Tlte 11.1m0 f IhiIS WOLk ’I’ 10” tudy rhe plausma” B- endorphin levels in ca e. of preeclamptic and eclamptic ca . in comparison to that in normal pregna.ne This stud may explain orne of the unresolved pathophy iological change’ in toxaemia f pregnancy. |