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Abstract ’l:he po!l!llble tole Of ca1clu. in the pathogenesis of l!!Isentll11 hypertension had zecleved lncxea:lea attention. SOlie 8’tudle’s had suggested a I,?O,551tlve cot”relation, bfOtween se-tu. total calcl~lII levell1 and til. helqhtof blQod p:te!l!ll,lr,1!!’ (Keste1oot and Geboers, 1982). However, otlllH reports had l~l!le~ the opposite possIbility, that an actual deficiency of calcilJ_, .uy 5QllehoW’ be causal (Hcearro,n, 1982 and VLllar et ”,1., u~rn . Bel1zan et al., l19B3b), in a stUdy on JS normotensive primIgravIdae wit.h notllliJl ’Pregnancy had found th.lt tile e.llllclulIl-supplelllented 91:01111h,a>d significantly lowe:: dlastol1c blood pl:es15ure tha:n the control group betveen the twentLeth ana the twenty fourth weeks of g:estatlon, Kovever. no d~f ference was ol):!un~:ved at terll”, Bellzan and Villar, 11980l, had found that no~mal VOmen ”,Lth 10’”’ calc1tJ. 1ntake have ,an lncl:case tn tIle,a’n acte.c:ial blood pl:eS5Ure tll”t predlSpoll.ell thelll to the developllent of pl:eqnaney-ll1duce’d hypectenslon (PUn durlnq the 1a:lt ])<11:1: of qelS1:ilItlon. |