EARLY ARTERY REMODELING IN RATS WITH FETAL ZINC RESTRICTION

ARRANZ C; SANCHEZ R; VEIRAS LC; MASSARA L; CERNIELO M; COSTA M.A; TOMAT AL

Milan

Congreso; 21th European Meeting on Hypertension; 2011

European Society of Hypertension

We have shown that inadequate zinc intake during fetal life and lactation programs in adult rats hypertension, kidneymorphological and physiological alterations. In young rats we observed myocytes remodelling and reduced NOsynthase (NOS) activity in males (m) and females (f) rats. Objective: To evaluate vascular alterations in growing andadult zinc deficient rats and to compare the effects in m and f rats.Methods: Wistar rats were exposed from the beginning of pregnancy up to adulthood: low (L, 8 ppm) or control(C,30 ppm) zinc diet. At day 6, 21 and 81, m and f offspring of each group of mothers (Cm, Lm, Cf and Lf) weresacrificed to perform morphological studies in thoracic aorta sections stained by heamatoxylin-eosin (intimathickness(μm); media thickness(μm)) and picrosirius red (perivascular collagen thickness(μm), and signs of fibrosisin the media layer). NOS activity with L-(U14C)-arginine was also determined in thoracic aorta at 21 and 81 days.Results: Zinc deficient rats showed reduced vascular NOS activity (pmol Cit/g tissue.min) at 21 (C: 225 ± 4; L: 1725*) and 81 days (C: 231 ± 5; L: 167 ± 6*). Perivascular collagen thickness was increased in Lm and Lf since day 21(Cm:16±1;Lm:24±1*;Cf:12±1;Lf:23±2†) up to 81 days (Cm:46±1;Lm:71±6*;Cf:43±1;Lf:64±2†).No signs of fibroticprocesses were observed in the media layer of the thoracic aorta in any of the experimental groups.*p<0.01vsCm;†p<0.01vsCf, # p<0.01 vsLm. n=6 for each group.Conclusion: Zinc restriction during fetal life and postnatal growth induces a hypotrophic remodeling of large arteriesthat was observed since early postnatal life and persist until adulthood. These alterations were accompanied byan increase of the perivascular collagen and were similar in male and female offspring.The decrease of vascular NOSactivity and the inadequate growth in conduct arteries would impair vascular smooth muscle relaxation and would bereflected in a normal or abnormal posnatal vascular function in response to increases in flow and in shear stress.