Zinc restriction during fetal life and growth: role of the renin angiotensin system in the cardiovascular alterations in the adult lif

ARRANZ C, GOBETTO N, MENDEZ GARRIDO F, JURIOL L, VEIRAS L, HERRERA L, AGUIRRE S, CANIFFI C, TOMAT A, GIRONACCI MM, COSTA MA.

Congreso; 23rd European Meeting on Hypertension and Cardiovascular Protection; 2013

The aim was to evaluate renal renin angiotensin system (RAS) in rats exposed to zinc deficient diet during fetal life and to compare males (m) and females (f) rats, in order elucidate the mechanism involved in this hypertension programming model.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 81, we evaluated in offspring (Cm, Lm, Cf and Lf):1) Systolic blood pressure(SBP, mmHg), 2)maximal contractile response (Emax) in thoracic aortic rings. Isometric tension (g) was recorded by a force-transducer, in presence of Ang II (10-10, 10-6) ; 3) AngII receptors (AT1 R) labeling in kidney by inmunohistochemical technique (polyclonal anti-rabbit AT1 R antibody ); 4) the expression of angiotensin-converting enzyme (ACE) mRNA in renal tissue by reverse-transcription and quantitative real-time PCR reactions ( L levels/C levels, control groups were considered as calibrators with a given value of 1). Results: Only Lm showed increased SBP (Cm:124±3 vs Lm:141±5 *). Emax to Ang II was higher in Cm than Cf rats (0.57±0.056 vs 0.27±0.017*) and in Lm (0.27±0.027 *) this parameter was decreased compared with Cm, without changes in f. Inmunohistochemical of AT1R in renal tissues revealed that Cm showed strongest labeling that Cf rats. Zinc deficient diet in male and female rats induced an increase in the expression of AT1R in renal tissue.Zinc deficiency induced an increase of renal ACE expression in males (fold change: 6.4±0.6, p < 0.001 vs Cm rats), but no changes were observed in f (1.1±0.1, ns). Values are means±SEM, n= 6, two ways ANOVA and Bonferroni post- test. *p