SEXUAL DIMORPHISM IN RENAL ANGIOTENSIN RECEPTORS GENE EXPRESSION: SEX CHROMOSOME COMPLEMENT INVOLVEMENT

DADAM, F.; CAMBIASSO, M.J.; PORCARI, C.; GODINO, A.; VIVAS, L.; CAEIRO, X.

CABA

Congreso; 2do. Congreso de la Federación de Sociedades de Neurociencias de Latinoamérica y el Caribe (FALAN); 2016

SAN

The process of biological sex differentiation (development of a givensex) involves genetic and hormonal developmental steps. This study aimed todefine whether sex chromosome complement (SCC) may differentially modulate sexdifferences in renal basal ANG II and ANG-(1-7) receptor expression. For thispurpose, we used gonadectomized mice of the "four core genotype"  model, in which the effect of gonadal sex andSCC is dissociated, allowing comparisons of sexually dimorphic traits betweenXX and XY females as well as in XX and XY males. Renal or Kidney cortex and medulla were collected and relative geneexpression of AT1aR, AT2R, and MasR were assessed by qPCR. Data showed that SCC modulates mRNA levels forboth, AT2R and MasRat the renal cortex. Regardless of sex (male or female) XX-SCCmice expressed higher levels of AT2R and MasR gene expression when compared to XY-SCCmice {F(1,12)=6,13, p<0.05; F(1,21)=5,14, p<0,05 resp.}. The analysis of MasR gene expression also showed asignificant effect of the interaction of SCC and gonadal sex {F(1,12)=4,59;p<0,05}. XX-female mice showed a significant increase in mRNA MasRlevelswhen compared with XY-female mice. These results, in agreement withour central brain data, reveal a modulatory effect of SCC on AT2R and MasR geneexpression with an enhancement of the vasodilator and natriuretic arm of RAS inXX-SCC mice, that may underlie sex differences in the regulation of arterialpressure. Supported: ANPCyT,ISN,SECyT,Mincyt-Cba,CONICET.