Furthermore, the increased levels of Giα were shown to be associated with hypertension and not with hypertrophy, due to the fact that heart and aorta from Nω-nitro-L-arginine methyl ester-(L-NAME)-induced hypertensive rats, which do not have cardiac hypertrophy exhibited enhanced levels of Giα-2 and Giα-3 proteins as well as mRNA, whereas the levels of Gsα protein were unaltered [31]. The gene discussed is GNAS; the disease is cardiac hypertrophy.