The present observation that AT2 receptor antagonist PD123319 inhibits the Ang II mediated cardiac hypertrophy is in agreement with our earlier observation with AT2 deficient mice which lost hypertrophic response to Ang II. It is important to note that normalization of blood pressure by hydralazine prevented cardiac hypertrophy which indicates that pressure load is essential for the hypertrophy in agreement with existing reports as discussed above myocyte stretch and tension induce expression of AT2. In summary, the present results of in vivo and in vitro studies demonstrate that PLZF activates GATA4 gene transcription and plays a significant role in the AT2-mediated cardiac hypertrophic response to Ang II. Different insults inflicting hepatocyte damage, such as alcohol or acute and chronic viral infections, may eventually lead to cirrhosis and intra-hepatic portal hypertension. Anatomical changes such as fibrotic scar and regenerative nodule formation that result in mechanical Acipimox compression of the hepatic vasculature have been traditionally implicated as the dominant cause for increased intrahepatic vascular resistance, the hallmark of sinusoidal-type PH. It is similarly acknowledged, L-Ornithine however, that hepatic stellate cells play a pivotal role in this process. A common pathway in PH pathogenesis due to increased intra-hepatic resistance involves activation of HSCs from a quiescent, vitamin A storing subendothelial cells to myofibroblast-like cells, endowed with a contractile, proinflammatory and fibrogenic properties. Together, HSC-associated anatomical changes contribute to increased mechanical resistance to blood flow, while contractile activity of activated HSCs might contribute to increased hemodynamic pressure. The sinusoidal endothelium is distinguished by openings that, together with discontinuities in the basement membrane are essential for proper permeability through this unique low resistance/low pressure microvascular network. Accordingly, matrix deposition within the space of Disse and closure of endothelial fenestrations �Cprocesses that together underlie sinusoidal capillarization- impede the rapid exchange of solutes between the sinusoidal space and hepatocytes, causing increased resistance to portal blood flow and PH.