Splanchnic and systemic vasodilation: the experimental models.

Experimental models are a sine qua non condition for unraveling the specific components and mechanisms contributing to vascular dysfunction and arterial vasodilation in portal hypertension. Moreover, a careful selection of the type of animal model, vascular bed, and methodology is crucial for any investigation of this issue. In this review, some critical aspects related to experimental models in portal hypertension and the techniques applied are highlighted. In addition, a detailed summary of the mechanisms of arterial vasodilation in portal hypertension is presented. First, humoral and endothelial vasodilators, predominantly nitric oxide but also carbon monoxide and endothelium-derived hyperpolarizing factor, and others are discussed. Second, time course and potential stimuli triggering and/or perpetuating splanchnic vasodilation are delineated. Finally, a brief general overview of vascular smooth muscle signaling sets the stage for a discussion on cotransmission, receptor desensitization, and the observed impairment in vasoconstrictor-induced smooth muscle contraction in the splanchnic and systemic circulation during portal hypertension.