Physiopathology of splanchnic vasodilation in portal hypertension

Figure 4 Hypothesis regarding the mechanisms and effects of the sympathetic post-ganglionic atrophy in splanchnic vasodilation. The afferent stimulus of portal hypertension, originating from pressure increases in portal or mesenteric vessels or microvasculature, reaches the brain stem cardiovascular nuclei through the afferent nerves. From there, post-ganglionic sympathetic nerve regression are mediated by efferent sympathetic nerves, leading to neurotransmission inhibition and vasoconstriction impairment mediated by norepinephrine (NE).