Editorial
Copyright ©2006 Baishideng Publishing Group Co.
World J Gastroenterol. Jan 28, 2006; 12(4): 526-538
Published online Jan 28, 2006. doi: 10.3748/wjg.v12.i4.526
Figure 4
Figure 4 Vascular hyporeactivity in cirrhosis may originate in the central nervous system, the autonomic nervous system, from local mediators, or within the smooth muscle cell/heart muscle cell. An autonomic dysfunction may act at cardiac, arterial, and arteriolar levels. Vasodilators and vasoconstrictors may act variably at cardiac, arterial, and arteriolar levels. At the smooth cellular (arteriolar) level, hyporeactivity may be caused by increased concentrations of vasodilators (NO, nitric oxide; CGRP, calcitonin gene-related peptide; ANP, atrial natriuretic peptide; TNF-α, tumor necrosis factor-alpha; endocannabinoids; CO: carbon monoxide) and/or decreased sensitivity to vasoconstrictors (ET-1: endothelin-1).