The effect of endothelin-1 on pancreatic diseases in patients who smoke.

Endothelin (ET) is a peptide secreted by the endothelial cells of blood vessels. It has a very strong vasoconstricting effect. Endothelin-1 (ET-1) is present in the blood in low concentrations, but in response to the stimulus of cigarette smoking, it can be released into the interior of blood vessels in substantial quantities, resulting in rapid vasoconstriction. ET-1 activity causes ischemia and hypoxia in many organs, particularly in the pancreas. The destructive action of tobacco smoke components on the cells of the pancreas is known, but so far the mechanisms of these changes are not fully understood. It has been suggested that ET-1 may play a major role in this process. By inducing vasoconstriction in the pancreas, with a subsequent disruption in its blood flow, ET-1 leads to structural changes in this organ and to exocrine and endocrine dysfunction. ET-1 also has the ability to induce secretion of pro-inflammatory cytokines (IL-1, IL-6), which intensify existing pancreatitis and lead to the progression of this disease. ET-1 can stimulate collagen production in the pancreas, which contributes to the formation of fibrosis in patients with chronic pancreatitis. Nicotine from tobacco smoke intensifies insulin resistance in patients with diabetes. High insulin concentrations induce the secretion of ET-1 by the endothelial cells of the pancreas. By inducing vasoconstriction and subsequent tissue hypoxemia, ET-1 can cause a decrease in peripheral glucose utilization and contribute to the progression of type 2 diabetes. ET-1 is considered a risk factor for pancreatic diseases, particularly acute ischemia and pancreatitis.