Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma kallikrein releases bradykinin when activated by gram-negative septicemia or irreversible hemorrhagic shock. Pancreatitis releases glandular kallikrein causing hypotension and increased vascular permeability. Bradykinin in the brain produces hypertension. Renal kallikrein is released by high arterial pressure, vasodilators, low doses of noradrenaline, angiotensin II, mineralocorticoids and rapid volume expansion. It has a biphasic relation to sodium excretion. In essential hypertension, kallikrein release into the blood and urine is low and facilitates hypertension. High renin in Bartter's syndrome is balanced by high PGE and kallikrein without hypertension.
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PMID:Kallikrein, kininogen and kinins in control of blood pressure. 37 13

Excretion of adrenaline was increased in patients with chronic recurrent pancreatitis, excretion of noradrenaline tended to decrease although the content of this amine exceeded 1.5-2-fold its normal concentration in individual patients; excretion of DOPA was unaltered. Hyperlipoproteinemia was found in the majority of the patients. Maximal level of the adrenaline excretion was mainly observed in the patients with high activity of the trypsin inhibitor in blood serum as well as with the high ratio trypsin inhibitor/trypsin. An increase in the adrenaline excretion correlated with hypercholesterolemia and to a lesser extent--with hypertriglyceridemia. The most pronounced hypertriglyceridemia was typical for the patients with alcoholic abuse. Relationship between catecholamines and extrasecretory functions of pancreatic gland as well as with hyperlipoproteinemia in pancreatitis is discussed. An increase in the total antitryptic activity might be caused by activation of the sympathoadrenal system or by hyperproduction of adrenaline.
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PMID:[Excretion of catecholamines and lipid composition of blood in patients with chronic pancreatitis]. 640

Staphylococcal intoxication caused distinct alterations in content of biogenic amines estimated in salivary, lacrimal and pancreatic glands. Development of pancreatitis was accompanied by a decrease in content of adrenaline and noradrenaline in all the glands studied, while histamine content was increased in pancreas and-unaltered in salivary and lacrimal glands.
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PMID:[Levels of biogenic amines in the salivary and lacrimal glands in experimental staphylococcal pancreatitis in rats]. 650 85

Pancreatic ductal adenocarcinoma (PDAC) is among the leading causes of cancer deaths and is unresponsive to existing therapy. Smoking and alcohol-induced pancreatitis are among the risk factors for PDAC. We have previously reported that beta-adrenergic receptors (beta-ARs) stimulate the proliferation and migration of human PDAC cells in vitro by cAMP-dependent signaling and that the nicotine-derived nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) activates this pathway directly in vitro while additionally stimulating the release of noradrenaline/adrenaline by binding to alpha7 nicotinic acetylcholine receptors (alpha7 nAChR) in hamsters. In this study, we have tested the hypothesis that the beta-AR antagonist propranolol prevents the development of PDAC induced in hamsters with ethanol-induced pancreatitis by NNK. We found that propranolol had strong cancer preventive effects in this animal model. Western blots of pancreatic duct cells and PDAC cells harvested by laser capture microscopy showed significant upregulation of the alpha7 nAChR associated with significant inductions of p-CREB, p-ERK1/2, and increases in epidermal growth factor and vascular endothelial growth factor in PDAC cells of hamsters not treated with propranolol. These effects were reversed by treatment with propranolol. Our data suggest that propranolol may prevent the development of PDAC by blocking cAMP-dependent intracellular signaling, cAMP-dependent release of epidermal growth factor, and PKA-dependent release of vascular endothelial growth factor while additionally downregulating the alpha7 nAChR by inhibiting cAMP-mediated subunit assembly. We conclude that increased cAMP signaling is an important factor that drives the development and progression of PDAC and that the inhibition of cAMP formation is a promising new target for the prevention and adjuvant therapy of PDAC.
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PMID:Prevention of pancreatic cancer by the beta-blocker propranolol. 1938 37