pancreastatin and Disease-Models--Animal

Hypertension significantly increases the risk of hyperglycemia in patients. It is known that chromogranin (CgA) and pancreastatin (PST) are involved in regulation of blood pressure and endocrine function of the pancreas. However, still little is known about the physiology of these hormones' secretion in hypertension. The objective of the study was to examine the effects of hypertension on pancreatic islet cells containing CgA and PST in rats. The studies were carried out on the pancreas of rats. After 6 week period of the renal artery clipping procedure, eight 2K1C rats developed stable hypertension. Cells containing CgA and PST were detected using immunohistochemical method. The hypertension significantly decreased the number of pancreatic endocrine cells immunoreactive to CgA and PST antisera. The differences between the hypertensive and normotensive rats concerned not only the number of endocrine cells but also intensity of reactions. In conclusion, the research results indicate that hypertension causes the diminished biosynthesis of CgA and PST in the pancreas of rats and suggests the participation of those peptides in pancreatic disorders occurring in a state of elevated blood pressure.

Topics: Animals; Chromogranin A; Disease Models, Animal; Hypertension, Renal; Immunohistochemistry; Islets of Langerhans; Male; Rats; Rats, Wistar

Acute myocardial infarction causes neurohumoral activation characterized by increased sympathetic activity. CgA is a protein released during sympathoadrenal stress from neuroendocrine tissue. Recently, increased CgA concentrations in circulation have been reported and suggested to be an independent predictor of mortality after acute myocardial infarction.. Eighteen pigs underwent 1 h of regional myocardial ischemia followed by 3 h of reperfusion. Blood samples were collected every hour and plasma CgA was measured with two radioimmunoassays.. We found a 30% increase in plasma N-terminal CgA 1 h after re-establishment of coronary blood supply. On the other hand, plasma pancreastatin did not change in response to ischemia or reperfusion but decreased during the entire experiment.. Our results suggest a differentiated CgA response in myocardial reperfusion after local cardiac anoxia that may reflect tissue-specific post-translational processing and release.

Topics: Adrenal Glands; Amino Acid Sequence; Animals; Chromogranin A; Disease Models, Animal; Female; Hemodynamics; Myocardial Ischemia; Myocardial Reperfusion; Myocardium; Natriuretic Peptides; Pancreatic Hormones; Peptides; Swine; Time Factors; Troponin T