ABSTRACT
Traditionally, diuretics have been the only agents considered appropriate for initial antihypertensive treatment, and other drugs have been added sequentially. Diuretics may cause a number of adverse metabolic effects as well as a decrease in the quality of life for some patients. Currently, physicians are modifying their approach to treating hypertension and using alternatives to diuretics as initial therapy. Diuretics are often used in combination with many of the newer antihypertensive drugs. Some antihypertensive agents, such as the angiotensin-converting enzyme inhibitors, may blunt the adverse metabolic effects of the diuretics with which they are combined. This review discusses the advantages and disadvantages of beta-adrenergic blocking agents, calcium-channel blockers, and alpha-adrenergic blocking agents.
Subject(s)
Antihypertensive Agents/therapeutic use , Hypertension/drug therapy , Antihypertensive Agents/administration & dosage , Diuretics/administration & dosage , Drug Therapy, Combination , HumansABSTRACT
Gastroduodenal disease such as peptic ulcer and duodenitis is increased in patients with end-stage renal disease. Gastric hypersecretion of acid proposed as the underlying mechanism has been disputed because peptic ulcer has occurred even in those with normal or low gastric acid secretion. We studied the pancreatic exocrine secretion of bicarbonate (HCO3) and the concentration of plasma pepsinogens in addition to gastric acid secretion in 15 patients on chronic hemodialysis, 10 patients wih previous renal transplantation and compared them with 10 subjects without gastrointestinal or renal disease. We confirmed hypersecretion of gastric acid in renal disease. We confirmed hypersecretion of gastric acid in renal patients on chronic hemodialysis but not in transplant patients. In addition, we found basal but hyposecretion of HCO3 and hyperpepsinogenemia in both renal groups. These observations suggest that the high incidence of gastroduodenal disease in end-stage renal disease might, in part, be due to the simultaneous occurrence of gastric acid hypersecretion, basal hyposecretion of HCO3 by the pancreas, and hyperpepsinogenemia.