Clinical pharmacology of diuretic agents with special reference to chlorothiazide (diuril).

The factors responsible for congestive heart failure as a clinical syndrome may be multiple. Although decreased cardiac output relative to inflow produces a moderate increase in venous pressure, there is a concomitant decrease in renal blood flow which may contribute to a decreased renal excretion of sodium. There is also a decrease in hepatic inactivation ( ? due to congestion) of adrenal cortical sodium-retaining hormone. Sodium retention produces at least a transient hypertonicity of the blood which may stimulate hypothalamic osmo-receptors, resulting in increased antidiuretic hormone secretion. Subsequent water retention produces a marked increase in venous pressure to further the development of edema. Thus, the rational therapeutic approach to the problem of congestive heart failure includes the exhibition of agents to increase cardiac output and increase renal blood flow, decrease venous pressure, decrease hepatic failure to inactivate steroids, decrease antidiuretic hormone activity, and decrease the abnormal renal retention of sodium. However, it is the renal retention of (or failure to excrete) sodium that assumes a major role in the pathogenesis of edema and it is this factor that concerns us therapeutically as we discuss diuretic agents. The purpose of this report is to describe the clinical pharmacology of diuretics with special attention to chlorothiazide (Diuril*).