dihydroergotoxine and Edema

The adaptability of the kidney in heart-failure is restricted. This is due to a sympathetically mediated renal vasoconstriction, forming part of a sympathetically induced general rearrangement of haemodynamics. This is reflected in a rise of the total peripheral vascular resistance and of the right auricular pressure and can be normalized to a large extent by sympathetic gamma-blockade. The renal vasoconstriction reduces the glomerular filtration rate and, thus, the tubular sodium load. Simultaneously, possibly by the same sympathetic stimulus, more renin is liberated from the juxtaglomerular apparatus. This increases the production of angiotensin and in turn, raises the production of aldosterone. By the combined effect of the reduced glomerular sodium load and aldosterone-mediated increase in tubular reabsorption of sodium, sodium and water will be retained in the body. During the night-rest the load on the circulatory system diminishes. In the early stages of heart-failure this emergency circulatory reaction, therefore, subsides and the rise of the renal fraction of the cardiac output leads to the excretion of the retained fluid and is the basis of nocturia.

Topics: Blood Proteins; Capillaries; Chlorides; Circadian Rhythm; Dibenzylchlorethamine; Dihydroergotoxine; Edema; Extracellular Space; Glomerular Filtration Rate; Heart Failure; Hemodynamics; Humans; Hypertension; Juxtaglomerular Apparatus; Kidney; Regional Blood Flow; Renin; Sodium; Sympathetic Nervous System; Vasomotor System; Water-Electrolyte Balance

Topics: Dihydroergotoxine; Dystocia; Edema; Ergot Alkaloids; Female; Humans; Oxytocics; Oxytocin; Pre-Eclampsia; Pregnancy; Secale; Spasm; Toxemia; Uterus