atrial-natriuretic-factor and Acid-Base-Imbalance

Topics: Acid-Base Imbalance; Atrial Natriuretic Factor; Blood Flow Velocity; Constriction; Female; Fetal Blood; Fetal Distress; Humans; Hypertension; Infant, Newborn; Pregnancy; Pregnancy Complications, Cardiovascular; Prognosis; Respiratory Distress Syndrome, Newborn; Umbilical Arteries; Umbilical Cord

The common disorders of fluid, electrolyte and acid-base metabolism observed in patients with liver cirrhosis are hyponatremia, hypokalemia, respiratory alkalosis, and metabolic acidosis, in addition to an excess accumulation of body fluids with edema and ascites formation. It has been suggested that an impaired renal sodium excretion in liver cirrhosis is caused by rather an increase in tubular sodium reabsorption than a decrease in glomerular filtration rate. In order to explain the pathophysiological mechanisms involved in initiating and maintaining sodium retention in cirrhosis, three hypotheses, namely, the "underfilling" hypothesis, the "overflow" hypothesis, and the "pepipheral arterial vasodilation" hypothesis have been proposed. However, neither of them could not fully account for the pathogenesis and pathophysiology of the avid renal sodium retention in cirrhosis. Although it is undoubted that the abnormal renal sodium handling in cirrhosis is mediated mainly by the sympathetic nervous system and the certain humoral agents such as renin-angiotensin-aldosterone system, atrial natriuretic peptide, prostaglandins, kallikein-kinin system, antidiuretic hormone and so on, the precise mechanism of the enhanced tubular sodium reapsorption induced via these factors is not well understood and still remains to be elucidated.

Topics: Acid-Base Imbalance; Atrial Natriuretic Factor; Humans; Kallikreins; Kinins; Liver Cirrhosis; Renin-Angiotensin System; Water-Electrolyte Imbalance

Both micropuncture and clearance studies have shown that the anion excreted in the urine in response to the increased glomerular filtration rate and solute load induced by atrial natriuretic factor (ANF) depends on the pre-existing acid-base status. In normal animals, the kidney is relatively better at reabsorbing bicarbonate than chloride, as ANF increases luminal flow so that a chloruresis without bicarbonaturia ensues. In contrast, during chronic hypochloraemic metabolic alkalosis, alkalaemia renders the kidney unable to reabsorb the increment in filtered bicarbonate induced by ANF so that bicarbonaturia occurs with amelioration of the alkalosis. Since the relative magnitudes of chloride versus bicarbonate excretion rates in response to ANF are a function of the plasma anion concentrations, ANF tends to correct acid-base disorders.

Topics: Acid-Base Equilibrium; Acid-Base Imbalance; Animals; Atrial Natriuretic Factor; Bicarbonates; Female; Glomerular Filtration Rate; Rats; Rats, Inbred Strains