The contribution of atrial stretch receptors to salt and water homeostasis in the human.
Studies carried out in both the human and experimental animals provide reasonably strong evidence that receptors contained within the atria are involved in the control of body water. When atrial pressure is increased (and the atria distended) atrial receptor discharge is increased leading to an increase in urine flow and, depending upon the experimental condition, a less consistent increase in sodium excretion. At least two mechanisms appear to contribute to the renal response; inhibition of the secretion of antidiuretic hormone and inhibition of renal nerve discharge. None of the factors presently known to alter sodium excretion have been shown to account completely for the increase in sodium excretion. The failure of patients with chronically distended atria to experience a chronic diuresis appears to be partly the result of a resetting of atrial receptor sensitivity. Recent evidence suggests that the sensitivity of atrial volume receptors has a species variation.
D000818:Animals; D016275:Atrial Function; D001810:Blood Volume; D006332:Cardiomegaly / Q000652:urine; D004231:Diuresis; D004285:Dogs; D006325:Heart Atria / Q000294:innervation; D006331:Heart Diseases / Q000652:urine; D006439:Hemodynamics; D006706:Homeostasis; D006801:Humans; D007668:Kidney / Q000294:innervation / Q000502:physiology; D008465:Mechanoreceptors / Q000502:physiology*; D009200:Myocardial Contraction; D009318:Natriuresis; D013045:Species Specificity; D009435:Synaptic Transmission; D014667:Vasopressins / Q000037:antagonists & inhibitors; D014882:Water-Electrolyte Balance
D014667:Vasopressins