Evidence against ANP as a natriuretic hormone during atrial distension.
To determine whether natriuresis attributable to atrial natriuretic peptides (ANP) is obtained in response to atrial stretch after blockade of the afferent input and reflex diuresis from atrial receptors, urine flow and sodium excretion were measured in response to distension of a balloon in the left atrium with the vagi at 37 and 9 degrees C. It is known that during such a distension ANP plasma concentration is increased by the same amount whether or not the afferent vagal fibres are intact. In 11 chloralose anaesthetized dogs 22 distensions with the vagi at 37 degrees C increased urine flow 117.5% and increased sodium excretion 28.7%. In 11 distensions with the vagi at 9 degrees C, urine flow did not change but sodium excretion decreased significantly (-20.9%). Thus natriuresis could not be demonstrated in response to atrial stretch in anaesthetised dogs after blockade of the atrial receptor reflex. These results imply that under these conditions, in which ANP is reportedly released into plasma, ANP is not acting as a hormone. The results must call into question the suggestion that ANP is released into plasma in a concentration capable of causing a natriuresis as its normal physiological function.
D000818:Animals; D016275:Atrial Function; D009320:Atrial Natriuretic Factor / Q000502:physiology*; D001794:Blood Pressure; D003080:Cold Temperature; D004285:Dogs; D006339:Heart Rate; D045283:Natriuretic Agents / Q000502:physiology*; D012964:Sodium / Q000652:urine; D014556:Urine; D014630:Vagus Nerve / Q000502:physiology
D045283:Natriuretic Agents; D009320:Atrial Natriuretic Factor; D012964:Sodium