Investigations into the causes of the rise in aldosterone secretion during haemorrhage Part I

Abstract

The effect of haemorrhage on aldosterone secretion was studied in anaesthetized dogs with intact pituitary glands and kidneys subjected to the stress of adrenal vein cannulation. The following observations were made: Acute haemorrhage was followed by a significant rise in aldosterone secretion in about one half of the animals studied. In most of the remaining dogs, called non-reactors, premature stimulation of aldosterone secretion before the withdrawal of blood appeared to be the cause for the lack of response. This stimulation was traced in many instances to prolonged surgical ‘stress’, in others to incipient circulatory failure. Another reason for a high initial secretion rate of aldosterone was low dietary sodium intake continued for a week or more. Increase in aldosterone secretion after haemorrhage was unimpaired by sectioning the vagi or the splanchnic nerves, and by the absence of the proprioceptors of carotid sinus and thyro-carotid junction, or of liver, spleen and gastrointestinal tract. During haemorrhage there is secretion of medullary amines and anoxia develops. The effect of these factors on aldosterone secretion was tested by infusing adrenaline and noradrenaline in the splanchnotomized animal, and by carrying out exchange transfusions with plasma till the dog had lost 50 % of its red cells. Provided the initial aldosterone secretion was low enough, these procedures caused small rises in output of aldosterone, but constituted less effective stimuli than blood loss. Glucocorticoid secretion was in all animals maximal or near maximal and changed but little in the course of the experiments. The findings suggest that, in the intact dog, aldosterone secretion is influenced by a variety of factors, most of which act indirectly by releasingACTH, or renin, or both. The role ofACTHand of renin as mediators of the action of haemorrhage on secretion of aldosterone will be studied in part II.