Mechanism of Antidiuretic Effect of Beta Adrenergic Stimulation

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Abstract
The effect of beta adrenergic stimulation on renal-diluting capacity was examined in the dog. Beta adrenergic stimulation with intravenous isoproterenol significantly increased urinary osmolality (UOsm) and decreased free water clearance (CH2O), and these effects were rapidly reversible with cessation of the infusion. This antidiuretic effect of systemic beta adrenergic stimulation was comparable in innervated and denervated kidneys and was not associated with alterations in glomerular filtration rate or renal vascular resistance. Renal perfusion pressure was maintained constant in all of the experiments. The same dose of isoproterenol, which produced the antidiuretic effect and markedly stimulated cardiac beta adrenergic receptors when infused intravenously, was not found either to increase UOsm or to decrease CH2O when infused directly into the renal artery. Removal of the source of production and release of antidiuretic hormone (ADH) was, however, found to abolish the effect of intravenous isoproterenol on UOsm. A small effect on CH2O persisted and appeared to be related to an increase in arterial hematocrit. Thus, the results of the study exclude a major role of alterations in renal hemodynamics and renal innervation in the antidiuretic response to beta adrenergic stimulation with isoproterenol. They also provide no support for the hypothesis that beta adrenergic stimulation may directly alter the water permeability of the renal tubular epithelium. Rather the results suggest that the primary mechanism of the antidiuretic effect of beta adrenergic stimulation involves the integrity of the hypothalamoneurohypophyial system and the release of ADH.