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This Article Full Text Full Text (PDF) All Versions of this Article: 90/3/341    most recent expphysiol.2004.028654v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by McCormick, K. M. Articles by Kappagoda, C. T. Search for Related Content PubMed PubMed Citation Articles by McCormick, K. M. Articles by Kappagoda, C. T. Related Collections Respiratory

¹ Division of Cardiovascular Medicine, University of California, Davis, CA 95616, USA

The role of adrenergic receptors in the reflex diuresis in response to pulmonary lymphatic drainage was examined in anaesthetized, artificially ventilated New Zealand White rabbits. Pulmonary lymphatic drainage was obstructed by raising the pressure in a pouch created from the right external jugular vein. This pulmonary lymphatic obstruction results in a reflex increase in urine flow and sodium excretion. This reflex is abolished by renal denervation and by administration of L-NAME, a non-selective inhibitor of nitric oxide synthase. Also, infusion of the relatively selective neuronal nitric oxide synthase blocker, 7-nitroindazole sodium salt, into the renal medulla abolished the reflex diuresis. In this study the effects of adrenergic receptor antagonists on the reflex increase in urine were observed. Both ureters were cannulated in order to determine urine flow from both kidneys separately. Prazosin, an ₁ adrenergic receptor antagonist, was infused into the renal medulla of the right kidney, while the left kidney acted as control. Administration of prazosin in this manner did not block the reflex diuresis in response to pulmonary lymphatic obstruction in either kidney. However, rauwolscine, an ₂ adrenergic receptor antagonist, abolished the reflex increase in urine and sodium excretion in the ipsilateral kidney while preserving it in the contralateral kidney. These findings suggest that the increase in urine flow in rabbits caused by pulmonary lymphatic obstruction is dependent upon activation of ₂ adrenergic receptors within the renal medulla.

(Received 19 July 2004; accepted after revision 5 January 2005; first published online 14 January 2005)
Corresponding author C. T. Kappagoda: Division of Cardiovascular Medicine, Bioletti Way, TB 172, University of California, Davis, CA 95616 USA. Email: ctkappagoda{at}ucdavis.edu

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