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1 San Diego, California, United States
2 Div Nephrology, Dept Medicine, UC San Diego / VA Medical Center, San Diego, California, United States
3 Department of Pharmacology and Toxicology, University of Tuebingen, Tuebingen, Germany
4 United States
5 Pharmacology, UCSD, San Diego, California, United States
6 Pharmacology, University of California, San Diego, La Jolla, California, United States
7 Medicine and Pharmacology, University of California San Diego & VAMS, La Jolla, California, United States
* To whom correspondence should be addressed. E-mail: vvallon{at}ucsd.edu.
Activation of adenosine A1 receptors (A1R) can inhibit arginine-vasopressin (AVP)-induced cAMP formation in isolated cortical and medullary collecting ducts. To assess the in vivo consequences of the absence of A1R, we performed experiments in mice lacking A1R (A1R-/-). We assessed the effects of the vasopressin V2 receptor (V2R) agonist, 1-desamino-8-D-arginine vasopressin (dDAVP), on cAMP formation in isolated inner medullary collecting ducts (IMCD) and on water excretion in conscious water-loaded mice. dDAVP-induced cAMP formation in isolated IMCD was significantly greater (~2-fold) in A1R-/- compared to wild-type mice (WT) and, in contrast to WT, not inhibited by the A1R agonist N6-cyclohexyladenosine. A1R-/- and WT had similar basal urinary excretion of vasopressin, expression of aquaporin-2 protein in renal cortex and medulla, and acute increases in urinary flow rate and electrolyte-free water clearance in response to the V2R antagonist SR121463 or acute water loading; the latter increased inner medullary A1R expression in WT. Dose-dependence of dDAVP-induced antidiuresis after acute water loading was not different between the genotypes. However, A1R-/- had greater inner medullary expression of cyclooxygenase-1 under basal conditions and of the P2Y2 and EP3 receptor in response to water loading compared to WT mice. Thus, vasopressin-induced cAMP formation is enhanced in isolated IMCD of mice lacking A1R, but the adenosine-A1R/V2R interaction demonstrated in vitro is likely compensated in vivo by multiple mechanisms, a number of which can be "uncovered" by water loading.
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