Lithium administration and phosphate excretion.
The phosphaturic effect of parathyroid hormone (PTH), cyclic adenosine monophosphate (cAMP), acetazolamide (Az), and HCO3 loading was studied in normal, thyroparathyroidectomized (TPTX), and Li-treated dogs. PTH administration to normal animals markedly increased fractional excretion (F) of PO4 but had a blunted effect on FPO4 in the Li-treated animals. Cyclic AMP likewise markedly increased FPO4 in the normal animals but had a markedly blunted effect in the Li-treated animals. Az led to a significant increase in FNa, FHCO3, and FPO4 in the normal animals. In the Li-treated dogs, Az induced a significant natriuresis and bicarbonaturia but failed to increase phosphaturia. HCO3 loading in normal dogs caused a significant phosphaturia while having little effect on FPO4 in Li-treated dogs. HCO3 loading to TPTX dogs was associated with a lower FPO4 as compared to normal HCO3-loaded animals. These data suggest that Li administration not only blocks the adenyl cyclase-cAMP system in the renal cortex, but it may also interfere with a step distal to the formation of cAMP, since the phosphaturic effect of both PTH and cAMP was markedly diminished in Li-treated animals.
D000086:Acetazolamide / Q000494:pharmacology; D000067956:Adenylyl Cyclase Inhibitors; D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology; D000242:Cyclic AMP / Q000037:antagonists & inhibitors / Q000494:pharmacology; D004285:Dogs; D005260:Female; D007668:Kidney / Q000187:drug effects* / Q000502:physiology; D007672:Kidney Cortex / Q000201:enzymology; D008094:Lithium / Q000494:pharmacology*; D010280:Parathyroid Glands / Q000502:physiology; D010281:Parathyroid Hormone / Q000494:pharmacology; D010710:Phosphates / Q000652:urine*; D013961:Thyroid Gland / Q000502:physiology
D000067956:Adenylyl Cyclase Inhibitors; D001639:Bicarbonates; D010281:Parathyroid Hormone; D010710:Phosphates; D008094:Lithium; D000242:Cyclic AMP; D000086:Acetazolamide