Key Points
- To examine whether atrial natriuretic factor alters osmotic water permeability or urea permeability in isolated rat inner medullary collecting ducts stimulated by vasopressin.
- Perfused isolated terminal inner medullary collecting ducts from rats ex vivo.
- Administered rat ANF (1-28) at concentrations from 0.01 nM to 100 nM or exogenous cyclic GMP (0.1 mM) under submaximal vasopressin (10⁻¹¹ M) or cyclic AMP stimulation.
- Measured osmotic water permeability, urea permeability, and vasopressin-stimulated cyclic AMP accumulation.
- ANF significantly decreased vasopressin-stimulated osmotic water permeability in a dose-dependent manner (18% reduction at 0.01 nM, 46% at 0.1 nM, 48% at 1 nM, and 46% at 100 nM).
- Exogenous cyclic GMP mimicked this inhibition by decreasing osmotic water permeability by an average of 48%, and ANF reduced cyclic AMP-stimulated permeability by an average of 31%.
- ANF did not alter urea permeability or vasopressin-stimulated cyclic AMP accumulation, indicating an inhibitory site distal to cyclic AMP generation.
Structured PICO
PPopulationIsolated perfused terminal inner medullary collecting ducts (IMCDs) from rats
IInterventionAtrial natriuretic factor (rat ANF 1-28) at concentrations ranging from 0.01 nM to 100 nM, in the presence of vasopressin (10^-11 M)
CComparatorVasopressin (10^-11 M) alone
OOutcomeOsmotic water permeability (Pf)surrogate
ANF inhibits vasopressin-stimulated osmotic water permeability in the rat terminal IMCD, with cyclic GMP acting as the second messenger.