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Department Physiology and Biophysics, Instituto Ciências Biomédicas, Universidade de São Paulo, São Paulo 05508-900, Brazil
Luminal perfusion
with collected proximal fluid increases distal K+ secretion
compared with artificial solutions. Arginine vasopressin (AVP), present
in luminal fluid, might be responsible for this observation.
K+ secretion rate (JK) was measured by
K+-sensitive microelectrodes during paired luminal
stationary microperfusion with control and AVP-containing 0.5 mM
K+ solutions. JK was 1.34 ± 0.35 (n = 24 tubules)
nmol · cm
2 · s1
during perfusion with 109 M AVP, against
0.90 ± 0.12 nmol · cm2 · s1
(n = 21) in control (P < 0.02). With
109 M
AVP+106 M
-mercapto---cyclopenta-methylenepropionyl1,
O-Me-Tyr2-Arg8 vasopressin (MCMV), a specific
peptide V1-receptor antagonist, JK was
0.36 ± 0.067 against 0.77 ± 0.10 (control; n = 9)
nmol · cm2 · s1
(P < 0.01). With 106 M MCMV
alone, JK was 0.37 ± 0.04 against a control of
0.62 ± 0.06 (n = 19)
nmol · cm2 · s1
(P < 0.01). A peptide V2 antagonist had no such
effect. In Brattleboro rats, which do not produce endogenous AVP, MCMV
had no effect when given alone, although AVP still stimulated
JK. In conclusion, luminal AVP stimulates distal
JK significantly. The V1 antagonist MCMV inhibits the effect of AVP but also reduces JK
when given alone. This suggests that AVP acts luminally via
V1 receptors but also that there appears to be a background
effect of endogenous AVP blocked by the antagonist.
potassium; anti-V1; distal tubule; microperfusion
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