Vectorial efflux of cgmp and its dependence on sodium in the cortical collecting duct.. Stoos, Barbara A., and Jeffrey L. Garvin. Department of Hypertension and Vascular Research, Henry Ford Hospital, Detroit, MI 48202
APStracts 3:0247R, 1996.
Guanosine 3'5' cyclic monophosphate (cGMP) is an important second messenger which regulates transport in the nephron. We propose that the transport mechanisms which remove cGMP from the cell are different in the luminal and basolateral membranes of the cortical collecting duct (CCD). We examined efflux of cGMP from cultured and isolated perfused CCDs in response to atrial natriuretic factor (ANF) and nitric oxide (NO). In the presence of phosphodiesterase inhibition, these compounds resulted in preferential efflux of cGMP across the basolateral membrane in both cultured and isolated CCDs. In the presence of ANF, efflux was five times higher across the basolateral than the luminal membrane in cultured CCD cells (n = 14). In isolated CCDs, efflux across the basolateral and luminal membranes were 1.02 +/- 0.2 and 0.03 +/- 0.01 fmol/mm.min in the presence of ANF (n = 6; p &LT 0.007); and 0.87 +/- 0.21 and 0.02 +/- 0.01 fmol/mm.min in the presence of NO (n = 6; p &LT 0.011), respectively. Efflux across the basolateral membrane in the presence and absence of sodium was 37 +/- 7.3 vs 19.9 +/- 5 fmol/cm2.min, respectively, in cultured cells (n = 12; p &LT 0.044); and 1.02 +/- 0.2 (n = 6) vs. 0.41 +/- 0.12 (n = 5) fmol/mm.min in isolated perfused tubules (p &LT 0.042). There was no difference in luminal transport in the presence and absence of sodium in either model. We conclude that there are at least two different mechanisms involved in the removal of cGMP from the cell, one sodium-dependent and the other sodium-independent. The basolateral membrane appears to contain both, whereas the luminal membrane contains only the sodium-independent mechanism.

Received 13 January 1996; accepted in final form 12 June 1996.
APS Manuscript Number R62-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 July 96