gms | German Medical Science

27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Liga zur Bekämpfung des hohen Blutdrucks – Deutsche Hypertonie Gesellschaft e. V.

26. bis 29.11.2003, Bonn

Impaired expression of endothelial KCa-channels and EDHF-mediated vasodilations in experimental CRF

Vermindert Expression endothelialer KCa-Kanäle und EDHF-mediierter Vasodilatation bei experimenteller chronischer Niereninsuffizienz

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker I. Eichler - Charite Campus Benjamin Franklin (Berlin, D)
  • H. Schönfelder - Charite Campus Benjamin Franklin (Berlin, D)
  • S. Brakemeier - Charite Campus Benjamin Franklin (Berlin, D)
  • A. Knorr - Charite Campus Benjamin Franklin (Berlin, D)
  • I. Grgic - Charite Campus Benjamin Franklin (Berlin, D)
  • R. Köhler - Charite Campus Benjamin Franklin (Berlin, D)
  • J. Hoyer - Charite Campus Benjamin Franklin (Berlin, D)

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochV34

The electronic version of this article is the complete one and can be found online at:

Published: November 11, 2004

© 2004 Eichler et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.




Chronic renal failure (CRF) is associated with increased cardiovascular morbidity, abnormal arterial tone, and endothelial dysfunction. Small and intermediate-conductance Ca2+-activated K+-channels (KCa) are important regulators of endothelial function by mediating endothelial hyperpolarization which is prerequisite for endothelium-derived hyperpolarizing factor (EDHF)-meditated vasodilations. In the present study we tested the hypothesis whether an altered function of endothelial KCa and diminished EDHF-meditated vasodilation contribute to endothelial dysfunction in experimental CRF.


Endothelial KCa-currents and endothelium-dependent vasodilations in rat carotid arteries (CA) from SD rats were assessed by use of the patch-clamp technique and a pressure-myograph 8 weeks after either subtotal 5/6 nephrectomy (n=6) or sham operation (n=5).


In isolated EC, KCa-currents induced by cell dialysis with Ca2+ were significantly reduced in nephrectomized rats (18 pA ± 2 SE at Vhold of 0 mV, n=42) compared to sham-operated controls (40 pA ± 6 SE; P<0.0001, n=29). In phenylephrine-preconstricted CA, acetylcholine (ACh)-induced NO and prostacyclin-independent vasodilations were present in sham-operated rats (10 ± 1 % at 1 mM ACh), but almost absent in 5/6 Nx rats (2 ± 2%, P<0.05). 1-EBIO (100 mM), a selective opener of endothelial small and intermediate KCa induced vasodilation of 15 ± 4% in sham-operated rats, but was ineffective in 5/6 Nx-rats. In experiments without blocking NO and prostacyclin synthesis, endothelium-dependent vasodilation to ACh was significantly reduced by ~15 % in 5/6 Nx-rats.


Experimental CRF leads to a loss of EDHF-type vasodilation which is caused at least in part by an impaired functional expression of endothelial hyperpolarizing KCa. The loss of EDHF-type vasodilation may contribute to endothelial dysfunction and abnormal arterial tone in CRF.