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Journal of Experimental Biology, Vol 202, Issue 9 1151-1157, Copyright © 1999 by Company of Biologists
JOURNAL ARTICLES |
KO Stenslokken, L Sundin and GE Nilsson
Division of General Physiology, Department of Biology, University of Oslo, PO Box 1051, N-0316 Oslo, Norway and Department of Zoophysiology, University of Goteborg, S-413 90 Goteborg, Sweden. Goran.Nilsson@bio.uio.no.
Endothelin-1 (ET-1) has been shown to cause a considerable increase in the vascular resistance of fish gills. In trout, recent evidence suggest that this is the result of pillar cell contraction in the gill lamellae. Using epi-illumination microscopy to observe the gill lamellae of anaesthetised Atlantic cod (Gadus morhua), we show that ET-1 (100 ng kg-1, injected into the ventral aorta) causes an increase in pillar cell diameter, consistent with pillar cell contraction, and a shift of intralamellar blood flow from the lamellar sheet to the outer marginal channels. Simultaneously, there was an increase in ventral aortic blood pressure, a reduction in cardiac output, an increase in gill vascular resistance and a reduction in the oxygen partial pressure of venous blood. All these effects were blocked by the ETA/ETB receptor antagonist bosentan (5 mg kg-1). Pillar cell contraction is likely to be a mechanism for matching the functional respiratory surface area with the instantaneous respiratory needs of the fish.
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