Cardiovascular and gill microcirculatory effects of endothelin-1 in atlantic cod: evidence for pillar cell contraction
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.
Stenslokken
KO
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.
Sundin
L
Nilsson
GE