Cardiovascular and gill microcirculatory effects of endothelin-1 in atlantic cod: evidence for pillar cell contraction

• Published in: Journal of experimental biology Vol. 202 (Pt 9); no. 9; pp. 1151 - 1157
• Main Authors: Stenslokken, KO, Sundin, L, Nilsson, GE
• Format: Journal Article
• Language: English
• Published: England 01.05.1999
• ISSN: 0022-0949; 1477-9145
• DOI: 10.1242/jeb.202.9.1151

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.