Vasoactivity of the coronary artery of rainbow trout, steelhead trout, and dogfish: lack of support for non-prostanoid endothelium-derived relaxation factors

Abstract

This study surveyed and compared vasoactive responses of isolated coronary vessels from steelhead trout (Oncorhynchus mykiss), rainbow trout (also O. mykiss), and spiny dogfish (Squalus acanthias). The purpose of the investigation was twofold: to identify vasoactive controls that were possibly mediated by the vascular endothelium and to highlight the possible consequences on vasoactivity of the coronary lesions known to be present in the main coronary of salmonids but not dogfish. The test substances included acetylcholine, adenosine, adenosine triphosphate, adenosine diphosphate, serotonin, thrombin, bradykinin, prostaglandin F2α, prostaglandin I2, prostaglandin E2, and the fatty acids arachidonic acid, docosahexaenoic acid, and eicosapentaenoic acid. Acetylcholine, adenosine, adenosine triphosphate, adenosine diphosphate and prostaglandin F2α typically produced contractions. Use of endothelial removal techniques and antagonists failed to reveal any relaxations that might involve the endothelium. Thrombin and bradykinin had no vasoactivity. Serotonin, prostaglandin I2, and prostaglandin E2 produced relaxations that were not mediated by the endothelium. The powerful relaxations observed with prostaglandin I2 and prostaglandin E2 and the powerful contractions observed with prostaglandin F2α suggest a major role of prostanoids in coronary vasoactivity in fish. These prostanoid-mediated mechanisms, in addition to the previously demonstrated powerful contractions with endothelin-1, point to an important role for the endothelium. No major qualitative or quantitative differences in vasoactivity could be related to differences in coronary lesion severity.

Structural basis for control of secondary vessels in the long-finned eel Anguilla reinhardtii

“…Kågström et al (1996) examined the in vivo effects in O. mykiss of trout SP (tSP), which has three amino acid substitutions compared with mammalian SP (Jensen and Conlon, 1992), and found that it caused a significant increase in both systemic and coeliac resistance. In contrast to the effects of mammalian SP on coronary arteries (Farrell and Johnson, 1995), tSP had no vasodilator effect on relaxed or precontracted small gut arteries (Kågström and Holmgren, 1998). Based on this limited data set, it is difficult to interpret the presence of SP-like immunoreactivity or the signalling pathways involved in segmental and secondary vessels in A. reinhardtii.…”

“…In the coronary circulation of O. mykiss, 5-HT produces a dose-dependant vasodilatation, an effect that could be abolished by the addition of L-NA (N ω -nitro-L-arginine), a nitric oxide synthase (NOS) inhibitor (Mustafa et al, 1997). In contrast, Farrell and Johnson (1995) reported that although 5-HT induced vasodilatation in isolated coronary ring preparations from O. mykiss, this effect was endothelium independent. In addition, a number of studies have addressed the physiological effects of 5-HT in vivo.…”

Nitric oxide control of the dorsal aorta and the intestinal vein of the Australian short-finned eel Anguilla australis

“…These studies have proposed that prostaglandins released from the endothelium are responsible for mediating vasodilation (Olson and Villa, 1991;Sverdrup et al, 1994;Farrell and Johansen, 1995;Kågström and Holmgren, 1997;Miller and Vanhoutte, 2000;Park et al, 2000). However, the presence of an endothelial NO system in fish vasculature remains controversial because it has been reported that some vascular beds are dilated by NO purportedly released by the , and in the absence of an intact endothelium (C).…”

Cold-acclimation leads to differential regulation of the steelhead trout (Oncorhynchus mykiss) coronary microcirculation

“…Here, we demonstrate the feasibility/utility of microvessel techniques for fish research and show that the response of these vessels to several important vasoactive agents is concentration and temperature dependent. Interestingly, these responses often differ considerably from those observed in larger (conduit) vessels (i.e., coronary artery) (26,92,93) or in the whole coronary circulation (1,69,70).…”