Angiogenesis- growth of capillaries from a pre-existing network- can be induced in cold-acclimated fishes, where torpor onset and increased oxygen availability, suggests that the primary stimulus for angiogenesis is not metabolic. It was hypothesised that cold-induced angiogenesis was due to increased blood viscosity, therefore endothelial mechanotransduction of high shear stress, and that warm-induced capillary rarefaction was due to reduced shear stress. The reversal of elevated shear stress by vasoconstriction using the nitric oxide synthase inhibitor, L-NNA, and cyclooxygenase inhibitor, indomethacin had different effects. L-NNA administration hinted towards capillary regression at low temperatures but there was a trend towards increased capillarity at intermediate and high temperatures, whereas indomethacin had no effect. Neither warm acclimation nor vasodilatation using the α-adrenoceptor antagonist, prazosin, had an effect on capillarity. Investigation of the effects of NO on heart rate at high temperature showed NO may reduce heart rate at high temperature. However, this does not explain the trend towards an increase in capillarity with L-NNA at high temperature. Evidence is presented for the absence of eNOS in fishes suggesting either nNOS-derived NO or prostanoids are responsible for vascular tone. Microarray analyses were used to identify signalling pathways that would explain the discrepancies, but proved inadequate to reveal significant endothelial responses to cold acclimation.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:547524 |
| Date | January 2011 |
| Creators | Syeda, Fahima |
| Publisher | University of Birmingham |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://etheses.bham.ac.uk//id/eprint/3221/ |
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