NeuropharmacologyEffect of central urotensin II on heart rate, blood pressure and brain Fos immunoreactivity in conscious rats
Section snippets
Experimental procedures
Twenty-three male Sprague–Dawley rats weighing 282±8 g were kept in temperature- (22 °C) and light-controlled conditions (12-h light/dark), with ad libitum access to standard rat chow and water. All rats were weighed daily. All experimental procedures were approved by the Animal Experimentation Ethics Committee of the Howard Florey Institute under guidelines laid down by the National Health and Medical Research Council of Australia in line with the international guidelines on the ethical use of
HR and SBP
There was no significant change in sBP measured either 0–30 min or 60–90 min after i.c.v. administration of UII (Fig. 1a). At 0–30 min after i.c.v. treatment HR did not differ significantly between UII and aCSF treatments (Fig. 1b), but by 60–90 min following i.c.v. UII there was a large increase in HR compared with the same time period after aCSF (P=0.003) (Fig. 1b).
Plasma corticosterone and plasma glucose
Plasma corticosterone levels were significantly higher at 90 min after i.c.v. UII compared with after i.c.v. aCSF (614±72 and
Discussion
In this study we demonstrated that i.c.v. administration of UII to conscious rats causes similar responses to those that we have seen in conscious sheep (Watson et al., 2003), including increased secretion of corticosteroids, tachycardia and hyperglycemia. In addition, we observed activation of several brain nuclei involved in corticosteroid release. Together with our previous studies, these findings suggest that UII acts on specific brain nuclei to stimulate the hypothalamo-pituitary–adrenal
Conclusion
In conclusion, this study has shown that i.c.v. UII increases plasma corticosterone and glucose levels as well as HR in conscious rats. Significantly greater Fos-IR was seen initially in the CeA then later in the PVN, suggesting that the amygdala plays an important role in mediating the actions of i.c.v. UII. No staining was seen in the A5 area or caudal raphe nuclei, suggesting that these areas are not associated with the UII-mediated epinephrine release via an increase in sympathetic outflow
Acknowledgments
The authors are grateful to Dr. B. J. Oldfield for assistance with image analysis and to Craig Thomson for his excellent technical assistance. Preliminary results of this work have been published in abstract form (Watson and May, 2004a).
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Present address: Baker Heart Research Institute, PO Box 6492, St. Kilda Road Central, Melbourne, Victoria 3010, Australia.