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1 Department of Neuroscience, "Federico I" University Medical School, Naples, Italy
2 Department of Physiology and Biochemistry, University of Pisa, Pisa, Italy
3 Clinical Physiology, CNR, Pisa, Italy
* To whom correspondence should be addressed. E-mail: colantuo{at}unina.it.
Background The aim of the present study was to assess the effects of topically applied triiodothyronine (T3) and thyroxine (T4) on the arterioles of hamster cheek pouch microcirculation in-vivo. Methods and Results Microvessels were visualized using a fluorescent microscopy technique. Topical application of T3 (3.08, 30.8, 61.5, 307, 615, 6150 nM/l) consistently induced dose-dependent dilation of arterioles within 2.0 ± 0.5 min of administration. The application of T4 (150, 257, 514, 5140 nM/l) caused different dose-dependent effects: dilation at the three lower doses within 16 ± 2 min and rhythmic diameter changes at the highest dose. Aging of hamsters did not alter the arteriolar responses to T3 and T4. T3-induced dilation was countered by the inhibition of nitric oxide synthase with NG-nitro-L-arginine-methyl ester (L-NAME) or NG-nitro-L-arginine (L-NNA). Iopanoic acid (IPA), which inhibits types I and II 5'-deiodinase, abolished the dilation elicited by 514 nM T4 but did not affect T3-dependent dilation. 6-propyl-2-thiouracil (PTU), which inhibits type I 5'-deiodinase only, did not affect the dilation induced by T4. IPA and PTU did not impair arteriolar dilation induced by acetylcholine or sodium nitroprusside. Conclusions These results indicate that T3 induces arteriolar dilation, likely through nitric oxide release. The local conversion of T4 to T3 appears to be crucial for the dilation induced by T4.
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