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Acta Physiologica Congress

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Acta Physiologica 2009; Volume 196, Supplement 671
Scandinavian Physiological Society’s Annual Meeting
8/14/2009-8/16/2009
Uppsala, Sweden


VASODILATION BY PERIVASCULAR ADIPOSE TISSUE: UNALTERED IN SHR
Abstract number: P6

LI1 R, ANDERSEN1 I, NILSSON1 H

1Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, P.O.Box 432, S-405 30 Gothenburg, Sweden. [email protected]

Perivascular adipose tissue (PVAT) produces a variety of vasoactive substances and plays an essential role in regulating vascular function. Hypertension has been considered to result from changes of blood vessel properties and function of PVAT. A recent study has revealed a diminished anticontractile function of PVAT in hypertensive mesenteric artery rings compared with control (Gálvez et al. 2006). Here we used a different method and tested vaso-regulating effects of PVAT from spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) controls on hypertensive and normotensive vessels. In each experiment two small mesenteric arteries were isolated from SHR and two from WKY control and mounted in a Mulvany-Halpern myograph to measure their tension. PVAT was longitudinally removed from different vessels during dissection and saved for further use. Noradrenaline sensitivity was first determined directly on two types of vessels. PVAT was then carefully applied around arteries to investigate its effect on vascular function. Noradrenaline sensitivity was determined again and compared with the first one. We found that PVAT, regardless of which animal model it was taken from, has a dilator effect on WKY vessels (fat from WKY D(log EC50) 0.41±0.11, n=5; SHR D(log EC50) 0.33±0.09, n=5). In contrast with the previous results, a significant effect of PVAT was also observed on SHR vessels (fat from WKY D(log EC50) 0.28±0.08, n=5; SHR D(log EC50) 0.41±0.08, n=5). Our results suggest that the vasodilation function of PVAT is unaltered in SHR and hypertensive vessel preserves its ability of being regulated by PVAT. Further investigation is needed to explain the differences between two studies. Gálvez B, de Castro J, Herold D, Dubrovska G, Arribas S, González MC, et al. Arterioscler Thromb Vasc Biol. 2006;26(6):1297–302.

To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 196, Supplement 671 :P6

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