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Forced-swim induces subsensitivity to phenylephrine in the rat thoracic aorta

Stress may change vascular function. The aim of this report was to study the sensitivity to phenylephrine (PHE) in the thoracic aorta from rats submitted to forced-swim. Male Wistar rats (200-250 g) were submitted to three swimming sessions, one session/day (15, 30 and 30 min, respectively). Immediately after the last swimming session, the animals were sacrificed and thoracic aorta was isolated. Aortic rings (3-5 mm), with and without endothelium, were carefully obtained and were main-tained in Krebs-Henseleit solution (95% O2- 5% CO2, 37 ºC). Endothelial integrity was assessed by relaxation to acetylcholine (10 µM) in pre-contracted rings (PHE 0.1 µM). Concentration-effect curves to PHE were obtained (n = 5/group). There was no difference between control and stress groups in the maximum response to PHE of aortic rings with and without endothelium (p>0.05). Forced-swim induced subsensitivity to PHE in aortic rings with endothelium isolated from stressed rats (pD2 = 6.89 ± 0.07; p<0.05) compared to the control group (pD2 = 7.39 ± 0.06), without changes in aortic rings without endothelium. The in vitro inhibition of nitric oxide synthesis cancelled this subsensitivity. It is concluded that forced swim-induced-subsensitivity to PHE in thoracic aorta from rats seems to be caused by an increase in the activity of the endothelial nitric oxide system.

Stress; Phenylephrine; Subsensitivity; Aorta; Endothelium; Swimming


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