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Acta Physiologica Congress

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Acta Physiologica 2009; Volume 197, Supplement 672
The 60th National Congress of the Italian Physiological Society
9/23/2009-9/25/2009
Siena, Italy


REM SLEEP ENTAILS ARTERIAL HYPERTENSION IN HYPOCRETIN-ATAXIN3 NARCOLEPTIC MICE
Abstract number: P12

BASTIANINI1 S, BERTEOTTI1 C, ELGHOZI2 JL, LENZI1 P, LO MARTIRE1 V, FRANZINI1 C, SILVANI1 A, MIGNOT3 E, ZOCCOLI1 G

1Dipartimento di Fisiologia Umana e Generale, Univ.di Bologna; (Italy)
2Hopital Necker, Universit Descartes, Paris, (France)
3Center For Narcolepsy, Stanford University, (USA)[email protected]

Aim: 

Hypothalamic neurons releasing hypocretin (HCRT) neuropeptides are involved in sleep regulation, and their loss leads to narcolepsy. Acute HCRT injection reportedly elicits hypertension and tachycardia. Aim of this study is to investigate the role of HCRT in cardiovascular regulation during sleep, a condition characterized by wide changes in physiological functions.

Methods: 

Six narcoleptic mice with genetic ablation of HCRT neurons (HCRT-ataxin3 transgenic mice, TG) and 6 wild-type (WT) control mice were implanted with a telemetric blood pressure transducer (TA11PA-C10, DSI) and electrodes for discriminating wake-sleep states. Ten days later, recordings were performed for 3 days with the mice undisturbed and freely moving. Mean blood pressure (MBP) values were computed during wakefulness (W), rapid-eye-movement sleep (REMS), and non-REMS (NREMS) in the light and dark periods and analyzed with 3-way analysis of variance and t-test (significance at p<0.05).

Results: 

showed that in W and NREMS, MBP did not differ significantly between TG and WT mice either in the light or dark period. In REMS, MBP was significantly higher in TG than in WT mice both in the light (difference 7 ± 3 mmHg) and the dark (difference 13 ± 3 mmHg) period.

Conclusions: 

These results indicate that REMS entails arterial hypertension in narcoleptic mice especially during the dark period. Data suggest that chronic cardiovascular effects of HCRT may be different form acute ones.

To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 197, Supplement 672 :P12

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