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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia


PRELIMINARY DATA ON THE INFLUENCE OF RESTING TENSION UPON ENDOTHELIUM-DEPENDENT RELAXATION
Abstract number: PF18-151

Serban1,2 I.L., Oprisa1,2 C., Tucaliuc1 S.E., Branisteanu3 D.D., Serban1,2 D.N.

1Department of Physiology
2Center for the Study and Therapy of Pain
3Clinic of Endocrinology, University of Medicine and Pharmacy Grigore T. Popa, Iasi, Romania [email protected]

Aims: 

Endothelium-dependent relaxation (EDR) differs upon species, age, sex, hormonal status, vascular territory and caliber, vasodilating agent, pre-existing tone. There are few studies regarding the effect of tone, so we investigated the effect of resting tension upon the EDHF response.

Methods: 

We used isometric myography and mesenteric resistance arteries (2 mm rings; ~0.15 mm diameter) from male Wistar rats (200-250 g). After 2 h equilibration under a tension of 1 g or 2 g, the ring was precontracted by 0.01 mM phenylephrine and we tested EDR induced by 0.01 mM carbachol or the EDHF component of EDR (in presence of 0.01 mM L-NAME and 0.01 mM indomethacin). Results are expressed as residual active tension (RAT), % of precontraction level (mean ± SEM; n = 4).

Results: 

The chosen preparation does not display a myogenic response to stretch and carbachol does not decrease baseline tension. Contraction is ~25% stronger in rings pretensioned at 2 g, EDR is complete for both pretension levels, while the EDHF component is more ample (p < 0.01; Student's t-test) at 2 g (45.4 ± 3.1% RAT), vs. 1 g (62.7 ± 2.8% RAT).

Conclusion: 

The antagonism between myogenic response and the EDHF phenomenon is well known, but our novel observations indicate that the release/action of EDHF is potentiated by a simple increase of parietal tension, which may be of functional relevance in both acute and chronic increases of arterial pressure.

*CNCSIS grant A/1222 **CNCSIS grant interdisciplinary platform /68

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :PF18-151

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