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Articles in PresS, published online ahead of print July 11, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00454.2002
Submitted on May 30, 2002
Accepted on July 9, 2002
1 Department of Pharmacology and Therapeutics, Facultad de Medicina, Universidad Autonoma de Madrid, Madrid, Spain; Department of Physiological Sciences, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil
2 Department of Pharmacology and Therapeutics, Facultad de Medicina, Universidad Autonoma de Madrid, Madrid, Spain
3 Department of Pharmacology, Louisiania State University Health Sciences Center, New Orleans, Louisiana, USA
4 Department of Physiological Sciences, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil
* To whom correspondence should be addressed. E-mail: mariajesus.alonso{at}uam.es.
The involvement of nitric oxide (NO), prostaglandins and calcium-dependent potassium channel (KCa) activators on the negative modulation of phenylephrine-induced contractions was evaluated on isolated aorta (AO) and caudal (CAU) artery obtained from ouabain-treated rats for 5 weeks to induce hypertension. In ouabain-treated rats, the reactivity to phenylephrine was reduced in endothelium intact AO, but not CAU segments. Endothelial modulation of phenylephrine contraction, as demonstrated by endothelium removal, NO synthase (NOS) inhibition with L-NAME and aminoguanidine as well as KCa inhibition with tetraethylammonium, was more pronounced in segments from ouabain-treated animals and here greater effects were seen in AO than in CAU. An increased expression of eNOS and nNOS was seen in AO after ouabain treatment. In CAU, only eNOS was detected and ouabain treatment did not alter its expression. These results suggest that ouabain-induced hypertension is accompanied by increased NO release derived from eNOS and nNOS and increased release of an endothelial hyperpolarizing factor that presumably opens KCa, all of which contribute to the increased negative modulation of the phenylephrine contraction.
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