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Immunoreactivity for nitric oxide synthase and endothelin in the coronary and basilar arteries of renal hypertensive rats

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The ultrastructural localization of immunoreactivity to nitric oxide synthase (type-III and type-II) and endothelin-1 was examined by using pre-embedding peroxidase-antiperoxidase techniques in the coronary and cerebral basilar arteries in renal hypertensive rats. Renal hypertension was produced by excision of the right kidney and clipping of the left renal artery. Controls were normotensive sham-operated rats (right surgical nephrectomy; a clip inserted near the left renal artery). Both in controls and hypertensive rats, immunoreactivities for nitric oxide synthase-III and endothelin-1 were localized within subpopulations of endothelial cells. In addition, signs of translocation of nitric oxide synthase-III were noted from the cytoplasm to the Golgi complex in endothelial cells of the basilar artery of hypertensive animals. Neither controls nor hypertensive rats showed immunoreactivity for nitric oxide synthase-II. Preparations of the right coronary artery from hypertensive rats displayed fewer endothelial cells positive to nitric oxide synthase-III than in controls, although there were no significant changes in the distribution of endothelin-1-positive endothelial cells in the coronary artery of hypertensive rats. In contrast, the basilar artery from hypertensive rats displayed no changes in the percentage of endothelial cells immuno-positive either for nitric oxide synthase-III or for endothelin-1. In consequence, the ratio of nitric oxide synthase-III:endothelin-1 was reduced in the coronary but not in the basilar artery. Therefore, the nitric oxide/endothelin-1 system appears to play different roles in the coronary and cerebral circulations during renal hypertension.

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Received: 24 October 1996 / Accepted: 3 January 1997

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Shochina, M., Loesch, A., Rubino, A. et al. Immunoreactivity for nitric oxide synthase and endothelin in the coronary and basilar arteries of renal hypertensive rats. Cell Tissue Res 288, 509–516 (1997). https://doi.org/10.1007/s004410050836

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  • DOI: https://doi.org/10.1007/s004410050836

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