Article date: December 1991
By: Daniel Henrion, Jean‐Marc Chillon, Christine Capdeville‐Atkinson, Marion Vinceneux‐Feugier, Jeffrey Atkinson, in Volume 104, Issue 4, pages 966-972
Treatment of young rats with vitamin D3 plus nicotine produced 31 and 4 fold increases in the calcium content of the aorta and the mesenteric arterial bed, respectively.
Aortic rings and perfused mesenteric arterial beds from vitamin D3/nicotine‐treated animals showed a diminished contractile response to noradrenaline in vitro.
In vascular preparations from vitamin D3/nicotine‐treated animals, precontracted with noradrenaline, relaxation by the endothelium‐dependent vasodilator, carbachol, was attenuated but responses to sodium nitroprusside were not modified.
Prolonged treatment with the angiotensin I converting enzyme inhibitor, perindopril, at a dose (1 mg kg−1) which did not significantly modify blood pressure, failed to prevent vascular calcium overload.
Perindopril treatment diminished noradrenaline‐evoked vasoconstrictor responses of aortic rings in both groups, but restored responses in mesenteric arterial beds of vitamin D3/nicotine‐treated rats.
Perindopril treatment also restored the maximal responses to carbachol of both aortic rings and mesenteric arterial beds of vitamin D3/nicotine‐treated rats.
In conclusion, in the vitamin D3 plus nicotine model of calcium overload, reduced endothelial‐mediated relaxation can be prevented by perindopril treatment.
Treatment of young rats with vitamin D3 plus nicotine produced 31 and 4 fold increases in the calcium content of the aorta and the mesenteric arterial bed, respectively.
Aortic rings and perfused mesenteric arterial beds from vitamin D3/nicotine‐treated animals showed a diminished contractile response to noradrenaline in vitro.
In vascular preparations from vitamin D3/nicotine‐treated animals, precontracted with noradrenaline, relaxation by the endothelium‐dependent vasodilator, carbachol, was attenuated but responses to sodium nitroprusside were not modified.
Prolonged treatment with the angiotensin I converting enzyme inhibitor, perindopril, at a dose (1 mg kg−1) which did not significantly modify blood pressure, failed to prevent vascular calcium overload.
Perindopril treatment diminished noradrenaline‐evoked vasoconstrictor responses of aortic rings in both groups, but restored responses in mesenteric arterial beds of vitamin D3/nicotine‐treated rats.
Perindopril treatment also restored the maximal responses to carbachol of both aortic rings and mesenteric arterial beds of vitamin D3/nicotine‐treated rats.
In conclusion, in the vitamin D3 plus nicotine model of calcium overload, reduced endothelial‐mediated relaxation can be prevented by perindopril treatment.
DOI: 10.1111/j.1476-5381.1991.tb12534.x
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