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Cardiovascular Research 1997 33(1):188-195; doi:10.1016/S0008-6363(96)00197-6
© 1997 by European Society of Cardiology
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Copyright © 1997, European Society of Cardiology

Ramipril therapy improves arterial dilation in experimental hypertension

Nina Hutri-Kähönena,b, Mika Kähönena,c,*, Jari-Petteri Tolvanena, Wu Xiumina, Kirsimarja Sallinena and Ilkka Pörstia,d

aMedical School, University of Tampere, PO Box 607, FIN-33101 Tampere, Finland
bDepartment of Clinical Chemistry, Tampere University Hospital, PO Box 2000, FIN-33521 Tampere, Finland
cDepartment of Clinical Physiology, Tampere University Hospital, PO Box 2000, FIN-33521 Tampere, Finland
dDepartment of Internal Medicine, Tampere University Hospital, PO Box 2000, FIN-33521 Tampere, Finland

Objective: Angiotensin-converting enzyme (ACE) inhibition has been shown to restore impaired endothelial function in hypertension, but the roles of different mediators in enhanced endothelium-dependent dilation have not been fully characterized. Methods: The effects of ACE inhibition with ramipril (1 mg · kg–1 · day–1) on relaxation responses of mesenteric arterial rings in vitro were studied in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Results: The 12-week-long therapy effectively reduced blood pressure in SHR. In noradrenaline (NA)-precontracted arterial rings, endothelium-dependent relaxations to acetylcholine (ACh) as well as endothelium-independent dilations to isoprenaline and nitroprusside were more pronounced in WKY and ramipril-treated SHR than in untreated SHR. The cyclo-oxygenase inhibitor, diclofenac, which reduces the synthesis of dilating and constricting prostanoids, clearly enhanced the relaxation to ACh in untreated SHR, but was without effect in the other groups. The nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), attenuated the relaxations to ACh more effectively in untreated SHR than in the ramipril-SHR and WKY groups. However, when endothelium-dependent hyperpolarization was prevented by precontracting the preparations with potassium chloride (KCl), no significant differences were found in relaxations to ACh between the study groups. In addition, in NA-precontracted rings the diclofenac- and L-NAME-resistant relaxations to ACh were partially prevented by glibenclamide and apamin, inhibitors of ATP-dependent and Ca2+-activated K+ channels, respectively. Conclusion: Long-term ACE inhibition normalized blood pressure and enhanced arterial dilation in SHR. The improved endothelium-mediated relaxation following ramipril therapy could be attributed to reduced release of cyclo-oxygenase-derived constricting factors and augmented endothelium-dependent hyperpolarization in this type of experimental hypertension.

KEYWORDS ACE inhibitors; Rat, arteries; L-NAME; Blood pressure; Endothelium; Rat, spontaneously hypertensive

* Corresponding author. Tel. +358 3 2156111; Fax +358 3 2156170.


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