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Abstract

In a previous work, we demonstrated that vascular smooth muscle modifies endothelium-independent relaxations in spontaneously hypertensive rats (SHR) by releasing cyclooxygenase-derived contracting factors. On the other hand, angiotensin II (ANG-II) is involved in the production of cyclooxygenase-derived vasoconstrictors. We hypothesized that AT1 receptor antagonism with irbesartan could ameliorate vascular relaxations to SNP by decreasing the ANG-II-dependent production of cyclooxygenase-dependent contracting factors in smooth muscle cells. Twenty female SHR (aged 14 weeks) were used for the study. Half of the SHR were treated for 30 consecutive weeks with 50 mg/kg/day irbesartan administered with the chow. At the end of the treatment period, vascular reactivity of aortic rings was studied. Chronic treatment with the ANG-II AT1 receptor antagonist, irbesartan, significantly increased the relaxation response to SNP in aortic rings from SHR. Furthermore, the modification of the SNP-induced relaxations appears to be related to a lower production of cyclooxygenase-dependent contracting factors. Firstly, incubation of aortic rings from irbesartan-treated SHR with indomethacin did not significantly alter the relaxations in response to cumulative doses of SNP. Secondly, the dose-response curve to SNP for aortic rings from irbesartan-treated SHR was comparable to that obtained in aortic rings from non-treated SHR incubated in the presence of indomethacin. In conclusion, increased relaxation in response to the nitric oxide donor SNP in aortic rings from irbesartan-treated SHR could be related to a lower ANG-II-dependent production of cyclooxygenase-dependent contracting factors in smooth muscle cells. Further experiments are needed to validate these observations, but our findings open a new line of investigation into the mechanisms involved in improving vascular function with antihypertensive treatment.

Irbesartan, Angio tensin II, Indomethacin
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© American Journal of Hypertension, Ltd. 2001
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