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1 Department of Physiology, Tulane Hypertension and Renal Center of Excellence, and Tulane University Health Sciences Center, New Orleans, LA, USA
2 Departments of Medicine and Pharmacology, Houston VA Medical Center, and Baylor College of Medicine, Houston, TX, USA
* To whom correspondence should be addressed. E-mail: Fruzsi123{at}aol.com.
Vascular heme oxygenase (HO) metabolizes heme to form carbon monoxide (CO). CO inhibits nitric oxide (NO) synthase and promotes endothelium-dependent vasoconstriction. We reported HO-1-mediated endothelial dysfunction in Dahl salt-sensitive hypertension. Previous studies suggested that salt-sensitive hypertensive, but not spontaneously hypertensive rats (SHR) display endothelial dysfunction. This study examines the hypothesis that HO-1-mediated arteriolar endothelial dysfunction develops in deoxycorticosterone acetate (DOCA)-salt hypertensive rats, but not in SHR. Uninephrectomized (isoflurane anesthesia) male Sprague-Dawley rats received DOCA injections and saline drinking solution for 4 weeks. Sham surgery rats received vehicle injections and tap water. Blood pressure was elevated in DOCA and SHR rats compared to SHAM and Wistar-Kyoto (WKY) groups. Aortic HO-1 expression and blood carboxyhemoglobin levels were elevated in the DOCA group, but not in SHR. In isolated gracilis muscle arterioles, acetylcholine (ACh) caused concentration-related vasodilation in all groups with attenuated maximum responses in DOCA, but not in SHR arterioles. Acute pretreatment with an inhibitor of HO, chromium mesoporphyrin (CrMP), restored ACh-induced responses in DOCA arterioles to SHAM levels. ACh responses remained the same in SHR and WKY arterioles after CrMP treatment. These data show that HO-1 levels and activity are increased and arteriolar responses to ACh are decreased during DOCA-salt hypertension, but not in SHR. Furthermore, in DOCA-salt arterioles an inhibitor of HO restores ACh-induced vasodilation to SHAM levels. These results suggest that elevated HO-1 levels and activity, not resulting from hypertension per se, contribute to endothelial dysfunction in rats with DOCA-salt hypertension.
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