Increased Constrictor Tone Induced by Ouabain-Treatment in Rats.

*Biomedical Research Infrastructure Center, Winston-Salem State University, †Dept. of Obstetrics & Gynecology and ‡Hypertension Research & Vascular Center Wake Forest School of Medicine, Winston Salem, NC.
Journal of cardiovascular pharmacology (Impact Factor: 2.14). 04/2013; 62(2). DOI: 10.1097/FJC.0b013e3182955d33
Source: PubMed


Ouabain-induced hypertension in rodents provides a model to study cardiovascular changes associated with human hypertension. We examined vascular function in rats after long-term treatment with ouabain. Systolic blood pressure (SBP) was measured by tail-cuff plethysmography in male Sprague-Dawley rats treated with ouabain (Oua, ∼25 µg·day) or placebo for 8 weeks. Blood pressure increased in ouabain-treated animals, reaching 30% above baseline SBP after 7 weeks. At the end of treatment, vascular responses were studied in mesenteric resistance arteries (MRA) by wire myography. Contraction to potassium chloride (KCl) in intact and denuded arteries showed greater sensitivity in Oua-treated animals. Contraction to phenylephrine (PE) and relaxation to acetylcholine (ACh) were similar between groups with a lower response to sodium nitroprusside (SNP) in Oua-treated arteries. Sensitivity to endothelin-1 (ET-1) was higher in Oua-treated arteries. Na-K ATPase activity was decreased in MRA from Oua-treated animals, whereas protein expression of the Na-K-ATPase α2 isoform was increased in heart and unchanged in mesenteric artery. Pre-incubation with indomethacin (10M) or L-NAME (10M) abolished the differences in KCl response and Na-K ATPase activity. Changes in MRA are consistent with enhanced vascular smooth muscle cell reactivity, a contributor to the increased vascular tone observed in this model of hypertension.

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Available from: Victor M Pulgar, Jan 22, 2015
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    • "Nevertheless, the Na+/K+-ATPase α2 isoform is required for ouabain-induced hypertension because ouabain does not elevate arterial blood pressure in transgenic mice expressing the ouabain-resistant Na+/K+-ATPase α2 isoform [33]. In the mesenteric arteries in rats with ouabain-induced hypertension, the Na+/K+-ATPase α2 isoform was either increased [34] or unchanged [35]–[36]. In our rats, which were resistant to the pressor effects of ouabain, Na+/K+-ATPase α2 isoform mRNA was downregulated by 50% in the mesenteric arteries and by 66% in the aorta. "
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