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Functional knockout of the soluble guanylate cyclase alpha 1 subunit leads to gender-specific hypertension while retaining sensitivity to nitric oxide
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Functional knockout of the soluble guanylate cyclase alpha 1 subunit leads to gender-specific hypertension while retaining sensitivity to nitric oxide
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Blood pressure in mice with a targeted deletion of the soluble guanylyl cyclase alpha 1 subunit
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Gender-specific modulation of baseline vascular function and the response to arterial injury by soluble guanylate cyclase
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Soluble guanylate cyclase deficiency selectively abolishes NO-mediated pulmonary vasodilation and increases the pulmonary vascular remodeling response to chronic hypoxia