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1 Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, USA
2 Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, USA; Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota, USA
3 Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA
4 Pediatrics and Adolescent Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, USA; Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, Minnesota, Algeria
5 Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota, USA
6 Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, USA; Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, Minnesota, Algeria
* To whom correspondence should be addressed. E-mail: rkumar{at}mayo.edu.
IEX 1/gly96 is a growth and apoptosis-regulating, immediate early gene that is widely expressed in epithelial and vascular tissues. In vascular tissues, expression of the gene is induced by mechanical stretch, and over-expression of the gene prevents injury-induced vascular smooth muscle hypertrophy and neointimal hyperplasia. We now show that deletion of the gly96/IEX-1 gene in mice is associated with development of elevated blood pressure, cardiac hypertrophy and diminished fractional shortening of the left ventricle. Systolic blood pressure in conscious male gly96/IEX-1-/- mice is 20-25 mm Hg higher than in gly96/IEX-1+/+ mice. Serum and/or urine concentrations of sodium, potassium, creatinine, angiotensin II, corticosterone, aldosterone, epinephrine, nor-epinephrine, prostaglandin E2, thromboxane B2, prostaglandin 6 keto 1
, nitrites and nitrates, cyclic AMP and cyclic GMP are normal in gly96/IEX-1-/- mice. Alterations in dietary sodium intake do not alter blood pressure in gly96/IEX-1-/- mice. Aortic messenger RNAs for endothelial nitric oxide synthase, guanylate cyclase and cyclic GMP kinase 1 are increased in gly96/IEX-1-/- mice. Treatment with L-NAME or L-arginine does not alter blood pressure in gly96/IEX-1-/- mice. Gly96/IEX-1-/- mice respond to infused sodium nitroprusside with decrements in blood pressure similar to those seen in wild type littermate mice. In contrast to gly96/IEX-1 transgenic mice that have abnormalities in immune function, gly96/IEX-1-/- mice have normal lymphoid tissue architecture and a normal complement of T- and B-cells in lymphoid tissues. Ablation of the gly96/IEX-1 gene results in hypertension and cardiac hypertrophy suggesting a novel role for this gene in cardiovascular physiology.
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