Vanderbilt University

Nancy J. Brown, M.D.

Richard N. Armstrong Ph.D.Robert H. Williams Professor of Medicine
Professor of Pharmacology
Associate Dean for Clinical and Translational Scientist Development
M.D., Harvard Medical School, 1986 (Medicine)

Many environmental toxins promote vascular disease by inducing oxidative stress and consequent endothelial dysfunction. Studies in Dr. Brown’s laboratory have contributed to the understanding of the effect of endothelial fibrinolytic and vasoactive function in hypertension and in the metabolic syndrome.  Her group has elucidated the contribution of endogenous bradykinin to many of the beneficial effects of ACE inhibitors on endothelial function. On the other hand, activation of the kallikrein-kinin system by environmental factors can have negative consequences. Dr. Brown and members of the faculty in pharmacoepidemiology were the first to report an increased risk of ACE inhibitor-associated angioedema among black Americans. Together with Drs. Morrow and Ikizler she is studying the contribution of the kallikrein-kinin system to induction of oxidative stress in patients with the metabolic syndrome and in individuals with kidney disease.

Recent Publications

Byrd JB, Shreevatsa A, Putlur P, Foretia D, McAlexander L, Sinha T, Does MD, Brown NJ. Dipeptidyl peptidase IV deficiency increases susceptibility to angiotensin-converting enzyme inhibitor-induced peritracheal edema. J Allergy Clin Immunol. 2007 120:403-8

Brown NJ, Bradford J, Wang Z, Lea W, Ma L, Ma J, Vaughan DE, Fogo AB. Modulation of angiotensin II and norepinephrine-induced plasminogen activator inhibitor-1 expression by AT1a receptor deficiency. Kidney Int. 2007 72:72-81.

Muldowney JA 3rd, Painter CA, Sanders-Bush E, Brown NJ, Vaughan DE. Acute tissue-type plasminogen activator release in human microvascular endothelial cells: the roles of Galphaq, PLC-beta, IP3 and 5,6-epoxyeicosatrienoic acid. Thromb Haemost. 2007 97:263-71.

Chamarthi B, Kolatkar NS, Hunt SC, Williams JS, Seely EW, Brown NJ, Murphey LJ, Jeunemaitre X, Williams GH. Urinary free cortisol: an intermediate phenotype and a potential genetic marker for a salt-resistant subset of essential hypertension. J Clin Endocrinol Metab. 2007 92:1340-6.

Gumieniak O, Perlstein TS, Williams JS, Hopkins PN, Brown NJ, Raby BA, Williams GH. Ala92 type 2 deiodinase allele increases risk for the development of hypertension. Hypertension. 2007 49:461-6.

LeFebvre J, Shintani A, Gebretsadik T, Petro JR, Murphey LJ, Brown NJ. Bradykinin B(2) receptor does not contribute to blood pressure lowering during AT(1) receptor blockade. J Pharmacol Exp Ther. 2007 320:1261-7.

Motsinger AA, Donahue BS, Brown NJ, Roden DM, Ritchie MD. Risk factor interactions and genetic effects associated with post-operative atrial fibrillation. Pac Symp Biocomput. 2006 584-95.

Byrd JB, Adam A, Brown NJ. Angiotensin-converting enzyme inhibitor-associated angioedema. Immunol Allergy Clin North Am. 2006 26:725-37. Review.

Luther JM, Gainer JV, Murphey LJ, Yu C, Vaughan DE, Morrow JD, Brown NJ. Angiotensin II induces interleukin-6 in humans through a mineralocorticoid receptor-dependent mechanism. Hypertension. 2006 48:1050-7.

Pojoga L, Kolatkar NS, Williams JS, Perlstein TS, Jeunemaitre X, Brown NJ, Hopkins PN, Raby BA, Williams GH. Beta-2 adrenergic receptor diplotype defines a subset of salt-sensitive hypertension. Hypertension. 2006 48:892-900.

Murphey LJ, Malave HA, Petro J, Biaggioni I, Byrne DW, Vaughan DE, Luther JM, Pretorius M, Brown NJ. Bradykinin and its metabolite bradykinin 1-5 inhibit thrombin-induced platelet aggregation in humans. J Pharmacol Exp Ther. 2006 318:1287-92.

Ma J, Weisberg A, Griffin JP, Vaughan DE, Fogo AB, Brown NJ. Plasminogen activator inhibitor-1 deficiency protects against aldosterone-induced glomerular injury. Kidney Int. 2006 69:1064-72.

Brown NJ. Blood pressure reduction and tissue-type plasminogen activator release. Hypertension. 2006 47:648-9. Review.

Brown NJ, Muldowney JA 3rd, Vaughan DE. Endogenous NO regulates plasminogen activator inhibitor-1 during angiotensin-converting enzyme inhibition. Hypertension. 2006 47:441-8.

Williams JS, Williams GH, Raji A, Jeunemaitre X, Brown NJ, Hopkins PN, Conlin PR. Prevalence of primary hyperaldosteronism in mild to moderate hypertension without hypokalaemia. J Hum Hypertens. 2006 20:129-36.