Ade Adebiyi, PhD

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Assistant Professor
Phone: 901-448-1868
Fax: 901-448-7126
Full CV


2004 PhD: National University of Singapore, Singapore

Research Interest

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Our current research focuses primarily on the physiology and pathophysiology of renal hemodynamics. We utilize an integrative approach, including techniques drawn from cell and molecular biology, physiology, and pharmacology to investigate regulatory proteins, ion channels, and GPCRs that control renal vascular and glomerular functions. Current projects in the lab include:

  1. Control of renal microcirculation in adults and neonates.
  2. Mechanisms of altered microvascular function in acute kidney injury.
  3. Ca2+ signaling in glomerular mesangial cells.

Research Support


  • 07/01/2014 – 06/30/2019: R01DK101668, "Regulation of neonatal renal hemodynamics"
    Principal Investigator: Adebowale Adebiyi.
    Agency: National Institutes of Health (NIDDK)


  • 04/15/2009 – 03/31/2014: K01HL096411, "Vasoregulation by IP3 receptor coupling to TRPC channels"
    Principal Investigator: Adebowale Adebiyi
    Agency: National Institutes of Health (NHLBI)
  • 07/01/2006 - 06/30/2008: Postdoctoral Research Fellowship, "Regulation of the cerebral artery myogenic response by caveolin-1"
    Principal Investigator: Adebowale Adebiyi
    Agency: American Heart Association

Selected Publications

  1. Soni H, Buddington RK, ADEBIYI A. Postnatal kidney maturation regulates renal artery myogenic constriction. Journal of Perinatal Medicine 2014 (In press).
  2. ADEBIYI A, Soni H, John TA, Yang F. Lipid rafts are required for signal transduction by angiotensin II receptor type 1 in neonatal glomerular mesangial cells. Experimental Cell Research 2014; 324:92-104.
  3. ADEBIYI A. RGS2 regulates urotensin II-induced intracellular Ca2+ elevation and contraction in glomerular mesangial cells. Journal of Cellular Physiology 2014; 229:502-511.
  4. Soni H, ADEBIYI A. Pressor and renal regional hemodynamic effects of urotensin II in neonatal pigs. Journal of Endocrinology 2013; 217:317-26.
  5. ADEBIYI A, Thomas-Gatewood CM, Leo MD, Kidd MW, Neeb ZP, Jaggar JH. An elevation in physical coupling of type 1 inositol 1,4,5-trisphosphate (IP3) receptors to transient receptor potential 3 (TRPC3) channels constricts mesenteric arteries in genetic hypertension. Hypertension 2012; 60:1213-9.
  6. ADEBIYI A, McNally EM, Jaggar JH. Vasodilation induced by oxygen/glucose deprivation is attenuated in cerebral arteries of SUR2 null mice. American Journal of Physiology. Heart and Circulatory Physiology 2011; 301:H1360-8.
  7. ADEBIYI A, Narayanan D, Jaggar JH. Caveolin-1 assembles type 1 inositol 1,4,5-trisphosphate receptors and canonical transient receptor potential 3 channels into a functional signaling complex in arterial smooth muscle cells. Journal of Biological Chemistry 2011; 286:4341-8. ** Science Signaling Editor's Choice:  Gough NR. Coupled by Caveolin. Science Signaling 2011;4: ec50. **Featured paper: North American Vascular Biology Organization Publications Alert, March 2011.
  8. ADEBIYI A, Zhao G, Narayanan D, Thomas-Gatewood CM, Bannister JP, Jaggar JH.  Isoform-selective physical coupling of TRPC3 channels to IP3 receptors in smooth muscle cells regulates arterial contractility. Circulation Research 2010; 106:1603-12.
  9. ADEBIYI A, McNally EM, Jaggar JH. Sulfonylurea receptor-dependent and -independent pathways for KATP channel opener-mediated vasodilation. Molecular Pharmacology 2008; 74:736-43.
  10. 10.ADEBIYI A, Zhao G, Cheranov SY, Ahmed A, Jaggar JH. Caveolin-1 abolishment attenuates the myogenic response in murine cerebral arteries. American Journal of Physiology. Heart and Circulatory Physiology 2007; 292:H1584-92.