Education

Research Interest

The contraction of smooth muscle cells regulates many physiological processes, including blood pressure, parturition, gastrointestinal motility, and airway responsiveness. Alterations in smooth muscle contractility are involved in the pathophysiology of several conditions, including hypertension, stroke, pre-term labor, erectile dysfunction, urinary incontinence, and asthma.  However, smooth muscle contractility is regulated by numerous signal transduction molecules that are to a large extent, poorly understood.  We utilize a combination of molecular, physiological, and pharmacological tools, including RT-PCR, gene suppression, tension and pressure myography, calcium imaging, patch-clamp electrophysiology, and animal models to investigate signaling pathways that regulate smooth muscle contraction and their roles in disease pathophysiology.  We anticipate that our research will not only expand the current knowledge of signaling events that modulate smooth muscle contractility, it will ultimately provide potential therapeutic targets for the control of smooth muscle reactivity.

Research Support

NIH K01 HL096411, 2009-2014
"Vasoregulation by IP3 Receptor Coupling to TRPC Channels"
Role: Principal Investigator

Selected Publications

1. Bannister JP, Adebiyi A, Zhao G, Narayanan D, Thomas CM, Feng JY, Jaggar JH. Smooth muscle cell {alpha}₂{delta}-1 subunits are essential for vasoregulation by Ca_V1.2 channels. Circulation Research 2009; 105(10):948-55.
   
2. Zhao G, Adebiyi A, Blaskova E, Xi Q, Jaggar JH. Type 1 inositol 1,4,5-trisphosphate receptors mediate UTP-induced cation currents, Ca2+ signals, and vasoconstriction in cerebral arteries. American Journal of Physiology. Cell Physiology 2008; 295:C1376-84.
3. Adebiyi A, McNally EM, Jaggar JH. Sulfonylurea receptor-dependent and -independent pathways for KATP channel opener-mediated vasodilation Molecular Pharmacology 2008; 74(3):736-43.
4. Xi Q, Adebiyi A, Zhao G, Chapman KE, Waters CM, Hassid A, Jaggar JH. IP3 constricts cerebral arteries via IP3 receptor-mediated TRPC3 channel activation and independently of sarcoplasmic reticulum Ca2+ release. Circulation Research 2008; 102:1118-1126.
5. Zhao G, Adebiyi A, Xi Q, Jaggar JH. Hypoxia reduces KCa channel activity by inducing Ca2+ spark uncoupling in cerebral artery smooth muscle cells. American Journal of Physiology. Cell Physiology 2007; 292(6):C2122-128.
6. 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(3):H1584-1592.
7. Li A, Adebiyi A, Leffler CW, Jaggar JH. KCa channel insensitivity to Ca2+ sparks underlies fractional uncoupling in newborn cerebral artery smooth muscle cells. American Journal of Physiology. Heart and Circulatory Physiology 2006; 291(3): H1118-1125.
8. Adebiyi A, Adaikan PG. Effect of caffeine on response of rabbit isolated corpus cavernosum to high K+ solution, noradrenaline and transmural electrical stimulation Clinical and Experimental Pharmacology and Physiology 2004; 31: 82-85.
9. Adebiyi A, Adaikan PG, Prasad RNV. Oxytocic activity of thrombin: modulation of thrombin-induced gravid rat myometrial contractions by 5-hydroxytryptamine receptor antagonists. Journal of Perinatal Medicine 2004; 32: 126-131.
10. Adebiyi A, Adaikan PG, Prasad RNV. Pregnancy outcomes following pre- and post-implantation exposure of Sprague-Dawley rats to benzyl isothiocyanate. Food and Chemical Toxicology 2004; 42: 715-720.