Jeff C. Falcone, Ph.D.

Jeff C. Falcone, Ph.D.


JEFF C. FALCONE, Ph.D.
jcfalc01@louisville.edu
Associate Professor
Indiana University, 1989


My research endeavors are focused on the regulatory mechanisms controlling the local flow of blood to tissue (primarily skeletal muscle, intestine and kidney). We are investigating regulatory mechanisms whereby microscopic veins (venules) act as a sensor of changes in blood metabolites/nutrients and via second messengers either cause dilation or constriction of nearby microscopic arteries (arterioles).

Another emphasis involves examining the myogenic response of arterioles. The myogenic response refers to a pressure-induced mechanism within vascular smooth muscle. Simply described, arterioles will constrict to increases in pressure and dilate to decreases in intraluminal pressure. We have found that the myogenic response is enhanced (stronger) in arterioles from hypertensive compared to normotensive animals. Currently, we are investigating intracellular mechanisms associated with vascular smooth muscle contraction (calcium, protein kinase C, tyrosine kinases, mitogen activated kinases MAPK).

We have also been involved in studying the interaction between endothelial cells and vascular smooth muscle cells. Our interests are centered around nitric oxide, prostanoids, endothelin and hyperpolarizing factor. One recently funded aspect of our research asks the basic question of how microvasculature function changes with age, hypertension and/or diabetes.

Our studies involve the integration of multiple level hypotheses, technology, and protocols. Our approach to integrate across the spectrum is demonstrated by our in vivo and in vitro publications. Specifically, we have developed protocols for visualizing intracellular (either endothelial or vascular smooth muscle) calcium, and other probes such as: pH, sodium, potassium and even membrane potential in intact microscopic blood vessels. Furthermore, we can measure and analyze both content and activity of many intracellular pathway components which lead either to vasodilation or constriction. By focusing our research on specific cellular molecules and then by learning how these molecules interact within the cell and what effect they produce as tissue we can better appreciate and understand how tissues, organs and systems function in this complexity we call life.

PUBLICATIONS:

  1. J.C.Falcone, and H.G. Bohlen. EDRF from rat intestine and skeletal muscle venules causes dilation of arterioles. American Journal of Physiology 258: H1515-1523,1990.
  2. J.C.Falcone, L. Kuo, and G.A. Meininger. Endothelial cell calcium increases during flow-induced dilation in isolated arterioles. American Journal of Physiology 264: H653-H659, 1993. [Rapid]
  3. J.C.Falcone, H.J. Granger, and G.A. Meininger. Enhanced myogenic activation in skeletal muscle arterioles from spontaneously hypertensive rats. American Journal of Physiology 265: H1847-55,1993.
  4. J.C.Falcone, and G.A. Meininger. Arteriolar dilation produced by venule derived EDNO. Microcirculation 4(2): 303 - 310, 1997.
  5. V.V. Parekh, K.G. Maier, R.D. Roman, I.G. Joshua, J.C. Falcone and J.C. Passmore. The diminished role of G-protein, mitogen activated protein kinases (MAP-K) and tyrosine kinase (Tyr-K) in aging kidney cortex. Journal of Investigative Medicine 47(9): 462-467, 1999.
  6. J.C.Falcone, and G.A. Meininger. Endothelin mediates a component of the enhanced myogenic responsiveness of arterioles from hypertensive rats. Microcirculation 6: 305-313, 1999.
  7. Schuschke, D.A., J.C. Falcone, J.T. Saari, J.T. Fleming, S.S. Percival, S.A. Young, J.M. Pass, and F.N. Miller. Endothelial Cell Calcium Mobilization to acetylcholine is attenuated in copper-deficient rats. Endothelium 7(2): 83-92, 2000.
  8. Yu, J. Y. Wang, G. Soukhova, L.C. Collins and J.C. Falcone. Excitatory lung reflex may stress inspiratory muscles by suppressing expiratory muscle activity. Journal of Applied Physiology 90: 857-864, 2001.
  9. Tuttle, J.L. and J.C. Falcone. Endothelial arterioalar cell calcium and nitric oxide responses to adrenergic stimuli. Am. Journal of Physiology Heart Circ Physiol. 281: H873-H881, 2001.