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Julian H. Lombard, Ph.D.
Phone: (414) 955-8530 
Email: jlombard@mcw.edu
B.A. Biological Sciences, University of Texas-El Paso, 1969
M.S. Zoology, Arizona State University, 1971
Ph.D. Physiology, Medical College of Wisconsin, 1975
Research areas: Cardiovascular Physiology
  Molecular & Cellular Physiology

Current research in this laboratory utilizes television microscopy, optical Doppler velocity measurements, oxygen microelectrodes, electrophysiological techniques and molecular biology to investigate the mechanisms by which changes in oxygen availability regulate active tone in microvessels and small resistance arteries and how elevated dietary salt intake affects vascular control in salt-sensitive hypertension and in normotensive animals that are not salt-sensitive. We previously demonstrated that resistance vessels of hypertensive animals exhibit an enhanced constriction in response to elevated PO2 , and a reduced dilation in response to decreased PO2 . We have also found that consumption of a high salt diet leads to a dramatic reduction in the ability of blood vessels to relax and increase blood flow to critical organs, and that this occurs without an increase in blood pressure. A major goal of our work is to determine the mechanisms of the altered response of arterioles and small resistance arteries to changes in oxygen availability in hypertension. Another major goal of our laboratory is to identify the mechanisms by which high salt diet leads to impaired vascular function, even in the absence of an elevation in blood pressure. We are also investigating the role of circulating angiotensin II (ANG II) in maintaining normal vascular relaxation mechanisms using novel genetic rat strains [salt sensitive (SS) rats and consomic SS.13 BN rats) that differ in their ability to regulate their renin-angiotensin system and maintain normal circulating ANG II levels. In those studies, restoration of normal regulation of ANG II by substitution of the Brown Norway chromosome 13 (in SS.13 BN consomic rats) restores normal vascular relaxation mechanisms that are lost in SS rats, even when they are fed a low salt diet.  

Recent Publications:

Kunert, M.P., M.R. Dwinell, and J. H. Lombard.  Vascular responses in aortic rings of a consomic rat panel derived from the fawn-hooded hypertensive strain.  Physiological Genomics 42A:244-258 (2010). PMCID 3008365

Durand, M.J., and J.H. Lombard.  Introgression of the Brown Norway Renin Allele onto the Dahl Salt Sensitive Genetic Background Increases Cu/Zn SOD Expression in Cerebral Arteries.  Am. J. Hypertension 24:563-568 (2011). 

G. Raffai, M.J. Durand, and J.H. Lombard.  Acute and Chronic Angiotensin (1-7) Treatment Restores Vasodilation and Reduces Oxidative Stress in Mesenteric Arteries of Salt-Fed Rats.  Am. J. Physiol. (Heart and Circulatory Physiology) 301:H1341-H1342. (2011).

Drenjancevic-Peric I, Greene AS, Lombard JH.  Restoration of cerebral vascular relaxation in renin congenic rats by introgression of the Dahl R renin gene.  Am. J. Hypertension 23:243-248, 2010.  PMCID 2924749.

Durand MJ, Raffai G, Lombard JH.  Angiotensin (1-7) and low dose angiotensin II infusion reverse salt-induced endothelial dysfunction via different mechanisms in rat middle cerebral arteries. Am. J. Physiol (Heart and Circulatory Physiology) 299(4):H1024-1033, 2010.

Durand MJ, Moreno C, Greene AS, Lombard JH.  Impaired relaxation of cerebral arteries in the absence of elevated salt intake in normotensive congenic rats carrying the Dahl salt-sensitive renin gene. Am. J. Physiol (Heart and Circulatory Physiology) 299:H1865-1874, 2010. PMCID 3006280.

Lombard, JH.  Depression, Psychological Stress, Vascular Dysfunction, and Cardiovascular Disease:  Thinking Outside the Barrel.  J Appl Physiol 2010.  PM:20203070.

McEwen, S.T., S.F. Balus, M.J. Durand, and J.H. Lombard, J.H. Angiotensin II maintains cerebral vascular relaxation via EGF receptor trans-activation and ERK 1/2.  Am. J. Physiol. (Heart and Circulatory Physiology) 297: H1296-H1303, (2009).

Zhu J, Huang T, and Lombard JH. Effect of high salt diet on vascular relaxation and oxidative stress in mesenteric resistance arteries.  J Vasc. Res. 44: 382-390, 2007.

Zhu J, J. Friesema, I. Drenjancevic-Peric, R.J. Roman and J.H. Lombard. High salt diet impairs vascular Ca2+ signaling and nitric oxide production via ANG II suppression in rat aorta. Am J Physiol (Heart Circ. Physiol.) 291:H929-H938, 2006.

Drenjancevic-Peric I. S.A. Phillips, J.R. Falck, and J.H. Lombard. Restoration of normal vascular relaxation mechanisms in cerebral arteries by chromosomal substitution in SS.13BN rats.  Am J Physiol 289:H188-H195 (2005).

Drenjancevic-Peric I and Lombard JH. Reduced ANG II and oxidative stress contribute to impaired vasodilation in Dahl salt sensitive rats on low salt diet.   Hypertension 45 [Part 2] 687-691, (2005).

Wang J, Roman RJ, Falck JR, de la Cruz L, Lombard JH. Effects of high-salt diet on CYP450-4A w-hydroxylase expression and active tone in mesenteric resistance arteries. Am J Physiol Heart Circ Physiol. 2005 Apr;288(4):H1557-65.

Zhu J, Yu M, Friesema J, Huang T, Roman RJ, Lombard JH. Salt-induced ANG II suppression impairs the response of cerebral artery smooth muscle cells to prostacyclin. Am J Physiol Heart Circ Physiol. 2005 Feb;288(2):H908-H513.

Drenjancevic-Peric I, Greene AS, Kunert MP, Lombard JH. Arteriolar responses to vasodilator stimuli and elevated PO2 in renin congenic and Dahl salt-sensitive rats. Microcirculation. 2004 Dec;11(8):669-77.


Curriculum Vitae

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