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 John N. Lorenz, PhD
Professor
john.lorenz@uc.edu
The research activities in this lab are focused on the study of integrative physiology in a variety of genetically altered mice produced at UC and elsewhere. Recognizing that functional techniques must be made available in order to thoroughly evaluate the physiologic and integrative role of regulatory proteins using transgenic approaches, we have developed a facility that is able to perform in depth analyses of cardiovascular, renal, and pulmonary systems in the intact mouse. Methodologies include 1) evaluation of myocardial function in vivo using cardiac catheterization (pressure and volume measurements) and echocardiography, as well as in vitro using the Langendorff preparation (PowerPoint presentation illustrating methods used to evaluate cardiac function); 2) evaluation of renal function in anesthetized animals using clearance measurements of glomerular filtration rate, renal blood flow and electrolyte excretion; and 3) evaluation of pulmonary mechanics in both instrumented (pressure-flow measurements) and non-instrumented animals (plethysmography).
In addition to these activities, my lab is specifically engaged in research designed to evaluate the role of various ion transporters in the control of blood pressure and renal function. Using molecular techniques to produce mice lacking various kidney-specific transporters, we are studying the contribution of these transporters to overall fluid and electrolyte homeostasis. Presently, we are pursuing the phenotypic analysis of several knockout strains of mice including the NHE3, NHE2, ROMK, colonic H-K-ATPase, and NKCC1 knockouts. In addition, we have recently begun to investigate the mechanisms involved in balancing salt intake with urinary salt excretion. According to our hypothesis, this reflex, referred to as the anticipatory salt reflex, or the hepatorenal reflex, may involve the gastrointestinal peptides guanylin and uroguanylin as paracrine/autocrine mediators of a hepatorenal neural reflex. Using sophisticated techniques such as in vivo renal micropuncture and microperfusion, and renal nerve recordings, we hope to gain a more thorough understanding of the salt and fluid homeostatic mechanisms within the kidney. Ultimately, these studies investigating hemodynamics and fluid and electrolyte balance will provide insights to genetic basis of disease states such as hypertension. |
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Selected Publications:
- Emily M Bradford, Marian L Miller, Vikram Prasad, Michelle L Nieman, Lara R Gawenis, Mark Berryman, John N Lorenz, Patrick Tso and Gary E Shull (2010) CLIC5 mutant mice are resistant to diet-induced obesity and exhibit gastric hemorrhaging and increased susceptibility to torpor. Am J Physiol Regul Integr Comp Physiol 298, R1531-1542.
View original publication at AJP:Regu Online.
- Arshani N Wansapura, Valerie Lasko, Zijian Xie, Olga V Fedorova, Alexei Y Bagrov, Jerry B Lingrel and John N Lorenz (2009) Marinobufagenin enhances cardiac contractility in mice with ouabain-sensitive α1 Na+-K+-ATPase. Am J Physiol Heart Circ Physiol 296, H1833-1839.
View original publication at AJP:Heart Online.
- Elizabeth L Loreaux, Baksho Kaul, John N Lorenz and Jerry B Lingrel (2008) Ouabain-sensitive α1 Na,K-ATPase enhances natriuretic response to saline load. J Am Soc Nephrol 19, 1947-1954.
View original publication at JASN Online.
- John N Lorenz, Elizabeth L Loreaux, Iva Dostanic-Larson, Valerie Lasko, J Renee Schnetzer, Richard J Paul and Jerry B Lingrel (2008) ACTH-induced hypertension is dependent on the ouabain-binding site of the α2-Na+-K+-ATPase subunit. Am J Physiol Heart Circ Physiol 295, H273-H280.
View original publication at AJP:Heart Online.
- John N Lorenz, Lois J Arend, Rachel Robitz, Richard J Paul and A John MacLennan (2007) Vascular dysfunction in S1P2 sphingosine 1-phosphate receptor knockout mice. Am J Physiol Regul Integr Comp Physiol 292, R440-446.
View original publication at AJP:Regu Online.
- Iva Dostanic-Larson, John N Lorenz, James W Van Huysse, Jon C Neumann, Amy E Moseley and Jerry B Lingrel (2006) Physiological role of the α1- and α2-isoforms of the Na+-K+-ATPase and biological significance of their cardiac glycoside binding site. Am J Physiol Regul Integr Comp Physiol 290, R524-528.
View original publication at AJP:Regu Online.
- John N Lorenz, Iva Dostanic-Larson, Gary E Shull and Jerry B Lingrel (2006) Ouabain inhibits tubuloglomerular feedback in mutant mice with ouabain-sensitive α1 Na,K-ATPase. J Am Soc Nephrol 17, 2457-2463.
View original publication at JASN Online.
- John N Lorenz, Michelle Nieman, Jenine Sabo, L Philip Sanford, Jennifer A Hawkins, Noeet Elitsur, Lara R Gawenis, Lane L Clarke and Mitchell B Cohen (2003) Uroguanylin knockout mice have increased blood pressure and impaired natriuretic response to enteral NaCl load. J Clin Invest 112, 1244-1254.
View original publication at JCI.org.
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