John Lorenz - F1000 Faculty Member (since 23 November 2009)
Department of Molecular and Cellular Physiology, University of Cincinnati College of Medicine, Cincinnati, OH, USA
BIOGRAPHY
ACADEMIC POSITION:Professor, Department of Molecular and Cellular Physiology
EDUCATION:
Medical School University of Cincinnati
Internship University of Cincinnati College of Medicine
Residency University of Cincinnati College of Medicine
Fellowship University of Cincinnati College of Medicine
RESEARCH INTERESTS:
The research activities in my lab are focused on the study of integrative physiology in a variety of genetically altered mice produced at University of Cincinnati 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;
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 role of endogenous cardiac glycosides (such as ouabain) in cardio-renal regulation. These compounds act on Na,K-ATPase pumps that are expressed throughout the body. Recent development of mutant mice with altered differential sensitivity of the Na,K-ATPase pumps to ouabain serve as the model for these studies.
EVALUATIONS
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