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hormone/paracrine/autocrine regulation of the renal microcirculation, calcium signaling in vascular smooth muscle cells, pathophysiology of hypertension

UNC-Chapel Hill 

Education and Training

DePauw University, BA, Biological Sciences
Indiana University, PhD, Physiology

Areas of Interest

Abnormal renal function is a major cause of hypertension, and in conjunction with oxidative stress, is a major cause or contributor to the development of cardiovascular and renal disease, but our understanding of pathophysiological mechanisms and the possible contribution of abnormal renal function is incomplete. Our working hypothesis is that excess superoxide anion (O2-) generated by the specific activator NOXA1 of NADPH oxidase NOX1 distorts renal function to magnify vasoconstriction and to promote Na+ retention to produce hypertension. We postulate that these renal vascular and tubular mechanisms contribute to the prohypertensive actions of angiotensin II (ANG II) and can be reversed by genetic knockdown of NOX1/NOXA1 signaling or by administration of the antioxidant tempol. Pilot studies indicate that WT mice develop ANG II-induced hypertension (AIH), whereas NOXA1-null mice do not, but the renal phenotype of mice lacking NOX1/NOXA1 signaling is not known. Thus, the functional role of this signaling pathway in controlling the renal microcirculation and tubular function in AIH awaits investigation. Our comprehensive studies will combine genetic, biochemical, functional and histological approaches to characterize NOX/NOXA1 signaling in renal function in health and during the development and established phases of AIH and thereby fill this information gap.

Awards and Honors

NIH, Hypertension and Microcirculation Study Section, Ad hoc
NIH, Reviews, Heart, Blood and Lung Institute
NIH, NIDDK-Special Grants Review Comm (Subcomm D), Member
FASEB Summer Conferenceon Renal Hemodynamics, Organizing Comm Chair
American Heart Associate, Council-High Blood Pressure Research, Program and Awards Comm
Carl W. Gottschalk Lectureship, American Physiological Society
Visiting Professor, Center for Hypertension and Metabolic Diseases, University, Chongqing, China

Arendshorst, Bill
  • Phone Number

    919-966-1067 (Office Phone)

  • Address

    6341B Medical Biomolecular Research Building

    Campus Box 7545

    Chapel Hill, NC 27599-7545