Vasa recta pericyte density is negatively associated with vascular congestion in the renal medulla following ischemia reperfusion in rats

Author:

Crislip G. Ryan1,O’Connor Paul M.1,Wei Qingqing2,Sullivan Jennifer C.1

Affiliation:

1. Department of Physiology, Augusta University, Augusta, Georgia; and

2. Department of Cellular Biology and Anatomy, Augusta University, Augusta, Georgia

Abstract

Recent evidence suggests that a greater density of pericytes in renal cadaveric allografts is associated with better recovery following transplant. The physiological mechanism(s) through which pericyte density may be beneficial is not well understood. The goal of this study was to test the hypothesis that lower medullary pericyte density is associated with greater renal injury following ischemia reperfusion (IR) in a rat model, providing a basis for future studies to better understand pericytes in a pathological environment. To test our hypothesis, we determined the association between medullary pericyte density and renal injury in spontaneously hypertensive rats (SHR) following 45 min of warm bilateral IR. We found that there was a significant negative relationship between pericyte density and plasma creatinine (slope = −0.03, P = 0.02) and blood urea nitrogen (slope = −0.5, P = 0.01) in female but not male SHR. Pericyte density was negatively associated with medullary peritubular capillary (PT) congestion in both sexes following IR (male: slope = −0.04, P = 0.009; female: slope = −0.03, P = 0.0001). To further test this relationship, we used a previously reported method to reduce pericyte density in SHR. Medullary erythrocyte congestion in vasa recta (VR) and PT significantly increased following IR in both sexes when pericyte density was pharmacologically decreased (VR: P = 0.03; PT: P = 0.03). Our data support the hypothesis that pericyte density is negatively associated with the development of IR injury in SHR, which may be mediated by erythrocyte congestion in the medullary vasculature.

Funder

American Heart Association (AHA)

HHS | National Institutes of Health (NIH)

Publisher

American Physiological Society

Subject

Physiology

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