Renal medullary oxygenation decreases with lower body negative pressure in healthy young adults

Abstract

One in three Americans suffer from kidney diseases such as chronic kidney disease, and one of the etiologies is suggested to be long-term renal hypoxia. Interestingly, sympathetic nervous system activation evokes a renal vasoconstrictor effect that may limit oxygen delivery to the kidney. In this report, we sought to determine if sympathetic activation evoked by lower body negative pressure (LBNP) would decrease cortical and medullary oxygenation in humans. LBNP was activated in a graded fashion (LBNP; -10, -20, and -30 mmHg), as renal oxygenation was measured (T2*, blood oxygen level dependent, BOLD MRI; n = 8). At a separate time, renal blood flow velocity (RBV) to the kidney was measured (n = 13) as LBNP was instituted. LBNP significantly reduced RBV (P = 0.041) at -30 mmHg of LBNP (Δ-8.17 ± 3.75 cm/s). Moreover, both renal medullary and cortical T2* were reduced with the graded LBNP application (main effect for the level of LBNP P = 0.0008). During recovery, RBV rapidly returned to baseline, whereas medullary T2* remained depressed into the first minute of recovery. In conclusion, sympathetic activation reduces renal blood flow and leads to a significant decrease in oxygenation in the renal cortex and medulla.NEW & NOTEWORTHY In healthy young adults, increased sympathetic activation induced by lower body negative pressure, led to a decrease in renal cortical and medullary oxygenation measured by T2*, a noninvasive magnetic resonance derived index of deoxyhemoglobin levels. In this study, we observed a significant decrease in renal cortical and medullary oxygenation with LBNP as well as an increase in renal vasoconstriction. We speculate that sympathetic renal vasoconstriction led to a significant reduction in tissue oxygenation by limiting oxygen delivery to the renal medulla.

Keywords: renal oxygenation; renal reflexes; sympathetic activation.

Figure 1.

A: experimental design. B: study model diagram. C: nonmagnetic LBNP tank. The subject was placed in the MRI compatible LBNP tank, which was then slid into the bore of the magnet. Participants’ placed their arms on the chest to avoid scanning the artifact. BH, breath hold; LBNP, lower body negative pressure; MRI, magnetic resonance imaging.

Figure 2.

A: image of the left kidney taken in the coronal plane using the blood oxygen level-dependent (BOLD) magnetic resonance imaging technique in one subject at rest. B: segmented image of the region of interest (ROI). The darker region reflects the renal medulla. ROI is highlighted in red.

Figure 3.

Renal blood flow velocity (RBV) responses (A) and percent change in renal vascular resistance (RVR) (B) during lower body negative pressure (LBNP; −10 mmHg, −20 mmHg, −30 mmHg; n = 13). One-way repeated ANOVA was performed and showed significant main effect for both RBV (P = 0.041) and RVR (P = 0.018). For both variables, post hoc pairwise comparison (3 comparisons) with the Bonferroni method was followed. These comparisons revealed a significant decrease in RBV (P = 0.020) and increase in RVR (P = 0.006) at −30 mmHg of LBNP. Data are presented as means ± SE. *Significant difference from baseline, P < 0.05.

Figure 4.

Change from baseline for renal cortex T2* and renal medulla T2* response to lower body negative pressure (LBNP; −10 mmHg, −20 mmHg, −30 mmHg; n = 8). Two-way repeated ANOVA was performed and showed significant main effects for both the vascular territory (group; P = 0.0275) and the level of LBNP (time; P = 0.0008). Following post hoc pairwise comparison (3 comparisons) with the Bonferroni method for the significant main effects revealed a significant reduction at −30 mmHg of LBNP (P = 0.008 vs. baseline) for changes in medullary T2*. Data are presented as means ± SE. *Significant difference from baseline, P < 0.05.

Figure 5.

Renal blood flow velocity (RBV; n = 13) (A) and renal medullary T2* (n = 8) (B) responses during recovery after termination of lower body negative pressure (LBNP). Post hoc paired t tests revealed significant reduction in medulla T2* 30 s into recovery (R1; P = 0.002 vs. baseline) and immediate return to baseline of RBV. R1, 30 s; R2, 3 min; R3, 5 min 30 s into the recovery period. Data are presented as means ± SE. *Significant difference from baseline, P < 0.05.