Key result
Transient renal venous congestion reduces renal blood flow ~46%, demonstrating dissociation from urine flow.
Why the study?
The acute hemodynamic effects of venous congestion on renal blood flow and urine flow remained incompletely understood because most in vivo studies do not independently control arterial and venous pressures.
Does brief venous pressure elevation alter renal blood flow and urine flow under constant arterial pressure in rats?
Does brief venous pressure elevation alter renal blood flow and urine flow under constant arterial pressure in rats?
p-value: p=<0.05
Brief elevation of renal venous pressure under constant arterial pressure causes a dissociation between renal blood flow and urine flow, suggesting urine flow is primarily governed by pressure conditions rather than renal perfusion.
Background: Venous congestion is recognized as an important contributor to kidney dysfunction. Whereas arterial pressure (AP) promotes pressure diuresis, elevated venous pressure (VP) can induce renal edema and impair kidney function. However, the acute hemodynamic effects of venous congestion on renal blood flow (RBF) and urine flow (UF) have not been fully elucidated. Most in vivo studies do not control AP and VP independently, making it difficult to isolate the specific contribution of venous congestion. This study aimed to clarify the effects of brief VP elevation on RBF and UF under constant AP. Methods: Male Wistar–Kyoto rats (N = 7) were anesthetized. Carotid sinus pressure was fixed at 100 mmHg to minimize baroreflex influences. Mean AP was maintained at either 100 or 60 mmHg using a closed-loop feedback system that regulated blood volume via a syringe connected to the left common carotid artery. Venous congestion was induced by transiently occluding the inferior vena cava between the left and right renal veins for 5 min, followed by release. Renal VP was measured in the inferior vena cava above and below the occlusion site to monitor the right and left kidneys, respectively. UF from each kidney was collected separately from the corresponding ureter. Results: Snare occlusion increased the left VP to 26.83 ± 0.43 mmHg at an AP of 100 mmHg and to 18.15 ± 0.66 mmHg at an AP of 60 mmHg, while the right VP remained unchanged under both conditions. The left RBF significantly decreased after occlusion, reaching −45.73 ± 4.21% (P < 0.05) at 3 minutes under an AP of 100 mmHg and −54.45 ± 7.32% (P < 0.05) under an AP of 60 mmHg. These reductions persisted throughout the occlusion period. In contrast, the left UF exhibited a transient increase immediately after occlusion, followed by a gradual decline under both AP conditions. The right UF remained unchanged. After the release of the occlusion, the left RBF promptly returned to baseline, whereas the left UF showed a further decrease at 1 minute post-release. The left UF gradually recovered during the 10-minute post-release observation period at an AP of 100 mmHg but remained suppressed at an AP of 60 mmHg.Conclusion: A brief elevation of renal VP under constant AP caused a clear dissociation between RBF and UF, suggesting that UF is governed primarily by pressure conditions rather than renal perfusion. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
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Fukuda et al. (2026) studied Venous congestion (n=7). Transient occlusion of the inferior vena cava vs. Right kidney (unchanged venous pressure) was evaluated on Renal blood flow (RBF) at 3 minutes under an AP of 100 mmHg (p=<0.05). Brief elevation of renal venous pressure under constant arterial pressure decreased left renal blood flow by 45.73% (P<0.05) at 100 mmHg, demonstrating a dissociation between RBF and urine flow.
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