Key result
Mild hypoxia produced a larger pressure response in female rats with CKD compared to controls (ΔMAP 30 ± 6 vs. 12 ± 6 mmHg; P≤0.05) and augmented respiratory-sympathetic nerve coupling.
Why the study?
Carotid body feedback and hypoxia may enhance respiratory-sympathetic nerve coupling and drive increased blood pressure in chronic kidney disease.
Female rats with CKD exhibit heightened respiratory-sympathetic coupling at baseline that is further augmented by mild hypoxia, suggesting a potential mechanism for hypertension in CKD.
Answers are grounded in this paper and cite their sources.
Heightened respSNA augmented by hypoxia in female CKD rats may drive hypertension; leaves open translation to humans and need for prospective studies.
Carotid body feedback and hypoxia may serve to enhance respiratory–sympathetic nerve coupling (respSNA) and act as a driver of increased blood pressure. Using the Lewis polycystic kidney (LPK) rat model of chronic kidney disease, we examined respSNA in adult female rodents with CKD and their response to acute hypoxia or hypercapnia compared to Lewis control animals. Under urethane anesthesia, phrenic nerve activity, splanchnic sympathetic nerve activity (sSNA), and renal sympathetic nerve activity (rSNA) were recorded under baseline conditions and during mild hypoxic or hypercapnic challenges. At baseline, tonic SNA and blood pressure were greater in female LPK rats versus Lewis rats (all P < 0.05) and respSNA was at least two-fold larger [area under the curve (AUC), sSNA: 7.8 ± 1.1 vs. 3.4 ± 0.7 μV s, rSNA: 11.5 ± 3 vs. 4.8 ± 0.7 μV s, LPK vs. Lewis, both P < 0.05]. Mild hypoxia produced a larger pressure response in LPK [Δ mean arterial pressure (MAP) 30 ± 6 vs. 12 ± 6 mmHg] and augmented respSNA (ΔAUC, sSNA: 8.9 ± 3.4 vs. 2 ± 0.7 μV s, rSNA: 6.1 ± 1.2 vs. 3.1 ± 0.7 μV s, LPK vs. Lewis, all P ≤ 0.05). In contrast, central chemoreceptor stimulation produced comparable changes in blood pressure and respSNA (ΔMAP 13 ± 3 vs. 9 ± 5 mmHg; respSNA ΔAUC, sSNA: 2.5 ± 1 vs. 1.3 ± 0.7 μV s, rSNA: 4.2 ± 0.9 vs. 3.5 ± 1.4 μV s, LPK vs. Lewis, all P > 0.05). These results demonstrate that female rats with CKD exhibit heightened respSNA coupling at baseline that is further augmented by mild hypoxia, and not by hypercapnia. This mechanism may be a contributing driver of hypertension in this animal model of CKD.
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Saha et al. (2021) studied Chronic Kidney Disease. Mild hypoxia vs. Lewis control animals was evaluated on Change in mean arterial pressure (ΔMAP) during mild hypoxia (p=≤0.05). Mild hypoxia produced a larger pressure response in female rats with CKD compared to controls (ΔMAP 30 ± 6 vs. 12 ± 6 mmHg; P≤0.05) and augmented respiratory-sympathetic nerve coupling.
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