Background: Altered respiratory modulation of sympathetic nerve activity (SNA) is suggested to contribute to the development of hypertension. Chronic kidney disease (CKD) has a reciprocal relationship with hypertension however little is known regarding respiratory sympathetic modulation in CKD. Aim: To identify if respiratory-sympathetic coupling is altered in the Lewis Polycystic Kidney (LPK) rat model of CKD compared to the normotensive control Lewis rats. Methods: Experiments were performed in anaesthetised, vagotomised, paralysed and ventilated LPK and Lewis rats (n = 8/strain, mixed sex). Blood pressure, phrenic nerve activity (PNA) and splanchnic SNA (sSNA) were measured. Results: LPK rats exhibit impaired renal function (plasma creatinine LPK: 61.38 ± 10.83 vs Lewis: 13.38 ± 2.259 μmol/L; p < 0.001), higher blood pressure (LPK: 124.82 ± 7.96 vs Lewis: 92.62 ± 5.15 mmHg; p < 0.01) and increased tonic sSNA (LPK: 7.57 ± 0.87 vs Lewis: 2.67 ± 0.44 μv; p < 0.001). Respiratory related sympathetic excitation (the difference between peak and basal amplitude in PNA triggered average of the sSNA) was larger in the LPK rats (LPK: 7.55 ± 2.47 vs Lewis: 3.86 ± 0.78 μv; p < 0.05) and the temporal position of the post inspiratory peak from the onset of inspiration was shifted to the left (LPK: 0.55 ± 0.04 vs Lewis: 0.37 ± 0.02 s; p < 0.05) in room air. Conclusion: Our findings suggest that the respiratory-sympathetic coupling is modified in CKD and this altered modulation may be one of the underlying mechanisms of hypertension associated with CKD.
|Number of pages||1|
|Journal||Autonomic Neuroscience: Basic and Clinical|
|Publication status||Published - Nov 2015|
|Event||Meeting of the International Society for Autonomic Neuroscience (ISAN) (9th : 2015) - Stresa, Italy|
Duration: 26 Sep 2015 → 29 Sep 2015