  Respiratory modulation of sympathetic nerve activity (respSNA) was studied in
a hypertensive rodent model of chronic kidney disease (CKD) using Lewis
Polycystic Kidney (LPK) rats and Lewis controls. In adult animals under in vivo
anaesthetised conditions (n=8-10/strain), respiratory modulation of splanchnic
and renal nerve activity was compared under control conditions, and during
peripheral (hypoxia), and central, chemoreceptor (hypercapnia) challenge.
RespSNA was increased in the LPK vs. Lewis (area under curve (AUC) splanchnic
and renal: 8.7$\pm$1.1 vs. 3.5$\pm$0.5 and 10.6$\pm$1.1 vs. 7.1$\pm$0.2
$\mu$V.s, respectively, P<0.05). Hypoxia and hypercapnia increased respSNA in
both strains but the magnitude of the response was greater in LPK, particularly
in response to hypoxia. In juvenile animals studied using a working heart
brainstem preparation (n=7-10/strain), increased respSNA was evident in the LPK
(thoracic SNA, AUC: 0.86$\pm$0.1 vs. 0.42$\pm$0.1 $\mu$V.s, P<0.05), and
activation of peripheral chemoreceptors (NaCN) again drove a larger increase in
respSNA in the LPK with no difference in the response to hypercapnia. Amplified
respSNA occurs in CKD and may contribute to the development of hypertension.
