BACKGROUND: We have previously shown that Lewis polycystic kidney rats (LPK) exhibit increased sympathetic tone 1,2. This study aimed to examine baroreflex control of renal sympathetic nerve activity (RSNA) in the LPK, and changes associated with age. We further determined the role of the central component of baroreflex arc in the regulation of RSNA.
METHODS: Urethane anaesthetised male Lewis control and LPK aged 7–8 weeks (juvenile, n=17) and 12–13 weeks (adult, n=17) were studied. RSNA baroreflex function was determined by sigmoid analysis of the mean arterial pressure (MAP)-RSNA relationship, induced by phenylephrine (10–50 µg/kg) and sodium nitroprusside (50-70 µg/kg). Central pathways were tested by recording RSNA responses to electrical stimulation of the sensory afferent aortic depressor nerve (ADN; 5-second train, 4.0 V, 2.0-ms pulses, at 1–24 Hz).
RESULTS: Irrespective of age, LPK had elevated baseline levels of RSNA (juvenile, 7.3 ± 1.5 vs 3.6 ± 0.7 µV and adult, 4.9 ± 0.9 vs 2.6 ± 0.5 µV, P<0.05) and systolic blood pressure (P<0.05) compared to age-matched controls. RSNA baroreflex function was shifted rightward in both juvenile and adult LPK rats. In adult LPK, the gain (1.3 ± 0.2 vs 2.1 ± 0.2 %RSNA/mmHg, P<0.05) and range (65 ± 8 vs 98 ± 7% P<0.01) of RSNA were reduced compared to Lewis. In juvenile LPK, RSNA range was not altered, but the gain was markedly lower (1.5 ± 0.2 vs 3.3 ± 0.3 %RSNA/mmHg, P<0.001) compared to Lewis. Reductions in RSNA in response to ADN stimulation were lower in both adult and juvenile LPK (P<0.05).
CONCLUSIONS: LPK exhibit impaired baroreflex control of RSNA from 7 weeks of age, which progressively worsens as the disease progresses. Impaired baroreflex control of RSNA in LPK is contributed to by a deficit in the central component of the baroreceptor reflex arc.