The adipocyte-derived
hormone,
leptin, has emerged as an important regulator of regional sympathetic nerve activity (SNA) with pathophysiological implications in
obesity. Genetically engineered mice are useful to understand the molecular pathways underlying the SNA responses evoked by
leptin. However, so far the effect of
leptin on direct SNA in mice has been studied under
general anesthesia. Here, we examined the sympathetic responses evoked by
leptin in conscious mice. Mice were instrumented, under
ketamine/
xylazine anesthesia, with renal or lumbar SNA recordings using a thin (40 gauge) bipolar
platinum-
iridium wire. The
electrodes were exteriorized at the nape of the neck and mice were allowed (5 h) to recover from
anesthesia. Interestingly, the reflex increases in renal and lumbar SNA caused by
sodium nitroprusside (SNP)-
induced hypotension was higher in the conscious phase versus the anesthetized state, whereas the increase in both renal and lumbar SNA evoked by
leptin did not differ between anesthetized or conscious mice. Next, we assessed whether
isoflurane anesthesia would yield a better outcome. Again, the SNP-induced increase in renal SNA and baroreceptor-renal SNA reflex were significantly elevated in the conscious states relative to
isoflurane-anesthetized phase, but the renal SNA response induced by
leptin in the conscious states were qualitatively comparable to those evoked above. Thus, despite improvement in sympathetic reflexes in conscious mice the sympathetic responses evoked by
leptin mimic those induced during
anesthesia.