Abstract P053: Nicotine-induced Renal Inflammation in Genetic Hypertension is Not Dependent on Renal Sympathetic Nerve Activity

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2015-09, Vol.66 (suppl_1)
• Main Authors: Harwani, Sailesh, Chapleau, Mark W, Meyerholz, David, Abboud, Francois
• Format: Article
• Language: English
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hyp.66.suppl_1.p053

Abstract only We recently demonstrated that cholinergic stimulation with nicotine in vivo leads to renal inflammation and premature development of hypertension in Spontaneously Hypertensive Rats (SHR), but not in Wistar Kyoto (WKY) controls. Nicotine can stimulate immune cells directly and influence inflammation indirectly by increasing sympathetic nerve activity (SNA). We hypothesized that increased renal SNA contributes to nicotine-induced renal inflammation in SHR. We tested this hypothesis by measuring the number of CD68+ macrophages in kidneys of prehypertensive SHR (3-5 weeks old, n=7) and age-matched WKY rats (n=3) after subcutaneous infusion of nicotine via osmotic mini-pump (625 mcg/kg/hr) for 24 hours. Each rat was subjected to unilateral renal nerve denervation (RND) and sham surgery on the contralateral kidney 1 week before implanting the mini-pump. RND failed to abrogate nicotine-induced renal inflammation, actually increasing CD68+ macrophage infiltration in renal tubulointerstitium of SHR (110 ± 3 vs. 89 ± 1 cells/unit area in denervated vs. contralateral intact kidneys, respectively, p0.05). Renal norepinephrine content was measured by ELISA to confirm RND. We conclude that nicotine-induced renal macrophage infiltration in SHR is not dependent on renal SNA, and speculate that renal SNA may be anti-inflammatory in this model.