Abstract
We have shown that cholinergic stimulation induces a pro-inflammatory innate immune response in pre-hypertensive Spontaneously Hypertensive rats (SHR). Here we hypothesized that cholinergic stimulation induces renal infiltration of a CD68+ macrophage population, contributing to renal hypertension. To test this, we infused either saline or nicotine (15 mg/kg/day) via osmotic pumps in pre-hypertensive SHR and WKY over 2 weeks. We measured blood pressure (BP) by tail-cuff and harvested renal tissue at 24 hours after initiating infusion. The presence of CD68+ macrophages in renal parenchyma was assessed by immunohistochemistry. Nicotine increased the number of renal CD68+ macrophages in SHR (n=3) from 47±8 to 73±7 cells per 400x field (p<0.001), but not WKY (34±8 cells vs 41±7 cells per 400x field) (p>0.05), without increasing the BP at 24 hours. However, over 2 weeks, nicotine increased the BP in pre-hypertensive SHR from 123±4mmHg to 157±3mmHg (n=6, p<0.001), whereas saline did not (124±5mmHg vs 126±2mmHg, n=6, p>0.05). In contrast, nicotine had no effect on BP in the WKY. We conclude that cholinergic stimulation which is selectively pro-inflammatory in innate immune cells of the pre-hypertensive SHR also enhances CD68+ macrophage infiltration in the kidneys and may, thus, play a dual role in the development of hypertension in this genetic model of hypertension.
Published Version
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