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Vagal TRPV1‐containing afferent fibers mediate cerebral vasodilation by inhaled ammonia in rats

Irritation of the airways and lungs can induce cardiovascular responses in subjects as a part of physiological stress to noxious stimulation. The aim of this study was to investigate the effects and afferent pathways of inhaled ammonia (IA) on cerebral vascular resistance (CVR) in rats. To irritate the lower airways and lungs, ammonia vapor equilibrated over a 30% NH4OH solution was introduced via ventilator (1 ml, 30 s) in sodium pentobarbital anesthetized, ventilated and paralyzed male rats. Parietal craniotomy was performed to produce a 3.0‐mm‐diameter hole that exposed the left cortex. Cortical cerebral blood flow was assessed with laser Doppler flowmetry and arterial blood pressure was measured to calculate CVR. IA decreased CVR by 20.3±2.5% (n=22, P<0.05). Bilateral vagotomy attenuated the effects of IA on CVR from −7.9±2.8% to +4.2±5.2% (n=5, P<0.05). In another group, effects of IA on CVR before and after spinal transections at C6‐C7 were not significantly different (−20.2±3.1% vs −16.6±4.0%, n=6). Resiniferatoxin (2 μg/kg, i.v.) used to inactivate transient receptor potential vanilloid type 1 (TRPV1) containing fibers, attenuated IA‐induced effects on CVR (−24.6±4.3% vs −3.4±1.5%, n=11, p<0.01). These data suggested that a decrease of cerebrovascular resistance resulting from inhaled ammonia was mediated primarily by vagal TRPV1‐containing afferent fibers. (NS‐035471, HL‐075524)