Acute nicotine induced pressor response is in part due to interaction with baro reflex pathway

Abstract

Arterial baro-reception is regarded as one of the most powerful rapidly acting homeostatic mechanism regulating blood pressure. Investigation had suggested that nicotine may interact with aortic baro-receptors to produce its sustained presser response, an effect that had received little attention. Anaesthetized Wister albino rats were used. Bilateral carotid occlusion (BCO) method was used to introduce a predominantly sympathetically mediated cardiovascular reflex. Baroreceptor sensitivity (BS) test was assessed as gain in baroreflex function. Others BCO led to increases in mean arterial pressure (MAP) in normal rats (? Map 27 + 3.6mm HG) and increases in MAP induced by BCO was less after nicotine pretreatment (P<0.001). BCO also led to significant increases in heart rate in both normal and in nicotine treated rats but the increases shows no significant differences. Acute nicotine pretreatment reduced BS evoked by presser stimulus (phenylephrine) from 0.789, 0.039 and 0.004 beats per min mm HG-1 (P<0.001). The significant decreases in BCO reduced presser response by nicotine may be an indication of strong pre-existing sympathetic activation. Reduction of BS by nicotine may be an indication that nicotine do interact with beroreflex pathway either peripherally at the receptors or centrally to reset the system. Thus nicotine action on baro-reflex system could contribute to the sustained presser response it produced.

Key words: Baroreceptors, Means Arterial Pressure (MAP), Baroreflex, Baro - reception