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Dose‐dependent mechanisms mediate lipopolysaccharide (LPS) hypotension in male rats

Previous data from our laboratory indicate that lipopolysaccharide (LPS) initially lowers arterial pressure through a central mechanism that involves the preoptic anterior hypothalamic area (POA). In this study, we investigated how the inflammatory signal induced by peripherally injected LPS reaches the POA. Indeed, it is well known that LPS raises body temperature through two different mechanisms, depending on the dose. Low doses of LPS cause fever by activating vagal nerve afferents; high doses cause fever by activating receptors in the organum vasculosum of the lamina terminalis (OVLT). In the present study we found that the effect of a relatively low hypotensive dose of LPS (1 mg/kg iv) was blocked by subdiaphragmatic vagotomy or lidocaine injection into the nucleus tractus solitarius (NTS), but not by lidocaine injection into the OVLT or the area postrema in isoflurane anesthetized rats, suggesting that initiation of LPS hypotension is mediated by vagal nerve afferents. Neither vagotomy nor NTS lidocaine injection prevented the hypotension evoked by high dose LPS (15 mg/kg), however. Interestingly, lidocaine injection into the OVLT prevented the hypotension evoked by high dose LPS. These data indicate that LPS lowers arterial pressure initially by two different pathways. Low doses lower arterial pressure by activating vagus nerve afferents; high doses act through the OVLT.