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Renal sympathetic nerve activity and vascular reactivity to phenylephrine after
lipopolysaccharide administration in conscious rats
#MMPMID28242823
Julien C
; Oréa V
; Quintin L
; Piriou V
; Barrès C
Physiol Rep
2017[Feb]; 5
(4
): ? PMID28242823
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It has been proposed that sympathoexcitation is responsible for vascular
desensitization to ?(1)-adrenoceptor stimulation during lipopolysaccharide
(LPS)-induced systemic inflammation. The present study tested this hypothesis by
examining the effects of sympatho-deactivation with the ?(2)-adrenoceptor
agonist, dexmedetomidine, on mean arterial pressure (MAP), renal sympathetic
nerve activity (RSNA), and vascular reactivity to phenylephrine in conscious rats
with cardiac autonomic blockade (methylatropine and atenolol) following LPS
administration. In male, adult Sprague-Dawley rats (n = 5 per group), RSNA and
MAP were continuously recorded over 1-h periods, before and after LPS
administration (20 mg/kg iv), and finally after infusion of either saline or
dexmedetomidine (5 ?g/kg, then 5 ?g/kg/h iv). A full dose-response curve to
phenylephrine was constructed under each condition. After pooling data from both
groups of rats (n = 10), LPS significantly (P = 0.005) decreased MAP (from
115 ± 1 to 107 ± 2 mmHg), increased RSNA (to 403 ± 46% of baseline values) and
induced 4 to 5-fold increases in the half-maximal effective dose (ED(50)) of
phenylephrine (from 1.02 ± 0.09 to 4.76 ± 0.51 ?g/kg). During saline infusion,
RSNA progressively decreased while vascular reactivity did not improve. Treatment
with dexmedetomidine decreased MAP, returned RSNA to near pre-endotoxemic levels,
but only partially restored vascular reactivity to phenylephrine (ED(50) was
still threefold increased as compared with baseline values). These findings
indicate that only part of the decrease in vascular reactivity to
?(1)-adrenoceptor stimulation during endotoxemia can be accounted for by
sympathetic activation, at least on a short-term basis.
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