Why the study?
Does adenosine-induced hypotension affect preganglionic and postganglionic sympathetic nerve activity differently than sodium nitroprusside in anesthetized rats?
Does adenosine-induced hypotension affect preganglionic and postganglionic sympathetic nerve activity differently than sodium nitroprusside in anesthetized rats?
Adenosine-induced hypotension suppresses postganglionic sympathetic nerve activity via inhibition of ganglionic neurotransmission, unlike sodium nitroprusside.
Adenosine may inhibit ganglionic transmission in rat models; leaves open translation to human anesthetic hypotension.
The aim of this study was to examine the effects of adenosine (AD)-induced hypotension on preganglionic adrenal (aSNA) and postganglionic renal (rSNA) sympathetic nerve activity. rSNA (n = 10) and aSNA (n = 6) were recorded together with mean arterial pressure (MAP) and heart rate (HR) in chloralose-anesthetized, artificially ventilated rats. In each experiment, hypotension was induced by equihypotensive doses of AD (0.03-2.0 mg.kg-1.min-1) and sodium nitroprusside (SNP) (1-10 micrograms.kg-1.min-1). SNP induced a progressive reflex tachycardia and a reflex increase in rSNA to levels 159 +/- 35% above control at a MAP reduction of 55% of the normotensive control value. Equipotent doses of AD induced a decrease in HR and significantly less pronounced reflex increase in rSNA. The maximal increase in rSNA with AD was 55 +/- 19% at a MAP reduction of 30%. At higher infusions rates of AD, rSNA progressively declined toward the normotensive control values. However, AD elicited a progressive increase in preganglionic aSNA that was not significantly different from the increase seen during SNP infusion. It is concluded that AD-induced hypotension is associated with a suppression of postganglionic sympathetic nerve activity caused by an inhibition of ganglionic neurotransmission.
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Delle et al. (1988) studied this question.
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