Effects of drug-induced changes in resting blood pressure on classically conditioned heart rate and blood pressure in restrained rats.

Subsequent to receiving aversive classical conditioning (which led to a decelerative heart rate [HR] CR and a pressor–depressor blood pressure [BP] CR), 3 groups of restrained male Sprague-Dawley rats received iv infusion of Na nitroprusside (n?=?9; 40 μg/mg/min) to lower baseline BP, phenylephrine (n?=?10; 17 μg/mg/min) to raise baseline BP, or an equivalent volume of saline (n?=?9). Conditioning test trials during infusion revealed that hypotension produced by Na nitroprusside eliminated the HR CR and transformed the BP CR into a pressor-only reaction. Hypertension produced by phenylephrine facilitated the HR CR and changed the BP CR to a pressor-only response on trials in which baseline BP increases and baseline HR decreases were within restricted limits. Following drug withdrawal, the HR CRs of both drug groups and the BP CR of the phenylephrine group were attenuated. The UCRs to the shock UCS under phenylephrine were exaggerated and consisted of tachycardias and depressor BP changes, whereas, under Na nitroprusside, reduced tachycardias and depressor activity occurred. Results suggest that the loss of the vagally medicated HR CR under Na nitroprusside was due to baroreceptor-controlled inhibition of vagal discharge. The enhancement of the HR CR under phenylephrine was due to baroreceptor-influenced facilitation of vagal discharge. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)