The restriction of and opioid receptors impaired the hypotensive response seen after central 5 HT3 receptor stim-ulation. This may mean that during central 5 HT3 receptor arousal, central n opioid receptors exert a tonic, negative drive on blood-pressure. This tonic inhibitory drive applied by d opioid receptors is apparently restricted to animals in which central 5 HT3 receptors are activated since the government of naltrindole alone has no influence on animals in which central 5 HT3 receptors aren’t pharmacologically activated. Moreover, in supplier OSI-420 animals where central 5 HT3 receptors are pharmacologically stimulated, this tonic, inhibitory drive that opioid receptors and is determined by isn’t observed. The pattern of opioid receptors distribution in the mind is specific for every receptor subtype. Additionally the occurrence of the opioid receptors varies greatly in the different brain areas. These anatomic differences among the opioid receptors subtypes may possibly take into account their functional range. Moreover, it’s important to notice that, in the absence of central 5 HT3 receptor stimulation, none-of the opioid antagonists was capable of changing blood pressure, indicating that Cellular differentiation the lowering of endogenous opioid activity offered by these drugs, in the doses used, was unable to influence central blood pressure regulation. We have previously demonstrated that the restriction and the stimulation of central 5 HT3 receptors impair baroreflex activity. Certainly, no tachycardic response is observed after the hypotension that follows the stimulation of central 5 HT3 receptors by no bradycardia and m CPBG sometimes appears during hypertension that follows the blockade of central 5 HT3 receptors by ondansetron. Exactly the same phenomenon is observed here. There is no compensatory tachycardia in animals after key 5HT3 receptor stimulation by m CPBG. Also, in the number of animals receiving m CPBG but pretreated with naltrindole hypotension was reverted and a hypertensive response was evident without the associated bradycardia. In the present CTEP paper, it had been decided to study the results of pharmacological manipulations on opioid receptors and central 5 HT3 receptors by adding the drugs intracerebroventricularly instead of studying the effect of the drugs in any particular place of the mind. The method selected for this study is, therefore, appropriate for examining the cardiovascular effects created by these agents through their action on the central nervous system alone, excluding the variety of effects that would derive from their interaction with peripheral receptors. But, this experimental protocol doesn’t permit recognition of the specific brain areas involved in the responses observed here.