Most conceptual models of the organization of the cardiovascular system begin with the premise that the nervous system regulates the metabolic and nonmetabolic reflex adjustments of the circulation. These models assume that all the neurally mediated responses of the circulation are reactive, i.e., reflexes elicited by adequate stimuli. This target article suggests that the responses of the circulation are conditional in three senses. First, as Sherrington argued, reflexes are conditional in that they never operate in a vacuum but in a context together with other reflexes. Guided by functional utility, they interact rather than add. Second, as Pavlov argued, stimuli acquire meanings as a result of experience. This notion of stimulus effect plus the Sherringtonian notion of conditionality suggest that association is one of the ways stimuli eliciting cardiovascular reflexes acquire their meanings and thus their relative strengths. Finally, as Skinner and others have argued, operants are responses that act upon the environment to obtain consequences – that is, stimuli. As operants, cardiovascular responses fulfill a major biological need, functioning proactively. The cardiovascular response is an integral component of the animal's behavior regardless of whether it is an elicited reflex or the eliciting stimulus acquired its properties as a result of the genetic inheritance of the animal or through experience, or the cardiovascular response is emitted in anticipation of an environmental consequence. The main theses of this essay are: (1) behavior is an integrated set of responses and the circulation is one of the response systems comprising behavior; (2) behavior is, in part, determined by its functional significance within a context; (3) the contextual factors operative at the time of the behavior have a major role in determining which of the set of possible responses will determine the final act, that is, which behavior will be the effective response and which other behaviors will be concomitants.

Animal research suggests that central serotonergic neurons are involved in behavioral suppression, particularly anxiety-related inhibition. The hypothesis linking decreased serotonin transmission to reduced anxiety as the mechanism in the anxiolytic activity of benzodiazepines conflicts with most clinical observations. Serotonin antagonists show no marked capacity to alleviate anxiety. On the other hand, clinical signs of reduced serotonergic transmission (low 5-HIAA levels in the cerebrospinal fluid) are frequently associated with aggressiveness, suicide attempts, and increased anxiety. The target article attempts to reconcile such human and animal findings by investigating whether anxiety reduction or increased impulsivity is more Likely to account for animal behavioral changes associated with decreased serotonergic transmission. The effects of manipulating central serotonin in experimental anxiety paradigms in animals (punishment, extinction, novelty) are reviewed and compared with the effects of antianxiety drugs. Anxiety seems neither necessary nor sufficient to induce control by serotonergic neurons on behavior. Further evidence suggests that behavioral effects of anxiolytics thought to be mediated by decreases in anxiety are not caused by the ability of these drugs to reduce serotonin transmission. Blockade of serotonin transmission, especially at the level of the substantia nigra, results in a shift of behavior toward facilitation of responding. This behavioral shift is particularly marked when there is competition between acting and restraining response tendencies and when obstacles prevent the immediate attainment of an anticipated reward. It is proposed that serotonergic neurons are involved not only in behavioral arousal but also in enabling the organism to arrange or tolerate delay before acting. Decreases in serotonin transmission seem to be associated with the increased performance of behaviors that are usually suppressed, though not necessarily because of the alleviation of anxiety, which might contribute to the suppression.