Effects Of Catecholamines On The Activity Of Baroresponsive Neurons In The Nucleus Tractus Solitarius Of The Rat.

Abstract

The nucleus tractus solitarius (nTS) is a brainstem structure with an important role in the elicitation of the baroreceptor reflex. This reflex is triggered by increases in blood pressure, and serves to bring about decreases in heart rate and vascular resistance. Studies have revealed the presence of catecholaminergic nerve terminals within the nTS. While such findings suggest the involvement of catecholamines in autonomic regulation, little is known of catecholamine effects on the activity of individual nTS neurons receiving baroreceptive input. This issue was addressed by examining the responses to catecholamines of baroreceptive neurons in the rat nTS. Neuronal responses to microiontophoretically applied catecholamines were recorded extracellularly and correlated with responses to pharmacologically induced elevations of blood pressure. Responses to norepinephrine and epinephrine were further examined in the absence and presence of microiontophoretically applied antagonists selective for subclasses of alpha- and beta-adrenergic receptors. Of the 357 neurons studied, 193 responded to blood pressure elevation. One-hundred twenty-eight neurons responded in an inhibitory manner, while the remaining 65 were excited. Both classes of neurons were inhibited by application of catecholamines. No differences were found between the responses of the two groups of neurons. Responses to norepinephrine and epinephrine were antagonized in both groups of cells by the alpha-adrenergic antagonist tolazoline but not by the beta antagonist sotalol. Responses to norepinephrine were also blocked by the alpha-2 antagonist idazoxan, but the responses of only a few cells were blocked by the alpha-1 antagonist prazosin. In contrast, the effects of epinephrine were equally blocked by prazosin and idazoxan. These data indicate the presence of at least two groups of baroresponsive neurons in rat nTS. Neuronal activity in both groups was suppressed by catecholamine iontophoresis. The actions of epinephrine appeared to be mediated in either group by both alpha-1 and alpha-2 adrenergic receptors, whereas the actions of norepinephrine appeared to be primarily mediated by an alpha-2 receptor. However, this latter finding may reflect a possible methodological artifact. The results are discussed in relation to current knowledge regarding baroreceptor information processing in the nTS.