Nucleus of the solitary tract catecholaminergic neurons modulate the cardiovascular response to psychological stress in rats

Key points Exaggerated cardiovascular responses to stress increase risk for hypertension and cardiovascular disease, but the mechanisms controlling the magnitude of this response are not understood. Catecholaminergic neurons located in the hindbrain area termed the nucleus of the solitary tract (NTS) modulate the control of blood pressure and are activated by psychological stress, but their role in modulating the cardiovascular response to stress is unknown. In this study we lesioned these NTS catecholaminergic neurons and measured the cardiovascular and hormonal responses to psychological stress in rats. We showed that lesioning these neurons increases baseline blood pressure and causes an exaggerated blood pressure response to acute or repeated psychological stress, suggesting that physiological or pathophysiological inhibition of these neurons could lead to exaggerated stress responses and hypertension. These results help us understand the mechanisms that contribute to enhanced cardiovascular responses to psychological stress. Abstract Catecholaminergic neurons within the central nervous system are an integral part of stress-related neurocircuitry, and the nucleus of the solitary tract (NTS) plays a critical role in cardiovascular regulation. We tested the hypothesis that NTS catecholaminergic neurons attenuate psychological stress-induced increases in blood pressure and promote neuroendocrine activation in response to psychological stress. Anti-dopamine-beta-hydroxylase antibody conjugated to the neurotoxin saporin (DSAP) or saline vehicle was microinjected into the NTS to lesion catecholaminergic neurons in male SpragueDawley rats, and 17 days later the rats were subjected to 60 min of restraint stress for five consecutive days. DSAP treatment significantly enhanced the integrated increase in mean arterial pressure during restraint on the first (800 +/- 128 and 1115 +/- 116 mmHg (min) for saline- and DSAP-treated rats) and fifth days (655 +/- 116 and 1035 +/- 113 mmHg (min) for saline- and DSAP-treated rats; P < 0.01 for overall effect of DSAP treatment) of restraint. In contrast, after 60 min of restraint plasma corticosterone concentration was significantly lower in DSAP-treated compared with saline-treated rats (25.9 +/- 7 compared with 46.8 +/- 7 mu g dl-1 for DSAP- and saline-treated rats; P < 0.05). DSAP treatment also significantly reduced baseline plasma adrenaline concentration (403 +/- 69 compared with 73 +/- 29 pg ml-1 for saline- and DSAP-treated rats), but did not alter the magnitude of the adrenaline response to restraint. The data suggest that NTS catecholaminergic neurons normally inhibit the arterial pressure response, but help maintain the corticosterone response to restraint stress.