Experimental 'jet lag' causes sympathoexcitation via oxidative stress through AT1 receptor in the brainstem.

Circadian disruptions through frequent transmeridian travel, rotating shift work, and poor sleep hygiene are associated with an array of physical and mental health maladies, including the abnormal autonomic nervous system. We have demonstrated that the oxidative stress through AT(1) receptor in the brain activates sympathetic nervous system. The aim of the present study was to determine whether experimental 'jet lag' causes sympathoexcitation via oxidative stress through AT(1) receptor in the cardiovascular center of the brainstem (rostral ventrolateral medulla; RVLM) or not. Experimental 'jet lag' was made to normotensive (Wister-Kyoto rat; WKY rat) and hypertensive rats (stroke-prone spontaneously hypertensive rats; SHRSP) by the exposure to a 12 hour phase advance for 5 days. In WKY, 'jet lag' increases blood pressure and the activity of sympathetic nervous system via oxidative stress through angiotensin II type 1 receptor in the RVLM for 2 days only, and the changes are improved at 3 day after the initiation of 'jet lag'. In SHRSP, 'jet lag' also increases blood pressure and the activity of sympathetic nervous system via oxidative stress through angiotensin II type 1 receptor in the RVLM, and the changes are greater compared to those in WKY, and are maintained for the period of 'jet lag'. These results suggest that experimental 'jet lag' causes sympathoexcitation via oxidative stress through AT(1) receptor in the brain, especially in hypertension.