EFFECTS OF A SHORT-TERM HINDLIMB SUSPENSION ON CENTRAL AND PERIPHERAL NOREPINEPHRINE TURNOVER IN RATS

The loss of appropriate cardiovascular reflexes which contributes to the cardiovascular deconditioning observed after an exposure to actual or simulated microgavity (in man or animals) is well known, but the mechanisms responsible remain unclear. This protocol, a 2.5 h hindlimb suspension in rats, was undertaken to study the early adaptation of the sympathetic neurons involved in arterial pressure regulation: we determined central norepinephrine (NE) turnover in the brainstem catecholaminergic cell groups responsible for the central cardiovascular regulation i.e. A1, A2 (rostral and caudal), A5 and A6 cell groups and peripheral NE turnover in target organs (heart and kidneys). The NE turnover in suspended rats significantly decreased in rostral A2 (48% p<0.001), caudal A2 (52% p<0.001) and A5 (40% p<0.05) cell groups while it was unchanged in Al and A6 cell groups compared with rats attached to the suspension device but maintained in the horizontal position. The short term hindlimb suspension did not alter the NE turnover in cardiac atria and ventricles or in kidneys nor did it alter the blood variables studied (hematocrit, osmolality, plasma sodium, potassium, proteins and renin concentration). We concluded that a 2.5 h hindlimb suspension reduced noradrenergic neuron activity in A2 and A5 cell groups involved in the central control of arterial pressure and particularly in the baroreceptor reflex mechanisms. This duration was probably not sufficient to modify the NE turnover in the two peripheral organs studied.