抄録
We have previously demonstrated that the peripheral vasopressin system participates in the control of renal sympathetic nerve activity (RSNA) and Fos-like immunoreactivity (FLI), as a neuronal marker, in the paraventricular nucleus of the hypothalamus, via the vasopressin V1 receptor during central salt loading in conscious rats. However, it is important to examine the [Na+] near the osmosensitive region during central salt loading and determine whether or not the stimulation has physiological relevance. The [Na+]CSF electrode was prepared using a modification of a previous procedure [Nose H, et al., J. Appl. Physiol., 73 (1992)]. The tip of the double-barreled Na+-electrode was located at AP = -2.8, L = 0.9, V = 7.5 mm, lateral angle = 7.5; using a 22-mm 18-gauge stainless steel guide cannula. Rats were administered infusions of 0.15, 0.3, 0.67, and 1.0 M HS (hypertonic saline) at 1 μl/min for 20 min into the left LV under anesthesia, and changes in [Na+]CSF in the V3 were measured. For the 0.3, 0.67, and 1.0 M HS groups, the increase in [Na+]CSF reached the maxima (13.7 ± 1.2, 59.9 ± 3.8, and 89.7 ± 7.0 mEq/kg H2O) at 16, 12, and 20 min, respectively. The changes in cerebrospinal fluid [Na+] during i.c.v. administration of 0.3 M hypertonic saline were compatible with those expected for thermal dehydration. This smaller than predicted increase (38.8, 134.7, and 220.1 mEq/kg H2O, respectively) in [Na+]CSF might be due to rapid buffering by free water movement from extraventricular spaces in response to the osmotic gradient. [Jpn J Physiol 54 Suppl:S212 (2004)]
