Abstract
Several studies have shown that changes in plasma osmolality have an influence on the sympathetic nervous system, and that hypothalamic areas such as the paraventricular nucleus (PVN) play a significant role in these homeostatic adjustments. The aim of this study was to assess the role of the PVN in regulating sympathetic outflow in response to physiological hyperosmotic stimuli in a novel in situ decorticated arterially perfused preparation of rat. Rats (70–90g) were anaesthetised with halothane and decorticated, which included removal of the thalamus. The systemic osmotic stimulus was delivered by changing the perfusate (Ringer’s solution) from isotonic (290 mOsmol) to hypertonic (320 mOsmol) over 40s. This stimulus caused an increase in lumbar sympathetic nerve activity (LSNA; 29.3±5 %, n=10), which persisted until the isotonic perfusate was re-introduced. Following ablation of the hypothalamic paraventricular nucleus (PVN) hyperosmotic-induced sympatho-excitation was blunted in magnitude (11±3%, n=6). Bilateral PVN microinjections of either isoguvacine (60 nmol/60nl), for reversible inactivation, or blockade of ionotropic glutamate receptors (kynurenic acid; 6 μmol/60nl) both attenuated the hypertonic-induced increase in LSNA to 7±2% and 8±3%, respectively, from control (25±2%, n=5). In conclusion, we have demonstrated that the in situ preparation demonstrates appropriate responses to physiologically relevant osmolality changes as seen in vivo during acute salt-loading. Moreover, the PVN plays a major role in hyperosmotic-induced sympatho-excitation. British Heart Foundation funded research
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