Abstract
Accumulating evidence indicates that the vasopressin (VP) is locally released within the supraoptic and paraventricular (PVN) nuclei, autoregulating VP neuronal activity. Here, we tested if intranuclear VP release also influences presympathetic PVN neuronal activity. Patch‐clamp recordings from presympathetic PVN‐RVLM neurons showed that focal application of VP (1µM) evoked an inward current (~8pA, P< 0.002), depolarized Vm (4mV, P< 0.0001), and increased PVN‐RVLM firing activity (~780%, P< 0.0001), effects blocked by a V1a receptor antagonist. The expression of V1a receptors in PVN‐RVLM neurons was confirmed immunohistochemically. V1a receptor blockade hyperpolarized Vm (~4mV, P< 0.001) and reduced ongoing firing activity of PVN‐RVLM neurons (~70%, P< 0.002). VP excitatory effect on PVN‐RVLM neurons was blocked by rapid chelation of intracellular Ca2+ (P< 0.02), but was not dependent on an influx of extracellular Ca2+. Finally, the effect of endogenously released VP was dependent on the activity of endogenous aminopeptidases. In summary, our results indicate that endogenously released VP, likely from a magnocellular neurosecretory source, tonically excites presympathetic PVN neurons, constituting a functionally relevant intercellular signaling pathway in the generation of homeostatic patterns of neuroendocrine and autonomic activities by the PVN. Supported by NIH HL68725
Published Version
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