Organum vasculosum laminae terminalis contributes to increased sympathetic nerve activity induced by central hyperosmolality

Abstract

The contribution of the organum vasculosum laminae terminalis (OVLT) in mediating central hyperosmolality-induced increases of sympathetic nerve activity (SNA) and arterial blood pressure (ABP) was assessed in anesthetized rats. Solutions of graded NaCl concentration (150, 375, and 750 mM) were injected (150 μl) into the forebrain vascular supply via an internal carotid artery (ICA). Time-control experiments ( n = 6) established that ICA NaCl injections produced short-latency, transient increases of renal SNA (RSNA) and mean ABP (MAP) ( P < 0.05–0.001). Responses were graded, highly reproducible, and unaltered by systemic blockade of vasopressin V1 receptors ( n = 4). In subsequent studies, stimulus-triggered averaging of RSNA was used to accurately locate the OVLT. Involvement of OVLT in responses to ICA NaCl was assessed by recording RSNA and MAP responses before and 15 min after electrolytic lesion of the OVLT ( n = 6). Before lesion, NaCl injections increased RSNA and MAP ( P < 0.05–0.001), similar to time control experiments. After lesion, RSNA responses were significantly reduced ( P < 0.05–0.001), but MAP responses were unaltered. To exclude a role for fibers of passage, the inhibitory GABA-A receptor agonist muscimol was microinjected into the OVLT (50 pmol in 50 nl) ( n = 6). Before muscimol, hypertonic NaCl increased RSNA, lumbar SNA (LSNA), and MAP ( P < 0.05–0.001). After muscimol, both RSNA and LSNA were significantly reduced in response to 375 and 750 mM NaCl ( P < 0.05). MAP responses were again unaffected. Injections of vehicle (saline) into OVLT ( n = 6) and muscimol lateral to OVLT ( n = 5) each failed to alter responses to ICA NaCl. We conclude that OVLT neurons contribute to sympathoexcitation by central hyperosmolality.