Abstract

To determine effects of OVLT lesions on pressor and sympathetic responses to central hyperosmolality, rats were anesthetized and mean arterial pressure (MAP) and renal sympathetic nerve activity (SNA) were recorded. NaCl solutions (150, 375 and 750 mM) were injected (150 μl) via an internal carotid artery and MAP and renal SNA responses were recorded before, 15 and 60 min after lesioning (500 μA, 45 s) the OVLT (n=6). The location of OVLT was mapped by stimulus (0.5 Hz, 1 ms, 150 μA)-triggered averaging of renal SNA. Before lesion, hypertonic, but not isotonic, NaCl increased MAP (375 mM 11± 2.6 mmHg, 750 mM 21±2.2 mmHg) and renal SNA (375 mM 184±14%, 750 mM: 209±12%) (P<0.001 vs 150 mM). After lesion, renal SNA responses were reduced (P<0.001 vs 150 mM) at 15 min (375mM 135 ± 4%, 750mM 176±7%) and 60 min (375mM 132±8%, 750mM 166±8%). MAP responses were not significantly altered. To exclude a role for ‘fibers en passage’, the OVLT was inactivated with muscimol (100 pmol, 50 nl) (n=4). Before muscimol, hypertonic NaCl increased MAP (375mM 8±3.9 mmHg, 750mM 17±2.8 mmHg) (P<0.05), renal SNA (375mM 147±4%, 750mM 176±10%) and lumbar SNA (375mM 184±23%, 750mM 209±30%) (P<0.001). After muscimol, renal SNA (375mM 119±7%, 750mM 141±12%) and lumbar SNA (375mM 132±9%, 750mM 145±2%) responses were reduced at 15 and 60 min (P<0.001). Again, MAP responses were not altered. Since ICA NaCl elicited consistent responses in sham controls, it appears that lesions/microinjections were effective due to interruption of OVLT activity. We conclude that elevated SNA in response to central hyperosmotic NaCl depends, in part, on OVLT neurons. Support HL071645

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