Abstract
The paraventricular nucleus (PVN) plays a critical role in both renal sympathetic nerve activity (RSNA) and vasopressin (AVP) secretion by the neurohypophysis. AVP is also released from dendrites of magnocellular neurons within PVN. In addition to V1a receptors, data indicate V1b receptors are present on PVN neurons. We tested the hypothesis that inhibition of V1b receptors within the PVN inhibits increases in mean arterial pressure (MAP) and RSNA induced by AVP injection into PVN. Male Sprague Dawley rats were instrumented. Studies were performed in awake unrestrained rats at least 24 hr after recovery from anesthesia. Baseline MAP, heart rate or RSNA did not differ among the groups. Microinjection of 100 ng AVP into the PVN increased MAP from 138.2 ± 3.1 (baseline) to 151.0 ± 3.2 mmHg (10 min, P<0.01). RSNA increased 47 ± 6.6%baseline (P<0.01). Pre‐injection with 100 ng of the V1b blocker nelivaptan significantly inhibited the pressor, tachycardic and RSNA responses (P<0.05 vs control). Experiments performed after ganglionic blockade with chlorisodamine indicate that the pressor response to central AVP is also in part due to an increase in plasma AVP. Vehicle did not block any of the responses. These findings support the concept that V1b receptors within PVN may be activated by dendritic release of AVP that stimulates both RSNA and peripheral release of AVP.
Published Version
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