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1 Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR, USA
* To whom correspondence should be addressed. E-mail: brooksv{at}ohsu.edu.
Water deprivation is associated with regional increases in sympathetic tone, but whether this is mediated by changes in brainstem regulation of sympathetic activity is unknown. Therefore, this study tested the hypothesis that water deprivation increases excitatory amino acid (EAA) drive of the rostral ventrolateral medulla, by determining if bilateral microinjection of kynurenate (KYN; 2.7 nmol) into the RVLM decreases arterial pressure more in water-deprived compared to water-replete rats. Plasma osmolality was increased in 48 hr water deprived rats (313±1 mOsm/Kg H2O; P<0.05) compared to 24 hr water deprived rats (306±2 mOsm/Kg H2O) and water replete animals (300±2 mOsm/Kg H2O). KYN decreased arterial pressure by 28.1±5.2 mmHg (P<0.01) in 48 hr water-deprived rats, but had no effect in water-replete rats (-5.9±1.3 mmHg). Variable depressor effects were observed in 24 hr water-deprived animals (-12.5±2.4 mmHg, ns); however, in all rats the KYN depressor response was strongly correlated to the osmolality level (P<0.01; r2=0.47). The pressor responses to unilateral microinjection of increasing doses (0.1, 0.5, 1.0, 5.0 nmol) of glutamate were enhanced (P<0.05) during water deprivation, but the pressor responses to iv phenylephrine injection were smaller (P<0.05). These data suggest that water deprivation increases EAA drive to the RVLM, in part by increasing responsiveness of the RVLM to EAA such as glutamate.
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