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1 Physiology and Pharmacology, Oregon Health & Science University, Portland, OR, USA
* To whom correspondence should be addressed. E-mail: brooksv{at}ohsu.edu.
To test the hypothesis that high osmolality acts in the brain to chronically support mean arterial pressure (MAP) and lumbar sympathetic nerve activity (LSNA), the osmolality of blood perfusing the brain was reduced in conscious water deprived and water replete rats by infusion of hypotonic fluid via bilateral non-occluding carotid (ic) catheters. In water deprived rats, the ic hypotonic infusion, estimated to lower osmolality by ~2%, decreased MAP by 9±1 mmHg and LSNA to 86±7% of control; heart increased by 25±8 bpm (all P<0.05). MAP, LSNA and heart rate did not change when the hypotonic fluid was infused iv. The ic hypotonic fluid infusion was also ineffective in water replete rats. Prior treatment with a V1 vasopressin antagonist did not alter the subsequent hypotensive and tachycardic effects of ic hypotonic fluid infusion in water deprived rats. In summary, acute decreases in osmolality of the carotid blood of water deprived, but not water replete, rats decreases MAP and LSNA and increases heart rate. These data support the hypothesis that the elevated osmolality induced by water deprivation acts via a region perfused by the carotid arteries, presumably the brain, to tonically increase MAP and LSNA and suppress heart rate.
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