Key result
Injections of hyperosmotic solutions into the anteroventral third ventricle of rats resulted in short latency drinking, antidiuretic, and pressor responses, with neural substrates distinct from angiotensin.
Hypothesis-generating for central osmotic control of thirst and pressor responses; leaves open translation to human cardiovascular disease.
Injections of hyperosmotic solutions (1- to 5-microliter injections of NaCl or sucrose solutions ranging in osmolarity from 0.34 to 0.90 osmol/l) into the anteroventral third ventricle (AV3V) of rats resulted in short latency drinking antidiuretic, and pressor responses. AV3V injections or infusions of combined angiotensin-hyperosmotic NaCl solution did not result in drinking greater than the sum of drinking to angiotensin and hyperosmotic NaCl separately administered. Differences in water versus saline drinking fluid preferences provided a behavioral dissociation of angiotensin and hyperosmotic sensitive neural mechanisms. Comparison of AV3V and lateral preoptic injection sites provided an additional separation since angiotensin was equally effective at both sites whereas osmotic stimulation was more effective at the AV3V site. AV3V lesions have previously been reported to abolish drinking, antidiuretic, and pressor responses to angiotensin and hyperosmotic stimulation. The data reported here provide additional evidence that angiotensin and hyperosmotic stimuli may both act on tissue surrounding AV3V but suggest that the neural substrates for these stimuli are not identical.
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Buggy et al. (1979) studied this question. Injections of hyperosmotic solutions (NaCl or sucrose) and/or angiotensin vs. Separate administration or lateral preoptic injection sites was evaluated on Drinking, antidiuretic, and pressor responses. Injections of hyperosmotic solutions into the anteroventral third ventricle of rats resulted in short latency drinking, antidiuretic, and pressor responses, with neural substrates distinct from angiotensin.
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