Effect of DOCA/salt hypertension on CRF expression in the amygdala and the autonomic stress response in conscious rats

- The cardiovascular response to stress was evaluated in DOCA/salt hypertension.
- Stress-related pressor responses were similar in DOCA/salt and controls.
- Stress-induced tachycardia was significantly altered by DOCA/salt hypertension.
- Baroreflex function increased after stress offset in normotensive controls only.
- Amygdaloid CRF gene expression was significantly reduced in DOCA/salt hypertension.

The effects of DOCA/salt treatment on amygdala-area CRF gene expression and the autonomic response to air jet stress (AJS) were evaluated in conscious male Sprague Dawley (SD) rats. Fifteen days of DOCA/salt treatment significantly increased resting arterial pressure (AP), decreased resting heart rate (HR) and significantly reduced regional CRF mRNA compared to controls (23 ± 7% vs. 100 ± 26%) independent of changes in regional CRF receptor expression. Twenty min of AJS elicited a rise in AP (~ 15 mm Hg) that was similar in both DOCA/salt animals (n = 11) and controls (n = 6). Alternatively, increases in HR were significantly different in the DOCA/salt animals compared to controls; including one group of DOCA/salt animals (n = 5) which responded with an attenuated HR response at the onset of AJS (low-responders) and a second group (n = 6) which demonstrated an elevated HR response to AJS (high-responders), specifically during the last 10 min of AJS. The divergent HR responses to AJS in the DOCA/salt animals were linked to differences in resting heart rate variability. During recovery HR returned to baseline within 10 min in both control and the low responder DOCA group but indicators of spontaneous baroreflex gain only increased significantly in controls. HR in the high-responder DOCA animals did not return to baseline during the same period. These results show that DOCA/salt treatment triggers downregulation of CRF gene expression in the region of the amygdala and significantly alters the HR response to acute stress but does not alter the pressor response to stress compared to normotensive controls.