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1 Vascular Biology Center, Medical College of Georgia, Augusta, GA, USA; Department of Physiology, Medical College of Georgia, Augusta, GA, USA
2 Vascular Biology Center, Medical College of Georgia, Augusta, GA, USA; Department of Physiology, Medical College of Georgia, Augusta, GA, USA; Department of Pharmacology, Medical College of Georgia, Augusta, GA, USA
3 Vascular Biology Center, Medical College of Georgia, Augusta, GA, USA; Department of Physiology, Medical College of Georgia, Augusta, GA, USA; Department of Surgery, Medical College of Georgia, Augusta, GA, USA
* To whom correspondence should be addressed. E-mail: gdangelo{at}mail.mcg.edu.
Clinical studies have documented an abrupt rise in plasma endothelin-1 (ET-1) coincident with an increase in mean arterial pressure (MAP) during the response to acute stress. Because ET-1 has been implicated as a mediator of salt-sensitive hypertension, we examined the ETA and ETB receptor-dependent effects of ET-1 on the pressor response to acute environmental stress in ET-1-dependent hypertension. Stress was induced by restraint and administration of air jet pulses (3 minutes) in ETB receptor deficient (ETBsl/sl) rats maintained on diets containing normal salt (NS; 0.8% NaCl), high salt (HS; 8% NaCl), and HS plus the ETA receptor antagonist ABT-627 (5 mg/kg/day) on successive weeks. MAP and heart rate (HR) were chronically monitored by radiotelemetry. Total pressor response as determined by the area under the curve was significantly reduced in ETB sl/sl rats maintained on a HS vs. NS diet (-6.8±18.7 vs. 29.3±8.1 mmHg x 3 min, p<0.05). Conversely, the total pressor response was augmented in both wild-type (34.2±29.2 mmHg x 3 min, p<0.05 vs. NS) and ETB sl/sl rats (49.1±11.8 mmHg x 3 min, p<0.05 vs. NS) by the ETA receptor antagonist ABT-627. Blockade of ETB receptors in Sprague-Dawley rats caused an increase in basal MAP that was enhanced by HS and lowered by mixed ETA/ETB receptor antagonism; none of these treatments, however, had any effect on the pressor response. These data demonstrate that increasing endogenous ET-1 suppresses the pressor response to acute stress through ETA receptor activation in a genetic model of ET- 1-dependent hypertension. These results are consistent with reports that ET-1 can attenuate sympathetically mediated responses.
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