Effect of baroreceptor activation and systemic hypotension on plasma endothelin 1 and neuropeptide Y

Abstract

To determine whether endothelin (ET-1) and neuropeptide Y (NPY) release are controlled by the carotid sinus (CS) baroreceptor or local endothelial mechanisms, we isolated and pump perfused the CS in eight chloralose-anesthetized dogs and controlled systemic arterial pressure (SAP) with an elevated reservoir connected to both femoral arteries. This allowed the SAP to be kept constant while CS pressure was varied from 55.8 ± 2.0 (low CS) to 192 ± 1.9 (high CS) mmHg (1 mmHg = 133.3 Pa) or CS pressure to be kept constant while SAP was lowered to 53.9 ± 1.8 mmHg (low SAP). There was no significant change in ET-1 when CS pressure was varied (control, 2.08 ± 0.50; low CS, 2.18 ± 0.51; high CS, 2.11 ± 0.38 pg/mL), but ET-1 was significantly higher during low SAP (2.93 ± 0.49 pg/mL, p < 0.05). This increase was not observed with vagi and CS intact in six dogs or with vagi intact and CS constant in four dogs. In contrast, plasma NPY was significantly higher in the low CS condition (619.13 ± 66.87 pg/mL) versus high CS condition (528.88 ± 45.19 pg/mL, p < 0.05) and did not change during hypotension. In conclusion, NPY, but not ET-1, is affected by CS baroreceptor manipulation, and plasma ET-1 increases in response to hemorrhagic hypotension when modulating reflexes are abolished.Key words: endothelin 1, neuropeptide Y, carotid sinus baroreceptor, hemorrhage, cardiac output.