EFFECT OF BARORECEPTOR ACTIVATION AND SYSTEMIC HYPOTENSION ON PLASMA ENDOTHELIN-1 AND NEUROPEPTIDE-Y

To determine whether endothelin (ET-1) and neuropeptide Y (NPY) releas e are controlled by the carotid sinus (CS) baroreceptor or local endot helial mechanisms, we isolated and pump perfused the CS in eight chlor alose-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 p ressure was varied (control, 2.08 +/- 0.50; low CS, 2.18 +/- 0.51; hig h CS, 2.11 +/- 0.38 pg/mL), but ET-1 was significantly higher during l ow 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 consta nt in four dogs. In contrast, plasma NPY was significantly higher in t he 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 hypotensi on. In conclusion, NPY, but not ET-1, is affected by CS baroreceptor m anipulation, and plasma ET-1 increases in response to hemorrhagic hypo tension when modulating reflexes are abolished.