Baroreceptor inhibition of respiration in conscious rats infused with phenylephrine (PE) or angiotensin II (ANG II)

The study was designed to determine 1) if ANG II acts centrally to stimulate ventilation, thus countering baroreflex inhibition of ventilation and, 2) to test the comparative thresholds for cardiac and respiratory baroreceptor reflexes between PE and ANG II infusions. Ventilation, metabolism, mean arterial blood pressure (MAP) and heart rate (HR) were monitored in male Sprague-Dawley rats during infusion doses of PE and ANG II to raise MAP to 40 mm Hg. Following a 20 min control saline infusion, the presser agent was infused for 60 rain. In the first 40 min MAP was increased and then, while the presser infusion was maintained, MAP was returned to the control level with sodium nitroprusside (SNP). Infusion of PE at doses raising MAP 20 and 40 mm Hg caused equal increases in ventilation and metabolism but HR was progressively decreased. The addition of SNP to the PE infusion returned MAP to control levels causing the teflex bradycardia to be abolished while the increased ventilation and metabolism were sustained. Ventilation was not stimulated by infusions of ANG II (MAP +40 mm Hg) nor was there bradycardia. When ANG II was infused with MAP at control levels, there was no stiàulation of ventilation nor was there a significant increase in HR. Unlike dogs, 1) ANG II does not stimulate ventilation in rats and 2) rats have a higher threshold for the baroreceptor pressor reflex. Supported by MRC (Canada) and the OTS.

Duke Scholars

Author Julia K.L. Walker School of Nursing