In 14 anesthetized dogs (control group) and 7 anesthetized dogs treated by Hexamethonium bromide (Hexa group), arterial carbondioxide tension (PaCO
2), blood pH; renal plasma flow (RPF), renal blood flow (RBF), glomerular filtration rate (GFR), renal blood pressure (RBP) and renal vascular resistence (RVR) were measured before and during inhalation of 5% and 15% CO
2. Cardiac output was observed in the control group. In the control group, moderate respiratory acidosis caused vasodilatation as evedenced by increase in RPF, . RBF and GFR, and a decrease of RVR. Severe respiratory acidosis caused vasoconstriction as evidenced by decrease in RPF, RBF and GFR, and an increase of RVR. Cardiac output remained relatively unchanged during CO
2 inhalation. In the Hexa group, inhalation of 5% CO
2 caused increase in RPF, RBF and GFR and a decrease of RVR. Hexamethonium bromide did not block renovascular dilatation in such a moderate respiratory acidosis. Inhalation of 15% CO
2 in this group produced marked increases in RPF and RBF, and decreases in GFR and RVR; renovascular constriction observed in the control group was abolished by hexamethonium bromide. This observation confirms positive participation of sympathoadrenal mechanisms in regulation of renovascular responses and renal functions in respiratory acidosis.
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