Vascular reactivity in rats with glycerol-induced acute renal failure.
The vascular reactivity of rats with glycerol-induced acute renal failure was assessed in vitro and in vivo. The contractile responses to noradrenaline, angiotensin and potassium chloride of aortic strips and portal vein segments from uraemic rats were significantly smaller than the responses obtained in vessels from control animals. The pressor responses to angiotensin were reduced significantly in rats with acute renal failure when compared to those in control rats. The reduced vascular responses to a range of spasmogens suggests that in this model of renal failure there is a defect in some mechanism of vascular contraction common to all three constrictor agents.
D058186:Acute Kidney Injury / Q000503:physiopathology*; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D005990:Glycerol / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D014508:Urea / Q000097:blood; D014661:Vasoconstriction / Q000187:drug effects*
D000804:Angiotensin II; D011189:Potassium Chloride; D014508:Urea; D005990:Glycerol; D009638:Norepinephrine