The effect of glycerol-induced acute renal failure upon cardiac reactivity in the rat: influence of indomethacin treatment and renal pedicle ligation.

Cardiac chronotropic responses to isoprenaline, carbachol and electrical stimulation of the cervical sympathetic and vagal nerves were recorded in rats with glycerol-induced acute renal failure (ARF) and control rats. The experiments involving electrical stimulation of cardiac nerves were performed in rats which either had been pretreated with indomethacin (1 mg kg-1 twice daily for 2 days) or had undergone acute bilateral renal pedicle ligation. The findings from this investigation indicate that the reduced chronotropic responses to vagal stimulation in rats with glycerol-induced ARF are due to a reduction in acetylcholine release mediated by prostaglandins possibly originating from the damaged kidneys. The diminished response to cervical sympathetic stimulation results from a decreased postsynaptic response to beta-adrenoceptor stimulation.

Vascular reactivity in experimental acute renal failure.

Vascular reactivity in-vivo and in-vitro was examined in rats with acute renal failure produced by bilateral nephrectomy or intramuscular glycerol injection. Bilaterally nephrectomized rats displayed enhanced pressor responses to noradrenaline and angiotensin. However, the contractile responses to noradrenaline, angiotensin and potassium chloride of aortic rings and portal vein segments from nephrectomized rats were not significantly different from the responses obtained in vessels from sham-operated controls. Rats with glycerol-induced ARF which were pretreated with indomethacin had significantly lower pressor responses to noradrenaline and angiotensin than similarly treated control animals. Aortic rings from glycerol-injected rats produced significantly smaller contractions to noradrenaline than preparations from controls. This difference was not abolished by incubation of vessels with indomethacin. The findings suggest that the absence of kidneys or the presence of damaged renal tissue and not uraemia itself have pronounced but opposite effects on vascular reactivity. The depression of vascular reactivity in glycerol-induced ARF does not appear to be a result of increased production of prostaglandins.