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R E Cronin

Publications and source records attributed to R E Cronin.

40 records · Page 3Linked to original sources

Effect of beta-adrenergic blockade and inhibitors of angiotensin II and prostaglandins on renal autoregulation.

The role of the renin-angiotensin system and prostaglandins in renal autoregulation was investigated in dog kidneys in situ. Renal autoregulation during decreases in renal arterial pressure (RAP) was examined in animals pretreated with a competitive antagonist of angiotensin ii, [1-sarcosine, 8-glycine] angiotensin II, or one of two chemically dissimilar inhibitors of prostaglandin synthetase, indomethacin and meclofenamate. Because of recent evidence suggesting a role for an intrarenal beta receptor in regulating renin release, renal autoregulation was also examined in animals treated with the beta-adrenergic blocking agent propranolol. In all groups of animals constancy of glomerular filtration rate (GFR) and renal blood flow (RBF) was observed after substantial decreases in RAP to a range of 70-90 mmHg. These studies therefore do not provide evidence in support of a role for angiotensin II, prostaglandins, or an intrarenal beta receptor as mediators of the renal autoregulation of GFR or total RBF.

Angiotensin II↗

Role of solute excretion in prevention of norepinephrine-induced acute renal failure.

Infusion of 0.75 μ g/kgbw/min norepinephrine (NE), for 40 minutes, into one renal artery in anesthetized dogs, induced acute renal failure (ARF). Subsequently there was nearly complete reversal of function within 8 weeks. Isotonic saline volume expansion, or renal vasodilation plus diuresis by acetylcholine (into renal artery: 20 μg/min) did not protect against this type of ARF. Volume expansion with either 5 or 20 percent mannitol partly prevented the fall of GFR 3 hours after NE, this protection being correlated with the magnitude of the osmolar clearance at the time of the insult. IV furosemide (10 mg/kg + 10 mg/kg/h; fluid losses replaced) afforded an even better protection. Proximal tubular necrosis in the "protected" kidneys was as severe as in non-protected kidneys. Glomerular cell morphology (scanning electron microscopy) was not altered by the 40-minute NE infusions. Functional "protection" appeared to depend on solute diuresis at the time of insult.

Acetylcholine↗