各種β-遮断剤の腎動脈内投与によるレニン分泌ならびに腎機能におよぼす影響について
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Dogs were sodium depleted by feeding specially designed low-salt diet for 5-7 days as well as giving intramuscular injections of Furosemide (20 mg) on the first day. Normal dogs were given commercially available solid food. Effects of intrarenal arterial administration (IRA) of pindolol, a blocker of the beta-1 and beta-2, practolol, a specific beta-1 blocker, and isoproterenol, a stimulant of both beta-1 and beta-2 were studied using these experimental dogs anesthetized with pentobarbital sodium. Apart from other parameters, plasma renin activity (PRA) was measured by radioimmunoassay. (1) Sodium depletion increased heart rate (HR) and PRA, but decreased renal arterial pressure (RPA), renal blood flow (RBF), urine flow (UR) and urinary sodium excretion. These changes were significant when compared with the findings in normal dogs. (2) Pindolol (0.2μg/kg/min, IRA) and practolol (priming dose 10μg/kg, sustaining dose 10μg/kg/hr, IRA) caused slight decreases in RAP, RBF, glomerular filtration rate (GFR), UF and urinary excretion of sodium and potassium, but did not influence PRA in neither normal nor sodium depleted dogs. (3) In the normal dogs, isoproterenol (0.02μg/kg/min, IRA) lowered RAP but increased HR slightly. It augmented RBF, UF, urinary excretion of sodium and potassium and PRA, but did not induce any change in GFR. (4) In the normal dogs pretreated with practolol (priming dose 10μg/kg, sustaining dose 10μg/kg/hr, IRA), the blocking agent did not practically act antagonistic against isoproterenol (0.02μg/kg/min, IRA) only to prohibit HR increase. Again in the normal dogs pretreated with pindolol (0.2μg/kg/min, IRA) all the stimulating effects of isoproterenol (0.02μg/kg/miri, IRA), i.e. on HR RBF, UF, urinary excretion of sodium and potassium and PRA were blocked completely. The above findings suggest that beta blocking agents do not inhibit renin release accelerated by sodium depletion, and that an increase in renin secretion and diuretic action by isoproterenol is performed through the beta-2 receptor.
- 1978-11-20
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