Experiments were performed on three groups of rats. The first group consisted of sodium loaded (SL) rats (high sodium diet, 10 meq Na/day, the second group consisted of sodium restricted (SR) rats (low sodium diet, 0.7 meq Na/day) and the third group consisted of hemorrhagic rats (HR), which were bled with 1-1,5% of the body weight. Blood pressure, glomerular filtration rate (GFR) and sodium excretion were measured. In some animals renal blood flow (RBF) was recorded with an electromagnetic flow meter. Adenosine was injected or infused into the thoracic aorta. Bolus injection of 10 nmoles adenosine resulted in a rapid and marked decrease of RBF (40%) in SR rats whereas in SL rats only a very small decrease of RBF (2%) was observed. Continuous infusion of adenosine (10(-7) moles/min) decreased GFR by 54% in SR rats and by 33% in HR rats, whereas GFR in SL rats did not change significantly. 5'-AMP decreased GFR in SR rats by 18% and in HR rats by 32%. Adenosine and 5'-AMP caused a slight fall in the systemic blood pressure, but this decrease could not account for the decrease of GFR. The sensitivity of kidney vasculature to adenosine parallelled high plasma renin activity (162 ng ang/ml-h in SR and 76 ng ang/ml-h in HR), elevated renal vascular resistance and low GFR. Simultaneous infusion of angiotensin (Hypertensin), 250 ng/min, in SL rats resulted in an increase of sensivity to adenosine infusion: GFR decreased by 21%. Our experiments demonstrated that a marked renal vasoconstriction caused by adenosine only occurs in rats in which renin-angiotensin system was stimulated.
The renal actions of the optically active isomers of the new diuretic drug ozolinone were studied by clearance, flowmeter and micropuncture techniques in rats. The levorotatory, but not the dextrorotatory isomer of ozolinone increased urine flow, urinary sodium and chloride excretion and enhanced sodium and chloride concentrations in early distal tubular fluid as checked by in situ microperfusion of Henle's loops. This indicates stereospecificity of the drug's diuretic action. However, both isomers of ozolinone equally inhibited maximal tubular secretion of paraaminohippurate and increased renal blood flow as measured by an electromagnetic flowmeter. Thus, the different renal target structures of ozolinone differ markedly with respect to stereoselectivity.
The criteria upon which diuretics are classified are based upon their site of action within the nephron. Carbonic anhydrase inhibitors act in the proximal tubule, high-ceiling diuretics in the ascending loop of Henle, the thiazides in the early distal tubule and the potassium-sparing diuretics in the late distal tubule and in the collecting duct. According to the localization of carbonic anhydrase acetazolamide acts on three different sites in the proximal tubule cells. The loop diuretics inhibit the secondary active chloride reabsorption. Experiments on the isolated stripped rabbit colon under the condition of stimulated chloride secretion reveal striking similarities between the receptors for chloride reabsorption in the luminal cell membranes of the ascending loop of Henle and in the serosal cell membranes of the colon. The potassium-sparing diuretics act by blocking sodium channels in the distal parts of the nephron. The lumen negative potential difference decreases and potassium secretion is diminished.
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