Properties of the macula densa mechanism for renin release in the dog

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Abstract
To study the macula densa mechanism for renin release, both the macula densa and the haemodynamic mechanisms were activated in anaesthetized dogs with denervated kidneys, either by renal arterial constriction to a renal arterial pressure (RAP) of 52 ±2 mmHg or by ureteral occlusion to a ureteral pressure of 95–105 mmHg, 20–25 mmHg below RAP. Renal arterial constriction increased renin release from 0.3+0.2 to 16 + 4 μg AI min‐1. At low RAP, renin release was subsequently reduced to 7 ± 3 μ AI min‐1when sodium excretion was raised far above control values by plasma volume expansion and acetazolamide infusion. Ethacrynic acid (3 mg kg‐1body wt.) restored renin release to pre‐expansion values, and a large dose (25 mg kg‐1body wt.) prevented renin release from falling even after unclamping the artery. During ureteral occlusion with stopped glomerular filtration, plasma volume expansion, acetazolamide and ethacrynic acid infusion did not alter renin release. On the other hand, β‐adrenergic stimulation by isoproterenol raised renin release equally (by 30–40 μg AI min‐1) before and after plasma volume expansion, during both renal arterial constriction and ureteral occlusion. Indomethacin (10 mg kg‐1body wt.) abolished renin release induced by ethacrynic acid infusion and ureteral occlusion. We conclude that the macula densa mechanism for renin release is inactivated by high NaCl reabsorption during plasma volume expansion and acetazolamide infusion, reactivated by inhibition of NaCl reabsorption with ethacrynic acid and completely inhibited by indomethacin. The degree of activation does not influence the renin release induced by β ‐adrenergic stimulation.