1. Micropuncture studies were performed in dogs to evaluate more directly the suggestion from clearance experiments that alpha-adrenergic stimulation enhances and beta-adrenergic stimulation depresses proximal sodium reabsorption. Experiments were performed during unilateral renal artery infusion of the appropriate drugs in the doses used in previous clearance studies.

2. To study pure beta stimulation, collections were made during alpha blockade with phenoxybenzamine and re-collections during the addition of beta stimulation with isoproterenol. No significant changes were noted in the ratio of inulin concentrations in tubular fluid and plasma (TF/P)In (1·49 ± 0·04 to 1·52 ± 0·05), absolute sodium reabsorption (23 ± 1 to 23 ± 3 nl/min), single nephron glomerular filtration rate (SNGFR) (75 ± 7 to 76 ± 15 nl/min) and the ratio of SNGFR to inulin clearance (SNGFR/CIn) × (106), (2·95 ± 0·4 to 2·65 ± 0·4).

3. To study pure alpha-adrenergic stimulation, collections were made during beta blockade with propranolol and again during the addition of alpha-adrenergic stimulation with nor-adrenaline. There were no significant changes in (TF/P)In (1·50 ± 0·09 to 1·42 ± 0·04), absolute sodium reabsorption (25 ± 7 to 17 ± 4 nl/min), SNGFR (68 ± 13 to 58 ± 10 nl/min) or SNGFR/CIn(× 106) (2·76 ± 0·6 to 2·51 ± 0·5).

4. CIn increased slightly after beta but not after alpha stimulations. p-Aminohippuric acid clearance (CPAH) and urine sodium excretion (UNaV) were not significantly different in either set of studies.

5. We conclude that neither alpha not beta adrenergic stimulation has a significant effect on proximal sodium reabsorption when infused in doses that do not alter renal haemodynamics.

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