1. Blood flow was measured in the renal cortex and medulla of anaesthetized rats by the hydrogen washout method. The effects of dopamine infusion were measured. 2. Low doses of dopamine (20 and 65 n‐mole.kg‐1.min‐1) caused only small increases in renal blood flow, and a higher dose (200 n‐mole.kg‐1.min‐1) caused vasoconstriction. After alpha‐blockade with phenoxybenzamine (9 mumole.kg‐1), all doses of dopamine caused vasodilatation in the cortex and medulla of the kidney. 3. This dopamine‐induced renal vasodilatation was almost abolished by sulpiride (0.7 mumole.kg‐1.min‐1), but was only slightly attenuated by propranolol (10 mumole.kg‐1). 4. Sulpiride did not significantly alter the renal blood flow responses to noradrenaline or isoprenaline, or the blood pressure responses to histamine, acetylcholine, 5HT, noradrenaline and isoprenaline. 5. In normal rats, infusion of sulpiride generally caused a reduction in renal cortical blood flow. This response showed a positive correlation with the initial blood pressure. 6. It is concluded that there are specific dopamine receptors in the renal vasculature of the rat, and that dopamine may play a role in the normal control of renal blood flow.

1. The effect of histidine and cysteine on the initial rate of zinc influx into rat and human erythrocytes in the presence of bovine serum albumin has been investigated. 2. The L-enantiomers of both amino acids promoted zinc influx into rat erythrocytes in a dose-dependent manner. L-Histidine, but not L-cysteine, also promoted zinc uptake into human erythrocytes. D-Histidine did not promote zinc uptake in either rat or human erythrocytes. In rat erythrocytes D-cysteine was significantly less effective than L-cysteine.3. The stimulation of zinc influx into rat erythrocytes by 20 mM L-histidine was approximately 4 1 times that seen with human erythrocytes. 4. The influx of zinc in the presence of varying concentrations of L-histidine was linearly related to the calculated concentration of the zinc-bis-histidine complex but not to that of the zinc-mono-histidine complex or the free ionic zinc concentration. 5. These results are discussed in relation to the nature of the transport mechanisms involved.

1. Histidine (2-40 mM) stimulated cadmium uptake into human erythrocytes incubated in the presence of 1 % bovine serum albumin to ensure that the free, ionic cadmium concentration was low. 2. The histidine-stimulated cadmium uptake correlated with the calculated concentration of the cadmium-bis-histidine complex rather than the cadmium-mono-histidine complex or free ionic cadmium. 3. The histidine stimulation of cadmium uptake was saturable and stereospecific. D-Histidine (10 mM) had no effect. 4. Cadmium and zinc were both able to inhibit 65Zn2+ uptake into erythrocytes incubated in the presence of 40 mM L-histidine. The relationships between the percentage inhibition of 65Zn2+ uptake and the calculated concentrations of cadmium-bis-histidine and zinc-bishistidine were very similar, which suggests that the metal histidine complexes compete for a common transport mechanism. 5. Pretreatment of the erythrocytes with N-ethylmaleimide using a protocol which is known to inhibit the system y+ amino acid transport mechanism had no effect on the histidine stimulation of metal transport.

1. A significant proportion of plasma zinc exists complexed with amino acids. The effect of amino acids on the accumulation of radioactive zinc by rat erythrocytes was studied in vitro, to investigate the hypothesis that zinc might be transported into cells as an amino acid‐zinc complex. 2. L‐Histidine (500 microM‐10 mM) stimulated 65Zn uptake; 50 mM‐L‐histidine gave a slight inhibition of uptake. D‐Histidine (500 microM‐10 mM) inhibited uptake in a dose‐dependent manner. A non‐zinc‐binding amino acid, L‐alanine, did not affect 65Zn uptake. 3. The effect of L‐histidine was sodium dependent and temperature dependent, but was DIDS insensitive. These properties suggest that zinc is being transported as a zinc‐histidine complex, utilizing an amino acid carrier system. Uptake of zinc in the presence of L‐histidine differed from the previously described ionic mechanism, and may represent a physiological route of uptake. 4. L‐Histidine stimulated efflux of 65Zn from pre‐loaded cells. 5. The relevance of transport of a zinc‐histidine complex is discussed with reference to histidinaemia, and as a significant zinc transport system in the presence of the very low ionic zinc concentrations found in plasma.

SUMMARY1. Blood flow through the inner cortex and outer medulla of the rat kidney was measured by the hydrogen wash-out technique.2. Renal nerve stimulation caused vasoconstriction in both cortex and medulla.This constriction was abolished or reduced by phenoxybenzamine (9 ,mole/kg I.v.), phentolamine (100 n-mole/kg) or prazosin (1P5 ,umole/kg).3. After prazosin (6 psmole/kg i.v.), renal nerve stimulation caused small but significant renal cortical vasodilatation. This vasodilatation was reversed by sulpiride (0-7 ,mole kg-' min1), but was unaffected by propranolol (10 #smole/kg) or atropine (4-3 ,smole/kg).4. These results indicate the existence of dopaminergic vasodilator nerves to the renal cortex of the rat.