Studies on renal vasomotion.
1. The present investigation was made on the left kidney of the dog. The animals were anaesthetized intravenously with pentobarbitone (30 mg/kg) and the kidneys were perfused with saline at room temperature (20 degrees -22 degrees C). The renal innervation was untouched.2. Stimulation of the left splanchnic major nerve at T10-T12, and of the renal nerves, consistently caused renal vasoconstriction.3. Repeated stimulation of both supradiaphragmatic vagi failed to induce any vasomotion in the kidney.4. The vasoconstrictor effect was not blocked by either nicotine or hexamethonium even in enormous doses (30,000 mug). This may indicate that renal ganglia do not exist, for these ganglion blockers would prevent transmission across the ganglia.5. Kidney perfusate, re-injected into the kidney after vasoconstriction induced by stimulation of the renal nerves, brought about a notable reduction in outflow. This effect was not observed when perfusate from a non-stimulated kidney was used. This points to the release of a vasoconstrictor substance after nervous stimulation.6. Acetylcholine (ACh) in concentrations ranging from 0.001 mug/ml. caused a reduction in renal outflow. Thresholds were extremely variable. Higher concentrations of ACh (100-1,000 mug/ml.) often induced vasodilatation. The vasoconstrictor effect of ACh was not blocked by atropine.7. Nicotine and hexamethonium (10,000-30,000 mug) induced blockade which elevated the threshold for ACh to values of 1,000 mug/ml.8. Noradrenaline (0.0001 mug/ml.) induced a strong renal vasoconstriction.9. Hydergine (5-10 ml. solutions in concentrations ranging from 15 to 30 mug/ml.) blocked the renal response to nerve stimulation. This suggests that the nature of the renal innervation is adrenergic.10. In diseased kidneys which show reduction of the lumen of the arterioles, the thresholds for ACh, nicotine and noradrenaline are greatly increased, which might explain why we failed to show any effect of these drugs on renal vasomotion in several kidneys, many of which were not examined histologically.11. The collision technique was applied in an attempt to discover the nature of the fibres activated by ACh. It was found that ACh greatly reduced the size of the action potentials generated by splanchnic stimulation. This would seem to indicate that these impulses are conducted antidromically by sympathetic postganglionic fibres.12. These findings are discussed in relation to the hypothesis that the renal innervation is chiefly adrenergic and that ACh acts as a sympathetic transmitter, liberating noradrenaline, and that this effect is blocked at postganglionic endings, or at some structure intervening between adrenergic nerve endings and the effector cells, or at sensory nerve endings.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D004285:Dogs; D004558:Electric Stimulation; D004877:Ergoloid Mesylates / Q000494:pharmacology; D006584:Hexamethonium Compounds / Q000494:pharmacology; D007668:Kidney / Q000098:blood supply* / Q000294:innervation; D009538:Nicotine / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D013153:Splanchnic Nerves / Q000502:physiology; D014630:Vagus Nerve / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000096:biosynthesis; D014666:Vasomotor System / Q000502:physiology*
D006584:Hexamethonium Compounds; D014662:Vasoconstrictor Agents; D009538:Nicotine; D004877:Ergoloid Mesylates; D000109:Acetylcholine; D009638:Norepinephrine