Role of Acetylcholine in the Renal Vasoconstrictor Response to Sympathetic Nerve Stimulation in the Dog
The renal blood vessels were studied for a cholinergic determinant of their response to renal nerve stimulation. In dogs anesthetized with morphine and chloralose, control values were: mean aortic blood pressure 147 ± 4 mm Hg, renal blood flow 257 ± 12 ml/min. Acetylcholine (ACh) in 1-, 10- and 100-µg doses (all drugs given into the renal artery) increased renal blood flow, whereas 1000 µg of ACh reduced renal blood flow by 35%. After atropine and physostigmine, 1 µg of ACh did not alter renal blood flow, while 10, 100 and 1000 µg of ACh reduced renal blood flow by 6, 40 and 72%, respectively. After reserpine pretreatment, ACh in all doses increased renal blood flow (range of the means from 20 to 30%). The vasoconstrictor action of ACh was also blocked by phentolamine, guanethidine and hexamethonium. The renal vasoconstrictor response to renal nerve stimulation was blocked by guanethidine, but not by hexamethonium. These observations suggest that hexamethonium opposes ACh by barring its entry into the nerve terminals, whereas guanethidine blocks the intraneuronal release of norepinephrine by ACh. The vasoconstrictor response to nerve stimulation was reduced by atropine and augmented by physostigmine. Hemicholinium, which blocks the synthesis of ACh, attenuated the renal vasoconstriction produced by nerve stimulation. The results suggest that ACh may function in the canine kidney to liberate norepinephrine during activity of the sympathetic nerves.
- autonomic control of renal blood vessels
- autonomic blockade of the release of norepinephrine
- hemicholinium and adrenergic neurotransmission
- Burn and Rand's hypothesis
- cholinergic mechanisms
- Accepted April 20, 1967.
- © 1967 American Heart Association, Inc.