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Nitroxidergic innervation in dog and monkey renal arteries
1Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
Hypertension (Dallas, Tex. : 1979)
|May 1, 1995
Summary
Neurogenic vasodilatation in renal arteries involves nitric oxide (NO) and adrenergic nerves. Inhibiting NO synthase potentiates vasoconstriction, highlighting the balance between these systems.
Area of Science:
- Physiology
- Pharmacology
- Neuroscience
Background:
- Neurogenic control of renal artery tone is complex.
- The roles of nitric oxide and adrenergic signaling in renal neurovasodilation require further elucidation.
Purpose of the Study:
- To investigate the mechanisms of neurogenic vasodilatation in canine and Japanese monkey renal arteries.
- To determine the involvement of nitric oxide and adrenergic pathways in renal neurovascular responses.
Main Methods:
- Isometric mechanical responses of renal arterial strips were recorded following nerve stimulation with nicotine.
- Pharmacological agents including hexamethonium, NG-nitro-L-arginine, L-arginine, prazosin, indomethacin, timolol, atropine, methylene blue, and oxyhemoglobin were used.
- Histochemical analysis identified NADPH diaphorase and nitric oxide synthase in perivascular nerves.
Main Results:
- Nicotine-induced contractions were blocked by hexamethonium and enhanced by NG-nitro-L-arginine, indicating NO-mediated inhibition.
- Prazosin reversed nicotine-induced contraction to relaxation, which was dependent on nitric oxide synthase and guanylate cyclase.
- NG-nitro-L-arginine potentiated adrenergic vasoconstriction, and this effect was reversed by L-arginine.
Conclusions:
- Renal arteries possess distinct nitric oxide-mediated vasodilator and adrenergic vasoconstrictor nerve fibers.
- Inhibition of nitric oxide synthase enhances adrenergic vasoconstrictor nerve activity, revealing a functional interplay.