Modulation of noradrenaline and neuropeptide Y (NPY) release in the pig kidney in vivo: involvement of alpha 2, NPY and angiotensin II receptors.

The modulation of the release of noradrenaline (NA) and neuropeptide Y-like immunoreactivity (NPY-LI) was investigated in the pig kidney in vivo. Under control conditions a reproducible co-release of NA and NPY-LI was obtained upon stimulation of the renal nerves with 5 Hz for 1 min. Infusion of peptide YY (PYY, 1 microgram/kg/min i.v.), which binds to NPY receptors, caused renal vasoconstriction and reduced the stimulation-evoked overflow of NA and NPY-LI by 24 +/- 4 and 33 +/- 11%, respectively (P less than 0.01). The PYY effect was reversible and was absent 1 h after the infusion. The alpha 2-adrenoceptor antagonist yohimbine (0.2 mg/kg i.v.) enhanced the overflow of NA and NPY-LI 2- to 3-fold. The angiotensin converting enzyme inhibitor captopril (5 mg/kg i.v.) did not significantly affect the overflow of NA or NPY-LI evoked by the nerve stimulation. Angiotensin II (0.5 microgram/kg/min i.v.), on the other hand, induced a reversible enhancement of the overflow of both NA and NPY-LI by 71 and 77%, respectively (P less than 0.01). Infusion of endothelin (0.2 microgram/kg/min i.v.), which reduced renal blood flow by a magnitude similar to that evoked by angiotensin II, did not significantly alter the nerve stimulation-evoked overflow of NA or NPY-LI. None of the administered drugs did significantly affect the percentage reduction in renal blood flow evoked by nerve stimulation. It is concluded that the release of NA and NPY-LI from sympathetic nerves in the pig kidney is inhibited in parallel via activation of NPY receptors by PYY and via alpha 2-adrenoceptors by endogenous NA.(ABSTRACT TRUNCATED AT 250 WORDS)