neuropeptide-y and apraclonidine

The concentration of neuropeptide Y in the aqueous humor (NPYaq) did not change during the circadian cycle in rabbits. However, NPYaq also did not decrease after superior cervical ganglionectomy or preganglionic section of the cervical sympathetic trunk (decentralization). Nor did NPYaq change after either stimulation, with para-aminoclonidine, or blockade, with rauwolscine, of prejunctional ocular alpha2-adrenergic receptors. Therefore, NPYaq does not reflect NPY release from ocular sympathetic nerves in rabbits.

Topics: Adrenergic alpha-Agonists; Adrenergic alpha-Antagonists; Animals; Aqueous Humor; Circadian Rhythm; Clonidine; Ganglia, Sympathetic; Ganglionectomy; Male; Neuropeptide Y; Rabbits; Sympathectomy; Yohimbine

Interactions between a alpha 2-adrenoceptor agonist and neuropeptide Y (NPY) binding sites have been studied in the rat medulla oblongata (MO) using biochemical binding techniques as well as quantitative autoradiography. Tritiated para-amino clonidine (3H-PAC; alpha 2-adrenoceptor agonist), idazoxan (3H-IDA; alpha 2-adrenoceptor antagonist) and iodinated neuropeptide Y (125I-NPY) were used as radioligands. (1) Neuropeptide Y (NPY; 10(-8) M) but not bovine pancreatic polypeptide (BPP) nor peptide YY (PYY 10 nM) increased the KD value of 3H-PAC binding sites. However, intraventricular administration of a high dose of NPY (1.25 nmol) did not change the 3H-PAC binding characteristics in MO membrane preparations of these animals. (2) GTP 10(-4) lowered the affinity of 3H-PAC binding. NPY (10 nM) had no additional effect, nor did NPY influence the GTP induced shift in potency of clonidine to displace 3H-IDA from its binding sites. (3) In the autoradiographical experiments NPY (10 nM) significantly reduced 3H-PAC binding (2 nM) in the nucleus tractus solitarius (NTS) area by 35%. (4) When clonidine, either given centrally in vivo (3.75 nmol) or in vitro (10 nM) the binding of 125I-NPY was reduced (34 and 24%, respectively) in the NTS. When the monoamine receptors were irreversibly blocked in vivo by N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ, 10 micrograms i.c. 24 h) 125I-NPY (0.5 nM) binding was increased by 137% in the NTS. This effect of EEDQ was prevented by pretreatment with the alpha 2-adrenoceptor antagonist idazoxan. These results provide support for a direct intramembrane interaction between the alpha 2-receptor and the NPY receptor within the NTS and may be of importance in central cardiovascular regulation.

Topics: Animals; Binding, Competitive; Clonidine; Dioxanes; Idazoxan; Kinetics; Male; Medulla Oblongata; Neuropeptide Y; Quinolines; Rats; Rats, Inbred Strains; Receptors, Adrenergic, alpha; Receptors, Neuropeptide Y; Receptors, Neurotransmitter; Subcellular Fractions