neuropeptide-y has been researched along with Hydronephrosis* in 3 studies
3 other study(ies) available for neuropeptide-y and Hydronephrosis
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Renovascular effects of neuropeptide-Y in the split hydronephrotic rat kidney: non-uniform pattern of vascular reactivity.
1. The renovascular effects of neuropeptide-Y (NPY) were examined in the split hydronephrotic rat kidney. 2. Systemic infusion of low non-pressor doses of NPY (0.2 micrograms kg-1 up to 5.0 micrograms kg-1) produced a non-uniform pattern of vascular reactivity. In general, a significant constriction of the proximal and distal arcuate artery was seen at all doses. No constriction was seen at the interlobular artery or the larger part of the afferent arteriole. These segments initially dilated during the lower dose infusions. The very distal part of the afferent arteriole adjacent to the glomerulus and the proximal efferent arteriole responded in a similar way to the arcuate arteries. 3. NPY, locally applied into the tissue bath at concentrations of 1 nmol l-1 up to 25 nmol l-1, produced non-uniform vascular reactions similar to those of intravenously infused NPY. At the considerably higher local dosage of 1.14 mumol l-1, all vascular segments revealed vasoconstriction. 4. NPY application did not attenuate effects of acetylcholine. This observation suggests that the mechanism of NPY-induced vasoconstriction does not rely upon antagonism of endothelium-derived vasodilatation. 5. The pattern of vascular reactivity to NPY was substantially different from that known for the vasoconstrictors noradrenaline and angiotensin II in our preparation. Topics: Acetylcholine; Animals; Arterioles; Blood Flow Velocity; Female; Hydronephrosis; Kidney; Kidney Glomerulus; Neuropeptide Y; Nitroprusside; Prazosin; Rats; Rats, Inbred Strains; Vasoconstriction | 1991 |
Differential effect of neuropeptide-Y on membrane potential of cells in renal arterioles of the hydronephrotic mouse.
1. The effects of neuropeptide-Y (NPY) on the membrane potential of vascular smooth muscle cells were studied in renal arterioles of hydronephrotic mouse kidneys. 2. Kidney vessels are only weakly coupled with length constants of less than 10 microns and are most probably 'multiunit' vessels. 3. The vasoconstrictor peptide NPY reversibly depolarizes only smooth muscle cells in arterioles at distances greater than 200 microns from the glomerulus, whereas no changes of the membrane potential can be evoked close to the glomerulus (distance less than 50 microns). 4. The depolarizations, when present, are dose dependent. 5. Regardless of distance from the glomerulus cells respond uniformly to application of the vasoconstrictor angiotensin II. Topics: Angiotensin II; Animals; Arterioles; Electrophysiology; Female; Hydronephrosis; Kidney; Membrane Potentials; Mice; Microelectrodes; Muscle, Smooth, Vascular; Neuropeptide Y; Vasoconstriction | 1991 |
Neuropeptide Y inhibits renin release by a pertussis toxin-sensitive mechanism.
The effects of neuropeptide Y (NPY) were studied in the isolated rat kidney, which was perfused at constant perfusion pressure with a synthetic medium. In this preparation NPY produced concentration (1-100 nM)-dependent inhibition of renin release and vasoconstriction. In kidneys perfused at constant flow, inhibition of renin release by NPY was even more pronounced, excluding a flow-dependent washout effect. The simultaneous infusion of the calcium channel antagonist methoxyverapamil (2 microM) or of the calmodulin inhibitor calmidazolium (1 microM) did not prevent these effects of NPY, suggesting that calcium-dependent reactions are not primarily involved. Inhibition of renin release by NPY was also observed in tissue pieces prepared from the hydronephrotic rat kidney, in which tubular elements are lacking. This indicates that inhibition of renin release by NPY is not dependent on the presence of macula densa cells or on changes of intrarenal hemodynamics. In isolated kidneys from rats pretreated with pertussis toxin (2 micrograms/100 g ip) both effects of NPY, renal vasoconstriction and inhibition of renin release, were almost completely abolished. The pertussis toxin-sensitive factor mediating the effects of NPY is most likely the Ni-coupling protein of the adenylate cyclase complex. Accordingly, our data suggest that NPY induces renal vasoconstriction and inhibits renin release by inhibition of adenylate cyclase activity in vascular smooth muscle and renin-producing cells. Topics: Adenylate Cyclase Toxin; Adenylyl Cyclases; Angiotensin II; Animals; Calcium; Colforsin; Guanfacine; Guanidines; Hydronephrosis; Imidazoles; Isoproterenol; Kidney; Male; Neuropeptide Y; Norepinephrine; Perfusion; Pertussis Toxin; Phenylacetates; Rats; Rats, Inbred Strains; Renin; Vascular Resistance; Virulence Factors, Bordetella | 1987 |