Carmine Zoccali1. 1. CNR-IBIM Epidemiologia Clinica e Fisiopatologia delle Malattie Renali e dell'Ipertensione Arteriosa, Ospedali Riuniti, Reggio Calabria, Italy. carmine.zoccali@tin.it
Abstract
PURPOSE OF REVIEW: I review recent knowledge on the interference of neuropeptide Y with energy balance and cardiovascular and renal disease and on the central regulation of bone mass. RECENT FINDINGS: Although neuropeptide Y is mainly seen as a vasoconstrictor, rats overexpressing the neuropeptide Y gene show reduced blood pressure and longer life span in comparison with control rats. Due to its strong mitogenic effects on vascular smooth muscle cells, neuropeptide Y induces occlusive lesions in a rat model of atherosclerosis induced by balloon angioplasty. The involvement of neuropeptide Y in experimental atherosclerosis is complex and may include also favourable, compensatory, mechanisms because, at physiological concentrations, it also activates a potent neoangiogenic response to ischemia. Subjects with a common genotype in the neuropeptide Y gene, which underlies increased intracellular neuropeptide Y storage, display slightly raised blood pressure, high serum cholesterol and increased carotid intima media thickness. In patients with end-stage renal disease high neuropeptide Y in plasma has been associated consistently with concentric left-ventricular hypertrophy and cardiovascular mortality. Finally, recent studies have shown that neuropeptide Y constitutes an important central regulator of bone mass and that it may be involved in inflammation and immune regulation. SUMMARY: Evidence has accrued in experimental animals that altered neuropeptide Y is involved in obesity and the attendant metabolic complications. Recent data also suggest that this peptide may play a role in atherosclerosis and related cardiovascular complications.
PURPOSE OF REVIEW: I review recent knowledge on the interference of neuropeptide Y with energy balance and cardiovascular and renal disease and on the central regulation of bone mass. RECENT FINDINGS: Although neuropeptide Y is mainly seen as a vasoconstrictor, rats overexpressing the neuropeptide Y gene show reduced blood pressure and longer life span in comparison with control rats. Due to its strong mitogenic effects on vascular smooth muscle cells, neuropeptide Y induces occlusive lesions in a rat model of atherosclerosis induced by balloon angioplasty. The involvement of neuropeptide Y in experimental atherosclerosis is complex and may include also favourable, compensatory, mechanisms because, at physiological concentrations, it also activates a potent neoangiogenic response to ischemia. Subjects with a common genotype in the neuropeptide Y gene, which underlies increased intracellular neuropeptide Y storage, display slightly raised blood pressure, high serum cholesterol and increased carotid intima media thickness. In patients with end-stage renal disease high neuropeptide Y in plasma has been associated consistently with concentric left-ventricular hypertrophy and cardiovascular mortality. Finally, recent studies have shown that neuropeptide Y constitutes an important central regulator of bone mass and that it may be involved in inflammation and immune regulation. SUMMARY: Evidence has accrued in experimental animals that altered neuropeptide Y is involved in obesity and the attendant metabolic complications. Recent data also suggest that this peptide may play a role in atherosclerosis and related cardiovascular complications.