IS NEUROPEPTIDE-Y A CONTRIBUTOR TO VOLUME-INDUCED HYPERTENSION

Hypertension often occurs with fluid overload. The most common mechani sm is considered to be mediated by increased cardiac output. Hemodialy sis (HD) patients frequently have large amounts of fluid overload. Neu ropeptide Y (NPY) is activated by stress and contributes to hypertensi on and heart failure. We speculated that NPY may be released by the st ress of fluid overload and, by its vasoconstrictor effect, may contrib ute to hypertension and heart failure. Plasma levels of NPY and other vasoconstrictors were studied in 20 HD patients with varying degrees o f fluid overload, and the relationship of NPY plasma levels to blood p ressure was analyzed. The plasma concentrations of NPY correlated with the degree of fluid overload (r = 0.89; P < 0.0001) and the mean arte rial blood pressure (r = 0.85; P < 0.0001). Seven patients had fluid o verload of greater than 6% of body weight. They had higher blood press ures and higher plasma concentrations of NPY than 13 HD patients with less than 5% of fluid retention (systolic blood pressure, 179 +/- 8.2 v 145 +/- 3.7 mm Hg, P = 0.007; NPY, 61 +/- 4.6 v 26.8 +/- 2.7 pmol/L, P < 0.001). In stepwise multiple regression analysis, NPY alone expla ined blood pressure elevation when analyzed with fluid overload and an giotensin II, renin, noradrenaline, and adrenaline levels, We hypothes ized that fluid overload in dialysis patients is a stress-inducing sta te that activates the sympathetic nervous system and releases the vaso constrictor NPY. The resulting inappropriate vasoconstriction may cont ribute to volume-induced hypertension and heart failure in a Vicious c ycle. We conclude that determination of plasma NPY levels may be usefu l as a marker of the clinical threat of overhydration, (C) 1998 by the National Kidney Foundation, Inc.