Abstract
The purpose of this study is to clarify the role of renal dopamine receptor in the pathogenesis of salt-dependent hypertension. Male Wistar rats were raised under three different conditions, control, 1% NaCl loading (NaCl) and 1% NaCl plus metoclopramide with a dose of 1.5mg/kg daily (MC), for 2 weeks. Then, renal plasma membranes were prepared by ultracentrifugation method, and maximal binding capacity (Bmax) and dissociation constant (Kd) were determined by Scatchard analysis using 3H-spiperone. And plasma aldosterone and prolactin concentration in these three groups were measured by radioimmunoassay.
Results: Systolic blood pressure measured tail-cuff method significantly elevated in MC group, but not control and NaCl group. Bmax of renal dopamine receptor was 535.9 ± 85.0 fmol/mg protein, 594.9 ± 159.3 fmol/mg protein, 529.1 ± 166.1 fmol/mg protein, in control, NaCl and MC group, respectively. Kd of renal dopamine receptor in NaCl group was significantly lower than control (p<0.05). Renal dopamine contents of NaCl and MC group were lower than control. There was a negative correlation between renal dopamine content and Bmax of renal dopamine receptor in NaCl group (r = - 0.95, p<0.02). In MC group, plasma aldosterone concentration was slightly higher than control and NaCl group,but there was no differences in Plasma prolactin concentration among these three groups.
Conclusion: These data suggests that renal dopamine receptor may participate in sodium transport in kidney, and that the impairment of dopaminergic activity may cause sodium-dependent hypertension.
