Article Text

  1. C. M.A van Dijk,
  2. X-P. Ni,
  3. M. H. Humphreys
  1. San Francisco General Hospital and UCSF, San Francisco


A high sodium diet (HSD) has been reported to be associated with markers of oxidative stress, and the superoxide dismutase mimetic Tempol lowers blood pressure in the spontaneously hypertensive rat (SHR) and some models of salt-sensitive hypertension. We have shown (Hypertension 2003; 42:962-967) that administration of Bromocriptine (B; 5 mg/kg ip daily for one week) causes salt-sensitive hypertension due to deficiency of the pituitary peptide γ-melanocyte stimulating hormone (γ-MSH); infusion of the peptide rapidly lowers blood pressure. We asked if Tempol would have a beneficial effect on mean arterial pressure (MAP) in this model as well. Sprague-Dawley rats were instrumented with radiotransmitters (Data Sciences Inc, Minneapolis, MN) for continuous measurement of distal aortic MAP in the conscious and unrestrained state. No change in MAP occurred in going from a normal (0.4%) sodium diet (NSD) to the HSD (8%) for one week, 103±5 vs. 104±6 mm Hg, while sodium excretion (UNaV) rose from 2.7±0.2 to 23.2±0.5 mmol/24 hr (p ≤.001). Treatment with B for another week increased MAP to 122±5 mm Hg (p ≤.05) with a slight reduction in UNaV to 19.3±2.5 mmol/24 hr. Addition of Tempol (1 mmol/L drinking water) for a final week resulted in no change in MAP (120±2 mm Hg) or in UNaV (19.5±2.2 mmol/24 hr). Urinary excretion of 8-isoprostane, a marker of renal oxidative stress, was increased during B treatment compared to the NSD (27.8±6.6 vs. 16.8±2.4 ng/24 hr, p ≤.05), and fell only slightly during Tempol treatment to 22.7±3.7 ng/24 hr (p = NS). These results confirm that B treatment results in salt-sensitive hypertension. This hypertension is accompanied by increased 8-isoprostane excretion, raising the possibility that the increased MAP may be linked to oxidative stress. However, Tempol, administered in a dose sufficient to correct hypertension in the SHR, did not affect MAP while lowering 8-isoprostane excretion modestly. These results do not support a major role of oxidative stress in the salt-sensitive hypertension resulting from B treatment.

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