Key result
Preventing volume expansion prevents high-salt-induced arterial pressure rises of ~27 mmHg in Dahl rats.
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Continuous measurement and servo control (SC) of total body weight of unrestrained rats were used to investigate the role of volume expansion in the development of hypertension in Dahl salt-resistant (SR) and Dahl salt-sensitive (SS) rats. A change in sodium intake from 1 to 20 meq/day was associated with an increase in total body weight of 7.2% in both SS and SR rats over 96 h. Plasma sodium (pNa) increased from 145.0 to 147.4 meq/l in both SS (n = 10) and SR (n = 10) rats. Only in the SS rats was the volume expansion associated with an increase in arterial pressure of 27 +/- 3 mmHg. Prevention of the volume expansion by SC blocked the rise in arterial pressure in the SS rats (n = 10) but increased pNa from 143.5 to 152.4 meq/l. Hematocrit fell from 36.6 to 27.5% in both non-SC groups but decreased less in SC groups (35.7 to 32.0%). Plasma volume expansion from 17.6 +/- 0.6 to 25.2 +/- 0.8 ml in non-SC rats was greatly blunted by SC. In non-SC rats, SS (n = 10) and SR (n = 9) rats an increase in salt intake was associated with a rise in cardiac output from 413 +/- 6 to 507 +/- 12 ml.min-1.kg-1 in both groups. These results indicate that fluid retention is required to trigger the rise of pressure in Dahl SS rats.
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Greene et al. (1990) studied Salt-sensitive hypertension (Dahl rat model). Servo control (SC) of total body weight during high sodium intake vs. Non-servo-controlled (non-SC) high sodium intake and Dahl salt-resistant (SR) rats was evaluated on Change in arterial pressure and total body weight. Prevention of volume expansion via servo control blocked the 27 +/- 3 mmHg rise in arterial pressure induced by high salt intake (20 meq/day) in Dahl salt-sensitive rats.
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