Abstract
To evaluate whether changes in central ouabain-like activity (OLA) play a role in the effects of dietary sodium on sympathetic outflow and blood pressure (BP), the effects of high vs. control sodium intake on BP, brain OLA, and responsiveness to exogenous ouabain were studied in young spontaneously hypertensive rats (SHRs) vs. Wistar-Kyoto (WKY) rats. At 4 weeks of age, the BP of SHRs was already significantly increased compared with that of WKY rats, and hypertension developed further with maturation. High sodium intake exacerbated the hypertension. Compared with WKY rats, in SHRs OLA in the hypothalamus was already increased at 4 weeks of age. High sodium intake increased brain OLA in both SHRs and WKY rats. However, high dietary sodium decreased pressor and sympathoexcitatory responses to exogenous ouabain only in SHRs. These results may indicate that in WKY rats on control sodium, endogenous OLA already exerts its maximal central effects and a further increase in OLA by high sodium intake does not cause hemodynamic changes, whereas in young SHRs the increase in brain OLA by high sodium intake may play a functional role in the pressor and sympathoexcitatory responses to high sodium.
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