This study determined whether clinical salt-sensitive hypertension (cSSHT)
results from the interaction between partial arterial baroreceptor impairment
and a high-sodium (HNa) diet. In three series (S-I, S-II, S-III), mean arterial
pressure (MAP) of conscious male Wistar ChR003 rats was measured once before
(pdMAP) and twice after either sham (SHM) or bilateral aortic denervation (AD),
following 7 days on a low-sodium (LNa) diet (LNaMAP) and then 21 days on a HNa
diet (HNaMAP). The roles of plasma nitric oxide bioavailability (pNOB), renal
medullary superoxide anion production (RMSAP), and mRNA expression of NAD(P)H
oxidase and superoxide dismutase were also assessed. In SHM (n=11) and AD (n=15)
groups of S-I, LNaMAP-pdMAP was 10.5±2.1 vs 23±2.1 mmHg
(P<0.001), and the salt-sensitivity index (SSi; HNaMAP−LNaMAP) was 6.0±1.9
vs 12.7±1.9 mmHg (P=0.03), respectively. In the SHM group,
all rats were normotensive, and 36% were salt sensitive (SSi≥10 mmHg), whereas
in the AD group ∼50% showed cSSHT. A 45% reduction in pNOB (P≤0.004) was
observed in both groups in dietary transit. RMSAP increased in the AD group on
both diets but more so on the HNa diet (S-II, P<0.03) than on the LNa diet
(S-III, P<0.04). MAP modeling in rats without a renal hypertensive genotype
indicated that the AD*HNa diet interaction (P=0.008) increases the likelihood of
developing cSSHT. Translationally, these findings help to explain why subjects
with clinical salt-sensitive normotension may transition to cSSHT.