What is the clinical evidence from this study?

Study design: Other. Population: Hypertension (Salt-sensitive and Essential). Intervention: Ovariectomy and High-Salt diet vs. Gonad-intact and Normal-Salt diet (0.4% NaCl). Primary outcome: Blood pressure (MAP) response to high-salt diet (p=0.05).

What does this research mean for the field?

Female sex hormones protect against high-salt-mediated elevations in blood pressure in salt-sensitive hypertension models but not in essential hypertension models, where resistance to salt-induced blood pressure increases is instead linked to greater renal nitric oxide synthase (NOS1) expression. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

May 15, 2014

Female sex hormones protect against salt-sensitive hypertension but not essential hypertension

Resultado clave

Ovariectomy significantly exacerbated high-salt diet-induced increases in mean arterial pressure in female Dahl salt-sensitive rats (p=0.05) but not in spontaneously hypertensive rats.

PICO estructurado

Población

Female spontaneously hypertensive rats (SHR) and Dahl salt-sensitive (DS) rats

Intervención

Ovariectomy (OVX) and high-salt (HS; 4% salt) diet for 2 wk

Comparador

Gonad-intact rats and normal salt (NS; 0.4% salt) diet

Resultado

Blood pressure (BP)surrogate

Female sex hormones protect against salt-sensitive hypertension in Dahl salt-sensitive rats but not in spontaneously hypertensive rats, likely due to differences in renal NOS expression.

Resultado numérico

valor p: p=0.05

Limitaciones

The study only examined females, so potential strain differences in male SHR and DS rats were not assessed.
The NOS activity assay reflects the potential of all NOS isoforms to produce NO and is not a measurement of in vivo NO production.
Isoform-specific NOS activity was not assessed.
The NOS activity assay was performed in the presence of optimal concentrations of cofactors, which may not reflect in vivo conditions.

Resumen

Initial studies found that female Dahl salt-sensitive (DS) rats exhibit greater blood pressure (BP) salt sensitivity than female spontaneously hypertensive rats (SHR). On the basis of the central role played by NO in sodium excretion and BP control, we further tested the hypothesis that blunted increases in BP in female SHR will be accompanied by greater increases in renal inner medullary nitric oxide synthase (NOS) activity and expression in response to a high-salt (HS) diet compared with DS rats. Gonad-intact and ovariectomized (OVX) female SHR and DS rats were placed on normal salt (NS; 0.4% salt) or HS (4% salt) diet for 2 wk. OVX did not alter BP in SHR, and HS diet produced a modest increase in BP. OVX significantly increased BP in DS rats on NS; HS further increased BP in all DS rats, although OVX had a greater increase in BP. Renal inner medullary NOS activity, total NOS3 protein, and NOS3 phosphorylated on serine residue 1177 were not altered by salt or OVX in either strain. NOS1 protein expression, however, significantly increased with HS only in SHR, and this corresponded to an increase in urinary nitrate/nitrite excretion. SHR also exhibit greater NOS1 and NOS3 protein expression than DS rats. These data indicate that female sex hormones offer protection against HS-mediated elevations in BP in DS rats but not SHR. We propose that the relative resistance to HS-mediated increases in BP in SHR is related to greater NOS expression and the ability to increase NOS1 protein expression compared with DS rats.

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