Key result
Short exposure to a 2% NaCl drinking solution significantly increased mean arterial blood pressure in rats without changing circulating blood volume, suggesting a neurogenic mechanism.
Why the study?
It was unclear whether the increase in arterial blood pressure from short-term high-salt intake relies on changes in circulating blood volume.
Does short exposure to high salt in drinking solution increase arterial blood pressure via changes in circulating blood volume in rats?
Does short exposure to high salt in drinking solution increase arterial blood pressure via changes in circulating blood volume in rats?
Short-term high salt intake induces hypertension in rats through a likely neurogenic mechanism associated with increased cerebrospinal fluid sodium, rather than through blood volume expansion.
Short high-salt exposure may raise BP in rats via autonomic imbalance; leaves open relevance to human salt-sensitive hypertension.
Evidence suggests that hypertension induced by high salt intake is correlated with an autonomic imbalance that favours sympathetic hyperactivity and an increase in vascular resistance, indicating a neurogenic component to this pathology. Although there are several animal models in which to study salt‐induced hypertension with prolonged exposure to a high‐sodium diet, here we sought to investigate whether the increase in arterial blood pressure of rats subjected to a short exposure to high salt, with 2% NaCl drinking solution instead of water, relies on changes in the circulating blood volume. Male Wistar rats were divided randomly into three groups: euhydrated (EU, n = 10), salt loaded (SL, n = 13) and water deprived (WD, n = 6). The SL rats exhibited a significant increase in mean arterial blood pressure, with a large low‐frequency component of systolic arterial blood pressure variability, when compared with the EU group. Circulating blood volume did not differ between SL and EU rats, but it was lower in WD rats. Compared with EU rats, the [Na + ] in cerebrospinal fluid was higher in SL rats and similar in magnitude to the WD rats. Plasma [Na + ] did not differ between SL and EU rats, but it was higher in WD rats. Collectively, our data suggest that the hypertension induced by a short exposure to high salt intake closely resembles a neurogenic mechanism, but not a blood volume‐dependent mechanism, with cumulative [Na + ] in the cerebrospinal fluid that could be associated with changes in the neurochemistry of autonomic nuclei, which are highly susceptible to osmotic stress related to high salt consumption.
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Gomes et al. (2023) studied Salt-induced hypertension (n=29). Short exposure to high salt (2% NaCl drinking solution) vs. Euhydrated (water) and water deprived was evaluated on Mean arterial blood pressure and circulating blood volume. Short exposure to a 2% NaCl drinking solution significantly increased mean arterial blood pressure in rats without changing circulating blood volume, suggesting a neurogenic mechanism.
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