Sodium-Selective Salt Sensitivity

Abstract

Abstract-We tested the hypothesis that the Na ϩ component of dietary NaCl can have a pressor effect apart from its capacity to complement the extracellular osmotic activity of Cl Ϫ and, thus, expand plasma volume. We studied 35 mostly normotensive blacks who ingested a low-NaCl diet, 30 mmol/d, for 3 weeks, in the first and third of which Na ϩ was loaded orally with either NaHCO 3 or NaCl, in random order (250 mmol/d). In subjects adjudged to be salt sensitive (nϭ18; ⌬ mean arterial pressure: Ն5 mm Hg with NaCl load), but not in salt-resistant subjects (nϭ17), loading with NaHCO 3 was also pressor. The pressor effect of NaHCO 3 was half that of NaCl: mean arterial pressure (millimeters of mercury) increased significantly from 90 on low NaCl to 95 with NaHCO 3 and to 101 with NaCl. The pressor effect of NaCl strongly predicted that of NaHCO 3. As judged by hematocrit decrease, plasma volume expansion with NaCl was the same in salt-resistant and salt-sensitive subjects and twice that with NaHCO 3 , irrespective of the pressor effect. In salt-sensitive subjects, mean arterial pressure varied directly with plasma Na ϩ concentration attained with all Na ϩ loading. In salt-sensitive but not salt-resistant subjects, NaHCO 3 and NaCl induced decreases in renal blood flow and increases in renal vascular resistance; changes in renal blood flow were not different with the 2 salts. Responses of renal blood flow and renal vascular resistance to NaHCO 3 were strongly predicted by those to NaCl. In establishing the fact of "sodium-selective" salt sensitivity, the current observations demonstrate that the Na ϩ component of NaCl can have pressor and renal vasoconstrictive properties apart from its capacity to complement Cl Ϫ in plasma volume expansion.

Dietary salt influences postprandial plasma sodium concentration and systolic blood pressure

“…18 The relationship between plasma chloride concentration and BP is not consistent, and a strong relationship was seen between BP and plasma sodium concentration. [18][19][20][21] Our study had several limitations. We did not measure atrial natriuretic peptide (ANP), renin and aldosterone, or vasopressin.…”

High Salt Intake Increases Blood Pressure via BDNF-Mediated Downregulation of KCC2 and Impaired Baroreflex Inhibition of Vasopressin Neurons

“…Increases in plasma sodium associated with a high level of dietary salt intake are linked to elevated BP in salt-sensitive hypertensive patients (He et al, 2013; He and Macgregor, 2012; Schmidlin et al, 2007), but the mechanisms underlying this effect are unclear. Hyperosmolality is a necessary consequence of hypernatremia and thus activates central osmoreceptors (Bourque, 2008).…”

“…High levels of dietary salt intake can significantly increase plasma sodium concentration and contribute to the development of salt-dependent hypertension (He et al, 2013; He and Macgregor, 2012; Schmidlin et al, 2007). However, the central mechanisms by which excess sodium can increase blood pressure (BP) remain poorly defined.…”

Neurogenic and Sympathoexcitatory Actions of NaCl in Hypertension

“…Indeed, Guyton’s theory of impaired renal pressure-natriuresis may explain the associated alterations in blood volume and peripheral resistance, but it is now well-recognized that salt-sensitive hypertension is a multi-system disorder that involves renal dysfunction, vascular abnormalities, and neurogenic or sympathetically-mediated increases in peripheral resistance. Support for a sympathetic component arises from several lines of evidence, including: 1) salt-sensitive hypertension is associated with activation of the sympathetic nervous system [8–11], 2) sympathetic nerve transection lowers blood pressure in salt-sensitive models [12–15], and 3) interruption of neurotransmission in various brain centers lowers sympathetic nerve activity (SNA) and/or arterial blood pressure (ABP) [16–21]. The unresolved question is of the unknown origin or identity of the factor(s) linking dietary salt intake to changes in these various brain centers and SNA to, ultimately, elevated ABP.…”