High Sodium Intake Impairs Small Artery Vasoreactivity in vivo in Dahl Salt-Sensitive Rats

Abstract

The effects of high sodium intake on the functionality of resistance arteries have been repeatedly studied in vitro, but no study has focused on salt-sensitive hypertension in vivo. We studied the in vivo reactivity of mesenteric small arteries (MSAs) to vasoactive agents in Dahl salt-sensitive (DS) rats with various sodium diets. Twenty-four male DS rats were randomized into 3 groups: LS (0.3% NaCl diet), NS (0.6% NaCl diet), and HS (8% NaCl diet). After a 12-week intervention, the diameter changes of the MSAs after noradrenaline (NA) and acetylcholine (ACh) exposure were detected by a microscope, and changes in blood perfusion through the MSAs were measured by full-field laser perfusion imaging. HS enhanced the constrictive response of the MSAs to NA and attenuated the relaxing response to ACh. Low sodium intake reduced the response of the MSAs to NA and promoted ACh-induced vasodilatation. HS also aggravated NA-induced blood perfusion reduction and impaired ACh-induced hyperperfusion of the MSAs. Pathologically, HS was associated with arteriolar structural damage and fibrosis of the MSAs. We conclude that sodium intake affects the responsiveness of the MSAs to vasoactive agents in DS rats and might play important roles in modulating blood pressure in hypertensive individuals.

Salt Restriction and Angiotensin-Converting Enzyme Inhibitor Improve the Responsiveness of the Small Artery in Salt-Sensitive Hypertension

“…In addition, in real life, excessive salt intake is a common problem in hypertensive individuals. High salt intake negatively influenced the response of resistant arteries to vasoactive agents, as confirmed by our previous study 16 . Therefore, we hope to further explore the relationship between resistance artery and BP from another perspective by limiting salt intake.…”

“…The plasma angiotensin II and aldosterone levels were measured by radioimmunoassay. The proximal small intestine and mesentery were removed and placed in a transparent chamber filled with a constant temperature physiological saline solution after pentobarbital sodium (30 mg/kg, Sigma-Aldrich) was administered intraperitoneally 16 . The mesenteric vessels maintained their perfusion and vascular tone in vivo and in situ .…”

“…These results for each rat were averaged from three segments of the MSAs. The optimal reaction concentrations [16] of both norepinephrine tartrate (NE) and acetylcholine chloride (ACh) were 10 μg/kg. The dynamic change in the MSA diameter was recorded immediately after NE and ACh injection, and the interval between injections was at least 15 minutes to ensure drug elution.…”

The Relationship between Low-Sodium Salt Intake and Both Blood Pressure Level and Hypertension in Chinese Residents

“…This notable decrease can be attributed to DBP’s primary sensitivity to peripheral vascular resistance, especially in the small arteries and capillaries [ 32 ]. Low-sodium salt intake initially reduces resistance in these peripheral vessels, thereby influencing the velocity and pressure of the blood flowing back to the heart, making DBP more responsive to changes in sodium intake [ 32 , 33 ]. Moreover, while the upper group analysis initially showed statistically significant effects before adjustments for dyslipidemia, diabetes, and central obesity—aligning with other studies in demonstrating a smaller reduction compared to SBP [ 26 , 30 , 34 , 35 , 36 ]—the significance dissipated after these adjustments.…”