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

Area of Science:

• Cardiovascular Physiology
• Renal Physiology and Hypertension
• Vascular Biology

Background:

• In vitro studies show sodium's effect on resistance arteries, but in vivo data in salt-sensitive hypertension is lacking.
• Salt-sensitive hypertension is a critical public health concern, necessitating in vivo investigation of vascular mechanisms.

Purpose of the Study:

• To investigate the in vivo effects of varying sodium intake on mesenteric small artery (MSA) reactivity in salt-sensitive hypertensive rats.
• To assess the impact of dietary sodium on vascular responses to vasoactive agents and structural integrity.

Main Methods:

• Dahl salt-sensitive (DS) rats were fed low (0.3% NaCl), normal (0.6% NaCl), or high (8% NaCl) sodium diets for 12 weeks.
• In vivo reactivity of MSAs was measured using microscopy for diameter changes and laser perfusion imaging for blood flow.
• Responses to noradrenaline (vasoconstrictor) and acetylcholine (vasodilator) were analyzed.

Main Results:

• High sodium intake enhanced MSA constriction to noradrenaline and reduced relaxation to acetylcholine.
• Low sodium intake decreased noradrenaline response and increased acetylcholine-induced vasodilation.
• High sodium aggravated noradrenaline-induced perfusion reduction and impaired acetylcholine-induced hyperperfusion, alongside arteriolar damage and fibrosis.

Conclusions:

• Dietary sodium intake significantly modulates the in vivo responsiveness of mesenteric small arteries in salt-sensitive hypertensive rats.
• These findings suggest sodium intake plays a crucial role in regulating vascular function and may contribute to blood pressure modulation in hypertension.