Small vessel membrane potential, sympathetic input, and electrogenic pump rate in SHR

Area of Science:

• Cardiovascular Physiology
• Hypertension Research
• Cellular Electrophysiology

Background:

• Vascular smooth muscle cell (VSM) transmembrane potential (Em) is critical for vascular tone.
• Hypertension is associated with alterations in VSM electrophysiology.
• Understanding these alterations is key to developing new treatments.

Purpose of the Study:

• To compare VSM transmembrane potential (Em) in situ and in vitro in hypertensive rats.
• To investigate the roles of sympathetic innervation and circulating factors in VSM depolarization.
• To elucidate the cellular mechanisms underlying altered VSM function in hypertension.

Main Methods:

• Comparative measurements of VSM Em in situ and in vitro in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats.
• Utilized topical suffusion and isolated vessel segments.
• Employed local sympathetic denervation (6-hydroxydopamine) and pharmacological/temperature challenges (ouabain, reduced temperature).

Main Results:

• Older SHR exhibited less polarized VSM compared to WKY rats.
• Sympathetic denervation normalized VSM Em in older SHR.
• Circulating factors selectively depolarized arterial VSM in situ.
• SHR VSM showed altered responses to ouabain and temperature reduction.

Conclusions:

• Sympathetic innervation contributes to VSM depolarization in established hypertension.
• Circulating factors influence arterial VSM Em, particularly in SHR.
• Temperature-sensitive mechanisms may be dysregulated in SHR VSM.