Key Points
- To evaluate the contribution of intact sympathetic innervation and norepinephrine to vascular smooth muscle transmembrane potential in mesenteric veins of spontaneously hypertensive rats.
- Measured in situ and in vitro transmembrane potential (Em) of vascular smooth muscle cells in 300–500 µm mesenteric veins from 13- to 15-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto controls (WKY).
- Evaluated the effects of neural blockade with 1 µg/ml tetrodotoxin (TTX) and cumulative concentrations of norepinephrine (NE) suffusion on in situ and in vitro venous Em.
- In situ baseline Em was significantly less negative in SHR (-34 ± 0.8 mV) than in WKY (-49 ± 1.3 mV), whereas in vitro Em values were similar between strains (-51 ± 1.0 mV in SHR vs. -54 ± 1.1 mV in WKY).
- In situ neural blockade with TTX hyperpolarized SHR venous Em to -45 ± 1.7 mV without affecting WKY, restoring a dose-dependent depolarizing response to norepinephrine in SHR that reached a plateau similar to WKY (-32 ± 0.9 mV at 6 µM NE).
Structured PICO
PPopulation13- to 15-wk-old anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive controls (WKY)
IInterventionSuffusion with physiological salt solution containing tetrodotoxin (TTX) and/or increasing concentrations of norepinephrine (NE)
CComparatorWistar-Kyoto normotensive controls (WKY) and in vitro measurements
OOutcomeTransmembrane potential (Em) in vascular smooth muscle cells of small veinssurrogate
The neurogenic vasoconstrictor component of vascular smooth muscle tone is significantly elevated in mesenteric veins of the spontaneously hypertensive rat model.