scholarly journals Structural motifs underlying voltage-dependent K+ channel function

1995 ◽  
Vol 48 (4) ◽  
pp. 918-922 ◽  
Author(s):  
Maurizio Taglialatela ◽  
Arthur M. Brown
Keyword(s):  
K Channel ◽  
Structural Motifs ◽  
Channel Function ◽  
Voltage Dependent

Structural Correlates of K+ Channel Function

Physiology ◽  
1994 ◽  
Vol 9 (4) ◽  
pp. 169-173 ◽  
Author(s):  
M Taglialatela ◽  
AM Brown
Keyword(s):  
Ion Channel ◽  
Ionic Currents ◽  
The Other ◽  
K Channel ◽  
K Channels ◽  
Functional Studies ◽  
Channel Function ◽  
Voltage Dependent ◽  
K Currents

More complementary DNAs have been cloned for Voltage-dependent K+ channels than any other voltage-dependent ion channel. Purely functional studies anticipated this result because K+ currents are far more diverse than voltage-dependent Na+, Ca2+, or Cl currents, the other types of voltage-dependent ionic currents commonly dealt with.

Reduced molecular expression of K+ channel proteins in vascular smooth muscle from rats made hypertensive with Nω-nitro-l-arginine

2005 ◽  
Vol 289 (3) ◽  
pp. H1277-H1283 ◽  
Author(s):  
Ian N. Bratz ◽  
Gregory M. Dick ◽  
L. Donald Partridge ◽  
Nancy L. Kanagy
Keyword(s):  
Smooth Muscle ◽  
Companion Paper ◽  
Muscle Membrane ◽  
K Channel ◽  
Channel Blockers ◽  
Western Blots ◽  
Channel Function ◽  
Voltage Dependent ◽  
Channel Expression ◽  
Smooth Muscle Membrane

Smooth muscle membrane potential ( Em) depends on K+ channels, and arteries from rats made hypertensive with Nω-nitro-l-arginine (LHR) are depolarized compared with control. We hypothesized that decreased K+ channel function, due to decreased K+ channel protein expression, underlies Em depolarization. Furthermore, K+ channel blockers should move control Em (−46 ± 1 mV) toward that in LHR (−37 ± 2 mV) and normalize contraction. The Em vs. K+ relationship was less steep in LHR (23 ± 2 vs. 28 ± 1 mV/log K+ concentration), and contractile sensitivity to K+ was increased (EC50 = 37 ± 1 vs. 23 ± 1 mM). Iberiotoxin (10 nM), an inhibitor of large-conductance Ca2+-activated K+ (BKCa) channels, depolarized control and LHR Em to −35 ± 1 and −30 ± 2 mV, respectively; however, effects on K+ sensitivity were more profound in LHR (EC50 = 25 ± 2 vs. 15 ± 3 mM). The voltage-dependent K+ (KV) channel blocker 4-aminopyridine (3 mM) depolarized control Em to the level of LHR (−28 ± 1 vs. −28 ± 1 mV); however, effects on K+ sensitivity were greater in LHR (EC50 = 17 ± 4 vs. 4 ± 4 mM). Western blots revealed reduced BKCa and KV1.5 channel expression in LHR arteries. The findings suggest that diminished expression of K+ channels contributes to depolarization and enhanced contractile sensitivity. These conclusions are supported by direct electrophysiological assessment of BKCa and KV channel function in control and LHR smooth muscle cells [see companion paper (Bratz IN, Swafford AN Jr, Kanagy NL, and Dick GM. Am J Physiol Heart Circ Physiol 289: H1284–H1290, 2005)].

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