May 1, 1990Open Access
View Full PaperThree different potassium channels in human atrium. Contribution to the basal potassium conductance.
Key Result
Basal potassium conductance in human and guinea pig atrial cells was mainly due to iK1 channels, with acetylcholine-induced currents playing only a modulatory role in human cells.
Structured PICO
P
Population
In vitro patch-clamp study of isolated single human and guinea pig atrial cells to evaluate basal and agonist-stimulated potassium conductance.
I
Intervention
Patch-clamp technique under basal conditions, or stimulated with 10(-5) M acetylcholine or 10(-4) M adenosine
C
Comparator
Guinea pig atrial cells under the same conditions
O
Outcome
Single-channel characteristics of potassium channels (iK1, iK(ATP), acetylcholine-sensitive) and their contribution to total basal potassium conductancesurrogate
Basal potassium conductance in human atrial cells is primarily driven by iK1 channels, with acetylcholine-sensitive channels playing a smaller modulatory role compared to guinea pig models, highlighting species-specific differences in autonomic modulation.
Abstract
We applied the cell-attached and inside-out patch-clamp technique under symmetrical isotonic potassium conditions on single human (and guinea pig) atrial cells. The human cells were isolated by a modified method to that described earlier. Our aim was twofold: 1) to study the single-channel characteristics of potassium channels in human atrial single cells, present under basal conditions (iK1 and iK(ATP] or when stimulated with 10(-5) M acetylcholine; and 2) to calculate the contribution of these three channel types to the total basal potassium conductance in human atrial cells, and to compare the results with data on guinea pig atrial cells under the same conditions. We found that in human cells 58% of the patches (n = 42/74) contained acetylcholine-sensitive potassium channels: their conductance was 42 +/- 1.2 pS and mean open time (tau o) was 1.7 +/- 0.5 msec. They showed sporadic openings in the absence of agonist, and activation by acetylcholine was G-protein dependent. In 16% of the patches (n = 7/44), adenosine (10(-4) M) activated the same channels, but the activity was lower than when stimulated by acetylcholine. In 18% of the patches (n = 9/51), an iK1 channel was present (conductance, 27 pS; tau o, 8.7 msec), whereas in the cell-attached mode, ATP-dependent channels were never seen. However, they were present in half of the inside-out patches on washout of ATPi (conductance, 73 pS; tau o, 1.4 msec). The basal potassium conductance (i.e., in the absence of any exogenous hormone or neurotransmitter) was mainly due to iK1 channels in both human and guinea pig cells, a finding that is in contrast with previous reports. However, the potassium current that is induced by acetylcholine is much higher in guinea pig than in human isolated cells; a fraction of it would suffice to fully determine the resting potassium conductance in guinea pig atrial cells, whereas it can play only a modulatory role in human cells. This difference could be important in species-specific autonomic modulation and antiarrhythmic drug action.