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The role of membrane depolarization in the contractile response of the rabbit basilar artery to 5‐hydroxytryptamine.
Author(s) -
Garland C J
Publication year - 1987
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1987.sp016783
Subject(s) - depolarization , contraction (grammar) , myogenic contraction , extracellular , repolarization , biophysics , membrane potential , basilar artery , muscle contraction , chemistry , anatomy , medicine , smooth muscle , electrophysiology , endocrinology , biology , biochemistry
1. 5‐Hydroxytryptamine (5‐HT, 10(‐9)‐10(‐4) M) depolarized and contracted smooth muscle cells (resting potential: ‐69.1 +/‐ 0.9 mV, n = 112) in isolated cylindrical segments of the rabbit basilar artery. 2. Simultaneous measurement of membrane potential and wall tension (n = 43, thirteen vessels) showed that the onset of 5‐HT‐induced depolarization coincided with the onset of smooth muscle contraction in the majority of cells studied. In addition, the onset of relaxation which followed the wash‐out of 5‐HT always preceded the onset of membrane repolarization by 52 +/‐ 8 s (n = 14). 3. In 30% of smooth muscle cells exposed to concentrations of 5‐HT greater than 10(‐6) M, fast rhythmic depolarizations (amplitude 10‐20 mV) were superimposed on the developing depolarization. Rhythmic membrane depolarization was always followed by rhythmic smooth muscle contraction, which peaked 2‐4 s after the peak of the fast depolarization. 4. Muscle contraction, but not depolarization, produced with concentrations of 5‐HT greater than 10(‐7) M, was significantly increased by the removal of intimal‐endothelial cells. 5. Smooth muscle depolarization recorded in the presence of increased extracellular K+ (greater than 5.2 mM) preceded the onset of smooth muscle contraction. For a similar change in membrane potential produced with either increased extracellular K+ or 5‐HT, the corresponding increase in arterial wall tension was always greater with 5‐HT. 6. The depolarization and contraction induced by 5‐HT was markedly reduced or abolished if extracellular Na+ was totally replaced, isosmotically, with either sucrose or Tris at pH 7.4. Normal‐sized contraction, but not depolarization, was recorded with 5‐HT in Na+‐free Tris solution at pH 8. 7. These observations suggest that 5‐HT‐stimulated contraction in cerebrovascular smooth muscle is largely a result of mechanisms other than depolarization of the smooth muscle cell membrane which it produces. However, high concentrations of 5‐HT (greater than 10(‐6) M) can stimulate additional depolarization, which has a faster time course and rhythmic nature. Discrete depolarizations of this type are responsible for initiating additional, phasic smooth muscle contractions.