Vascular actions of C-type natriuretic peptide in isolated porcine coronary arteries and coronary vascular smooth muscle cells

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Abstract

C-type natriuretic (CNP) caused concentration-dependent relaxations in porcine coronary arteries with a maximal relaxation (10-6 M) of 46%. Relaxations to CNP in isolated coronary arteries were significantly attenuated with potassium channel antagonists charybdotoxin (10-7 M) and glibenclamide (10-7 M). Membrane potential and K+ currents were measured in enzymatically dissociated smooth muscle cells from porcine coronary arteries with patch-clamp techniques in a whole-cell mode (n = 5). CNP caused K+ channel activation and membrane hyperpolarization in a dose-dependent manner. This hyperpolarization was markedly suppressed by the potassium channel inhibitor tetraethylammonium (TEA, 5 mM). These results demonstrate that CNP relaxes porcine coronary arterial smooth muscle by hyperpolarization of vascular smooth muscle through potassium channel stimulation.

Original languageEnglish (US)
Pages (from-to)765-771
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume205
Issue number1
DOIs
StatePublished - 1994

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C-Type Natriuretic Peptide
Potassium Channels
Vascular Smooth Muscle
Smooth Muscle Myocytes
Blood Vessels
Muscle
Coronary Vessels
Swine
Cells
Charybdotoxin
Membranes
Tetraethylammonium
Glyburide
Clamping devices
Patch-Clamp Techniques
Ion Channels
Membrane Potentials
Smooth Muscle
Chemical activation

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

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title = "Vascular actions of C-type natriuretic peptide in isolated porcine coronary arteries and coronary vascular smooth muscle cells",
abstract = "C-type natriuretic (CNP) caused concentration-dependent relaxations in porcine coronary arteries with a maximal relaxation (10-6 M) of 46{\%}. Relaxations to CNP in isolated coronary arteries were significantly attenuated with potassium channel antagonists charybdotoxin (10-7 M) and glibenclamide (10-7 M). Membrane potential and K+ currents were measured in enzymatically dissociated smooth muscle cells from porcine coronary arteries with patch-clamp techniques in a whole-cell mode (n = 5). CNP caused K+ channel activation and membrane hyperpolarization in a dose-dependent manner. This hyperpolarization was markedly suppressed by the potassium channel inhibitor tetraethylammonium (TEA, 5 mM). These results demonstrate that CNP relaxes porcine coronary arterial smooth muscle by hyperpolarization of vascular smooth muscle through potassium channel stimulation.",
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T1 - Vascular actions of C-type natriuretic peptide in isolated porcine coronary arteries and coronary vascular smooth muscle cells

AU - Wei, C. M.

AU - Hu, S.

AU - Miller, Virginia M

AU - Burnett, John C Jr.

PY - 1994

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AB - C-type natriuretic (CNP) caused concentration-dependent relaxations in porcine coronary arteries with a maximal relaxation (10-6 M) of 46%. Relaxations to CNP in isolated coronary arteries were significantly attenuated with potassium channel antagonists charybdotoxin (10-7 M) and glibenclamide (10-7 M). Membrane potential and K+ currents were measured in enzymatically dissociated smooth muscle cells from porcine coronary arteries with patch-clamp techniques in a whole-cell mode (n = 5). CNP caused K+ channel activation and membrane hyperpolarization in a dose-dependent manner. This hyperpolarization was markedly suppressed by the potassium channel inhibitor tetraethylammonium (TEA, 5 mM). These results demonstrate that CNP relaxes porcine coronary arterial smooth muscle by hyperpolarization of vascular smooth muscle through potassium channel stimulation.

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