Membrane electrical properties of vascular smooth muscle from the guinea pig superior mesenteric artery

Some electrical membrane properties of an isolated small artery, namely, the superior mesenteric artery of the guinea pig, were studied by intracellular microelectrodes. The mean resting membrane potential (E_m) was –54 mV. The average slope of theE_m vs. log [K]_o curve (between 10 and 100 mM [K]_o) was 32 mV/decade, and the curve extrapolated to a [K]_i of 160 mM. The ratio of Na⁺ permeability to K⁺ permeability (P_Na/P_K) at 4.0 mM [K]_o calculated from the Goldman constant-field equation (assuming Cl^– to be passively distributed) was 0.18 (E_m=–46 mV after a 5 min exposure to ouabain to suppress any electrogenic pump potential). The normal input resistance (R_in) averaged 8.5 m. Choline substitution for Na⁺ or amiloride, an agent known to depressP_Na, hyperpolarized the muscle to about –63 mV without a significant change inR_in. Ba²⁺ (0.5 mM) depolarized the muscle to –37 mV, increasedR_in to 15 m, and produced spontaneous action potentials in this normally quiescent artery; tetraethylammonium (TEA, 5 mM) enabled large overshooting action potentials to be produced upon stimulation. Glutamate of NO₃^– substitution for Cl^– produced an initial depolarization followed by a return to the original resting potential within 10 min; readdition of 25 mM Cl^– transiently hyperpolarized the muscle markedly, followed by a return to the originalE_m. These data indicate that Cl^– is passively distributed and does not contribute to the steady-state resting potential in this vascular muscle. The data also suggest that the relatively lowE_m in this arterial muscle is not due to a low [K]_i, but is due to a highP_Na/P_K ratio, presumably related to a low K⁺ conductance (g_K). Since Ba²⁺ and TEA⁺ are known to decrease restingg_K and K⁺ activation, the data also suggest that K⁺ activation could inhibit action potential generation.