Electrical and Mechanical Characteristics of Vascular Smooth Muscle Response to Norepinephrine and Isoproterenol
Effects of norepinephrine (NE) and isoproterenol on simultaneously recorded electrical and contractile activity in rat portal vein were studied using a sucrose-gaps technique. This vascular smooth muscle shows spontaneous phasic contractions correlated with bursts of action potentials. Norepinephrine (10-99 to 10-7 w/v) increases the duration of the bursts and shortens the interval between after an initial period of continuous spike discharge. The tension response is greater than can be accounted for by the increase in electrical activity. High NE concentrations (10-5) produce depolarization, decrease of spike amplitude, or even abolition of spikes and maintained contractions. Norepinephrine increases contracture tension of K+-depolarized portal vein without changing membrane potential. Electrical and mechanical activity is reinitiated in preparations inactivated by elimination of Ca2+ this may be due to release of bound calcium. Phenoxybenzamine abolishes the above NE responses. The typical response to isoproterenol (109 to 107) in a normal ionic environment consists of moderate depolarization, decreased burst duration, but increased frequency of bursts and inhibition of tension development which is not simply correlated with the change in electrical activity. This pattern resembles that produced by lowering [Ca2+]o. Contracture tension in high [K+]o is reduced by isoproterenol without changes in membrane potential. These responses to isoproterenol are abolished by propranolol. At high concentrations of isoproterenol (10-5) the inhibitory responses are not sustained, but revert to a pattern of activity resembling that induced by NE.
- membrane potential
- depolarized smooth muscle
- role of calcium
- rat portal vein
- Accepted September 1, 1967.
- © 1967 American Heart Association, Inc.