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PubMed1983

Effects of calcium antagonists on spontaneous and pharmacologically increased contractility of vascular smooth muscle.

Effects of calcium antagonists on spontaneous mechanical activity and pharmacological reactivity of isolated rat portal vein were investigated. Prenilamine (PREN) 2 X 10(-4) M, verapamil (VER) 2 X 10(-5) M and nifedipine (NIF) 3 X 10(-8) M abolished spontaneous phasic contractions. In veins incubated in calcium-free medium plus PREN, VER or NIF, readmission of calcium restored mechanical activity up to similar control values when [Ca2+]0 reached 4.88 mM. Contractures evoked by epinephrine (EPI) 2.5 X 10(-5) M or KCl 90 mM were diminished in a similar degree by all three antagonists, its pharmacological potency being NIF greater than VER greater than PREN. Tonic component of contracture was significantly more depressed than phasic. Contracture evoked by methoxamine 10(-4) M was impaired by prazosin 10(-8) M as well as by NIF 3 X 10(-10) M. The alpha1 antagonist also blocked EPI contractile effects. Comparative studies were performed in isolated rat tail ventral artery; contractions evoked by KCl 120 mM or EPI 5 X 10(-5) M or methoxamine 10(-4) M were differentially affected by calcium omission or by NIF 3 X 10(-8) M. Results support the hypothesis that calcium antagonists act mainly by interfering with calcium influx across cell membrane without selective action upon voltage or receptor operated channels.

Animals↗