Activation of calcium mobilization and calcium influx by alpha 1-adrenergic receptors in a smooth muscle cell line |
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| Authors: | E E Reynolds G R Dubyak |
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| Affiliation: | 1. Department of Pharmacology, University of Pennsylvania, Philadelphia, PA 19104 USA;2. Department of Biochemistry-Biophysics, University of Pennsylvania, Philadelphia, PA 19104 USA;1. Département de Mécanique, Université de Jijel, BP 98, Ouled Aissa, Jijel 18000, Algeria;2. LEAM, Université de Jijel, BP 98, Ouled Aissa, Jijel 18000, Algeria;3. LESEI, Université de Batna, avenue Chahid Boukhlouf, 05000 Batna, Algeria;1. Department of Physiology, Hôpital Bichat, Assistance Publique - Hôpitaux de Paris, 75018 Paris, France;2. Université de Paris, Paris, France;3. Hypertension Unit, Hôpital Européen Georges Pompidou, Assistance Publique - Hôpitaux de Paris, 75015 Paris, France |
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| Abstract: | Alpha 1-adrenergic receptor (alpha 1R) mediated increases in the cytosolic levels of free Ca+2 and the inositol phosphates were measured in a smooth muscle cell line, DDT1. Norepinephrine (NE) stimulated a rapid increase in cytosolic Ca+2 by two distinct components: 1) release of Ca+2 from intracellular sites (mobilization), and 2) influx of extracellular Ca+2. The mobilization component was not affected by removal of extracellular Ca+2 or addition of La+3 or Co+2 to the buffer. The influx component was abolished by EGTA, La+3, or Co+2, but was not affected by the voltage-operated Ca+2 channel blockers diltiazem or nifedipine. Depolarization of DDT1 cells with 100 mM KCl or with gramicidin did not induce Ca+2 influx. NE also increased inositol trisphosphate to 78% over basal levels within 1 minute. These results suggest that alpha 1R on DDT1 cells are coupled to both the mobilization of intracellular Ca+2 and to receptor-operated Ca+2 channels in the plasma membrane, and that polyphosphoinositide hydrolysis may play a role in these phenomena. |
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