The influence of receptor occupation on Ca++ influx-mediated vascular smooth muscle contraction.
A possible role of the agonist-induced intracellular calcium release process in mediating the utilization of the Ca++ ions which enter the smooth muscle cells during activation is proposed. The rate of refilling of the agonist-sensitive intracellularly bound calcium pool was found to be decreased when Ca++ influx was reduced by D-600 and increased when Ca++ influx was stimulated by KCl. Similarly, the rate of tension development in response to a stimulation of Ca++ influx by KCl was found to be slowed when the agonist-sensitive internal calcium pool had been depleted prior to addition of KCl and to be accelerated in the presence of an agonist capable of releasing this pool. These findings indicate that the agonist-sensitive internal Ca++ pool is capable of sequestering Ca++ which enters during the stimulation of Ca++ influx and that receptor occupation reduces the sequestration capacity of this pool. It is suggested that the agonist-induced internal calcium release process may play two roles in arterial smooth muscle activation: (1) the released Ca++ is directly involved in activation and (2) receptor occupation may reduce the ability of intracellular sites to sequester Ca++, thereby allowing more of the stimulated Ca++ influx to be utilized for activation.
D000818:Animals; D001665:Binding Sites; D002118:Calcium / Q000378:metabolism*; D005711:Gallopamil / Q000494:pharmacology; D066298:In Vitro Techniques; D007811:Lanthanum / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D011189:Potassium Chloride / Q000494:pharmacology; D011450:Prostaglandin Endoperoxides, Synthetic / Q000494:pharmacology; D011817:Rabbits; D014661:Vasoconstriction / Q000187:drug effects
D011450:Prostaglandin Endoperoxides, Synthetic; D005711:Gallopamil; C028429:U 44069; D011189:Potassium Chloride; D007811:Lanthanum; D002118:Calcium