Agonist-activated Ca^(2+) entry is important in many biological responses such as secretion and cell growth. In nonexcitable cells which have no voltage-operated Ca^(2+) channels (VOCC), agonist-receptor interaction can trigger Ca^(2+) entry across the plasmalemma via several entry pathways (Fig 1): (A) channels which are intrinsic structures of the receptor (receptor-operated channels),(B) channels which are coupled to receptors via a G-protein (G-protein-operated channels), (C) channels which are activated by some second messengers (second-messenger-operated channels), and(D) channels which open upon intraeellular nonmitochondrial Ca^(2+) store depletion (Ca^(2+) release-activated channels) resulting from inositol 1, 4, 5-trisphosphate-induced Ca^(2+) release or inhibition of Ca^(2+) re-uptake (see next section). Ca^(2+) entry
AIM: To examine the effects of tetrandrine (Tet) on the aggregation and ATP-release of rat washed platelets induced by several platelet activators. METHODS: Gel-filtration (Sepharose 2B) was used to isolate washed platelets from adult rats and the platelet aggragation and ATP-release were measured simultaneously. RESULTS: In the presence of Ca2 + 1 mmol · L-1, Tet 300 μmol·L -1 inhibited the aggregation induced by ADP ( 25 μmol · L -1), collagen (2.5 g·L-1), and thrombin (103 unit·L-1) by 62 %, 60 %, and 34 %, respectively. It also inhibited arachidonic acid (1 mmol · L-1)-induced aggregation. Elevating intracellular Ca2 + concentration with the Ca2 + ionophore, calcimycin (30 μmol · L-1), or by blocking the intracellular calcium pump with cyclopiazonic acid (5 μmol · L-1) initiated platelet aggregation, which was also inhibited by Tet. In Ca2+ -free medium, Tet still elicited an inhibitory effect on aggregation induced by ristocetin (2.5 g·L-1). Lower concentrations of Tet (30 nmol·L-1
