Parmodulins inhibit signaling mediated through platelet Gα_q, but not Gα₁₃. Platelets were incubated in the presence (black line) or absence (dark gray line) of (A) 10 μM parmodulin 1 (PM1), 3 μM parmodulin 2 (PM2), 10 μM parmodulin 3 (PM3), or 10 μM parmodulin 4 (PM4); or (B) 0.3 μM vorapaxar, 0.3 μM atopaxar, 1 μM SCH79797, or 3 μM BMS-200261, and subsequently stimulated with 5 μM SFLLRN. Reversibility was assessed after washing platelets incubated with PAR1 antagonists and exposing them to 5 μM SFLLRN (light gray line). (C) Platelets were incubated with parmodulins or orthosteric PAR1 agonists as described in (A) and (B), respectively, and evaluated for [Ca²⁺]_i flux after incubation with 5 μM SFLLRN. Data are presented as means ± SEM (n = 4). (D) Platelets were incubated with the indicated PAR1 antagonists at the concentrations described in the previous legends and subsequently exposed to vehicle (–) or 10 μM SFLLRN (+). Activation of RhoA after exposure to SFLLRN was evaluated.