**Core Concept**
The antagonism of leukotrienes' bronchoconstrictor effect by terbutaline in a patient with asthma involves a complex interplay between different receptor systems. Specifically, terbutaline acts on beta-2 adrenergic receptors, while leukotrienes exert their effects through cysteinyl leukotriene receptors.

**Why the Correct Answer is Right**
Terbutaline, a beta-2 adrenergic agonist, induces bronchodilation by stimulating beta-2 adrenergic receptors on bronchial smooth muscle cells. This leads to an increase in cAMP, which in turn relaxes the muscle cells and causes bronchodilation. Leukotrienes, on the other hand, exert their bronchoconstrictor effect by binding to cysteinyl leukotriene receptors on bronchial smooth muscle cells, leading to an increase in intracellular calcium and muscle contraction. The antagonism of leukotriene-induced bronchoconstriction by terbutaline can be explained by the concept of receptor-receptor interactions, where the activation of beta-2 adrenergic receptors by terbutaline can inhibit the action of leukotrienes on cysteinyl leukotriene receptors.

**Why Each Wrong Option is Incorrect**
**Option A:** This option is incorrect because it does not accurately describe the mechanism of action of terbutaline in relation to leukotriene receptor antagonism.
**Option B:** This option is incorrect because it implies a direct interaction between terbutaline and leukotriene receptors, which is not supported by the available evidence.
**Option C:** This option is incorrect because it suggests that terbutaline acts as an antagonist at leukotriene receptors, which is not the case.

**Clinical Pearl / High-Yield Fact**
It's essential to remember that the combination of beta-2 adrenergic agonists (like terbutaline) and leukotriene receptor antagonists (such as montelukast) can provide additive bronchodilatory effects in patients with asthma.

**Correct Answer:** C.