Phenylephrine-Induced Contraction in Guinea Pig Thoracic Aorta Is Triggered by Stimulation of α-Adrenoceptors Functionally Coupled with Store-Operated Ca Channels and Voltage-Dependent Ca Channels.

We examined whether the α-adrenoceptor (AR), which shows low affinity (pA < 9) for prazosin (an α-AR antagonist) and high affinity (pA ≈ 10) for tamsulosin/silodosin (α-AR antagonists), is involved in phenylephrine-induced contractions in the guinea pig (GP) thoracic aorta (TA). Intracellular signaling induced by α-AR activation was also examined by focusing on Ca influx pathways. Tension changes of endothelium-denuded TAs were isometrically recorded and mRNA encoding α-ARs/Ca channels and their related molecules were measured using RT-quantitative PCR.

Docosahexaenoic Acid Selectively Suppresses U46619- and PGF-Induced Contractions in Guinea Pig Tracheal Smooth Muscles.

We investigated the potential inhibitory effects of docosahexaenoic acid (DHA) on the contractions of guinea pig tracheal smooth muscles in response to U46619 (a thromboxane A (TXA) mimetic) and prostaglandin F (PGF) to examine whether this n-3 polyunsaturated fatty acid suppresses prostanoid-induced tracheal contractions. DHA (3 × 10 M) significantly suppressed tracheal contractions elicited by lower concentrations of U46619 (10 M) and PGF (5 × 10 M) (vs. control), although it did not suppress the contractions induced by higher concentrations (U46619: 10 M; PGF: 10 M).

Docosahexaenoic acid inhibits U46619- and prostaglandin F-induced pig coronary and basilar artery contractions by inhibiting prostanoid TP receptors.

Docosahexaenoic acid (DHA, an n-3 polyunsaturated fatty acid) inhibits U46619 (a TP receptor agonist)- and prostaglandin F-induced contractions in rat aorta and mesenteric arteries. However, whether these effects could be replicated in vasospasm-prone vessels, such as coronary and cerebral arteries, remains unknown. Here, we evaluated the changes in pig coronary and basilar artery tensions and intracellular Ca concentrations in human prostanoid TP or FP receptor-expressing cells.