Modulation of vascular responses of guinea-pig aorta by non-endothelial nitric oxide: A minor role for the endothelium.

Modulation of vascular responses of guinea-pig aorta by non-endothelial nitric oxide: A minor role for the endothelium. Vascul Pharmacol. 2019 Jul 23;:106580 Authors: Broadley KJ, Broadley HD Abstract Acetylcholine (Ach) causes vasodilatation by nitric oxide (NO) release from the vascular endothelium. Vasoconstrictors such as α-adrenoceptor agonists (phenylephrine) or thromboxane TxA2 mimetics (U46619) also release endothelial NO. Inhibition of nitric oxide synthase (NOS) with Nω-nitro-L-arginine (L-NAME) potentiates vasoconstriction by phenylephrine and the trace amine, β-phenylethylamine (PEA), indicating underlying opposing vasodilatation. However, the roles of the endothelium and NO in vasodilator and constrictor responses of guinea-pig aorta have not been examined and are the subject of this study. Guinea-pig thoracic aorta rings were set up in aerated Krebs solution (37 °C) and isometric tension recorded. Contractions to phenylephrine were fast onset, rapidly waned and antagonised by prazosin. PEA contractions were slow onset, sustained and not antagonised by prazosin and therefore not α1-adrenoceptor-mediated. PEA and phenylephrine contractions were enhanced by L-NAME whether endothelium was present or not. Ach produced only weak relaxation in a small proportion of endothelium intact U46619-constricted aortae, which were abolished by endothelium removal. In uncontracted aortae Ach caused small contractions, which like P...
Source: Vascular Pharmacology - Category: Drugs & Pharmacology Authors: Tags: Vascul Pharmacol Source Type: research