The vasoconstrictor agent phenylephrine selectively modulates endothelium‐ vs. smooth muscle‐mediated inhibition of myogenic tone in rat cremaster arteries (677.5)

Abstract

The α1‐adrenergic agonist phenylephrine (PE) is reported to impact endothelium‐mediated vasorelaxation by influencing vasoactive signals transferred from endothelium to vascular smooth muscle (VSM), however, it is unclear whether this putative process occurs in myogenically active vessels at physiologic pressures. In the present study, we have examined the impact of PE and the TP receptor agonist U46619 on endothelium‐dependent and independent vasorelaxation of cannulated rat cremaster arterioles pressurized to 70 mmHg in the absence of luminal flow. Vasorelaxant agents acting via the endothelium (i.e. 0.3 μM acetylcholine (ACh) and 3 μM SKA‐31) or directly on VSM (i.e. 10 μM adenosine (ADO), 10 μM SNP, 5 μM pinacidil) reversibly inhibited myogenic tone by 50‐80%. Bath addition of 25 nM PE evoked a modest constriction on top of the existing myogenic tone, but did not alter the magnitude of vasorelaxant responses to ACh and SKA‐31. However, ADO‐mediated vasorelaxation was somewhat depressed and the response to pinacidil was enhanced. In the presence of U46619 (5 nM), no clear effects on either endothelium‐dependent or ‐independent vasodilatory stimuli were noted. In summary, the cellular pathways activated by PE and U46619 in VSM do not appear to influence endothelium‐mediated inhibition of myogenic tone in cremaster arterioles, suggesting that myo‐endothelial communication is unaffected by signaling events occurring downstream of α1‐adrenoceptor or TP receptor activation in these vessels.Grant Funding Source: Supported by CIHR