The objective of this study was to characterize the α 1-adrenoceptor (α 1-AR) subtypes and evaluate the effect of acidosis on α 1-AR function and expression in goat superior mesenteric artery (GSMA).
GSMA rings were mounted in a thermostatically controlled (37.0°C ± 0.5°C) organ bath containing 20 ml of modified Krebs-Henseleit solution, maintained at pH o of 7.4, 6.8, 6.0, 5.5, 5.0, and 4.5. Noradrenaline (NA)- and phenylephrine (PE)-induced contractile response was elicited in the absence or presence of endothelium and prazosin at pH o of 7.4, 6.0, and 5.0. The responses were recorded isometrically by an automatic organ bath connected to PowerLab and analyzed using Labchart 7.1.3 software. Expression of α 1D-AR was compared at physiological and acidic pH o using reverse transcription-polymerase chain reaction (RT-PCR).
NA- and PE-induced contractile responses were attenuated proportionately with a decrease in extracellular pH (pH o), i.e. 7.4 → 6.8 → 6.0 → 5.5 → 5.0 → 4.5. Endothelium denudation increased the contractile response at both normal and acidic pH o. Prazosin (1 nM, 10 nM, and 0.1 μM) inhibited the NA- and PE-induced contractile response at pH o 7.4 and the blocking effect of prazosin was potentiated at pH o of 6.0 and 5.0. RT-PCR analysis for α 1D-AR in GSMA showed that the mRNA expression of α 1D-AR was decreased under acidic pH o as compared to physiological pH o.
(i) Adrenergic receptor mediates vasoconstriction in GSMA under normal physiological pH o, and α 1D is the possible subtype involved in this event (ii) acidosis attenuates the vasocontractile response due to reduced function and expression of α 1D-AR and also increased the release of endothelial-relaxing factors.