Thiocyanate induces vasoconstriction in rat-tail artery primed with norepinephrine.

The vasoregulating effects of thiocyanate (SCN-) were studied by means of a new rat tail artery perfusion model that uses constant driving pressure (1000 mm H2O). When a 30 mm long artery was perfused with 20 micromol/L verapamil, the flow rate increased 6%. Norepinephrine (10 to 1000 nmol/L) caused a dose-dependent flow inhibition. SCN- alone (0.05 to 5 mmol/L) had a slight, if any, effect on the arterial flow. However, when the artery was pretreated with norepinephrine (1000 nmol/L) for 10 minutes, followed by a basal-medium washout that left a 13% norepinephrine-induced flow inhibition, 0.05 to 5 mmol/L SCN- caused a marked flow rate reduction of between 20.4% +/- 9.8% and 28.0% +/- 21.8%, as calculated for the entire test perfusion. The decrease in flow rate correlated with the SCN- concentration (p < 0.05) and showed a clear reversibility. A similar SCN(-)-induced (0.05 mmol/L) vasoconstriction (p < 0.05) was seen when the artery was given a basal tone by continuous perfusion with low-dose norepinephrine, 10 nmol/L. Nifedipine (100 nmol/L) abolished the effect of 0.05 mmol/L SCN- but did not affect the norepinephrine priming. We conclude that SCN- amplifies the norepinephrine-induced vascular smooth muscle tone and that this may be caused by an altered calcium channel activity.