Tripamide (less than 10 μg/ml) does not modify the membrane potential and resistance, but does suppress the spike evoked by outward current pulses in the presence of 3-5 mM TEA[1].
In the mesenteric artery, Tripamide suppresses the amplitude of e.j.ps evoked by perivascular nerve stimulation. However, the facilitation process produced by repetitive stimulation is less affected by Tripamide[1].
In rats loaded orally with 25 ml/kg of normal saline, Tripamide (0.6-160 mg/kg) increases urine volume and sodium and chloride excretion in a dose-dependent fashion. Only at a dose of 160 mg/kg, there an increase in potassiumexcretion in rats[2].
Tripamide has anti-hypertensive effects, during administration to spontaneously hypertensive rats at a dose of 10 mg/kg/day for 4 weeks, tripamide doubled urine volume and sodium excretion, while potassium excretion is increased by <50% in rats[2].
References:
[1]. H Asada, et al. Effects of N-(4-azo-endo-tricyclo[5.2.1.0.(2.6)]-decan-4-yl)-4-chloro-3-sulfamoylbenzamide (E614; tripamide) on vascular smooth muscles. Gen Pharmaco. 1982;13(3):215-23.
[2]. Philip Hampel, et al. Azosemide is more potent than bumetanide and various other loop diuretics to inhibit the sodium-potassium-chloride-cotransporter human variants hNKCC1A and hNKCC1B. Sci Rep. 2018 Jun 29;8(1):9877.