High impact information on EDN3

• To characterize the ET receptors present in dog coronary arteries, competition binding assays with radiolabeled ET-1 using ET-1, ET-3, ETA receptor antagonist BQ-123, and sarafotoxin S6c were performed [1].
• Endothelin 3 (which stimulates endothelin A and B receptors) caused contractions of bronchi from autotransplanted lungs which were not different from those caused by endothelin 1 [2].
• Competitive inhibition of 125I-endothelin 1 by endothelin 3 was significant for a two-site binding model in membranes prepared from all bronchi and lung parenchyma [2].
• ET-1, ET-2, ET-3, and sarafotoxin caused dose-dependent accumulation of inositol phosphatase (IPs) and tracheal smooth muscle contraction [3].
• The amount of acetylcholine released by preganglionic stimulation for 10 min was concentration-dependently inhibited after exposure to ET-3 (10(-9)-10(-6) M) or IRL-1620, endothelin ET(B) receptor agonist (10(-8)-10(-5) M) [4].

Biological context of EDN3

• 5. Vasoconstriction induced by ET-3 (0.1 nM-0.3 microM) in porcine coronary arteries showed a concentration-response curve with two distinct phases in contrast to that seen with sarafotoxin S6c [5].
• Presumably ET-3 enhances the release of nitric oxide and prostaglandins and then renal vasodilation occurs [6].
• Continuous infusion of ET-3 in a dose of 5 ng/kg/min for 25 min increased both renal blood flow (RBF) and urine flow rate [6].
• Species-dependent differences in inotropic effects and phosphoinositide hydrolysis induced by endothelin-3 in mammalian ventricular myocardium [7].
• The maximum increase in splenic arterial vascular resistance was not significantly different for either ET-1, ET-3 or NA [8].

Anatomical context of EDN3

• Expression of PPET3 mRNA was detected throughout the organs examined, which included heart, lung, liver, kidney, spleen, stomach, pancreas, duodenum, colon, uterus, ovary and testis [9].
• Positive chronotropic responses to preganglionic stellate stimulation were inhibited by endothelin-3 (0.5-2 micrograms) given directly to the ganglia through the artery [10].
• Effects of endothelin-3 on ganglionic transmission were investigated in dog cardiac sympathetic ganglia [10].
• The relaxation by ET-3 was not affected by endothelium denudation nor treatment with NG-nitro-L-arginine, but was abolished or reversed to a contraction by treatment with indomethacin and markedly suppressed by tranylcypromine, a PGI2 synthetase inhibitor, or diphloretin phosphate, a prostaglandin receptor antagonist [11].
• ET-1 and ET-3 stimulated canine prostatic epithelial cell growth in vitro [12].

Associations of EDN3 with chemical compounds

• The rank order of molar potency in causing splenic capsular contraction was ET-1 greater than ET-3 greater than NA [8].
• Activation of endogenous thromboxane A2 biosynthesis mediates presynaptic inhibition by endothelin-3 of dog stellate ganglionic transmission [10].
• 5. The splenic vasoconstrictor responses to ET-1 and ET-3 were accompanied by reductions in spleen volume [8].
• The amount of acetylcholine released during preganglionic stimulation was reduced by exposure to endothelin-3 (10(-9) to 10(-6) M) [10].
• Furthermore, endothelin-3 (10(-7) M) stimulated the OKY-046- and indomethacin-sensitive formation of thromboxane A2 in the ganglia [10].

Other interactions of EDN3

• 6. These results suggest that the vasoconstriction induced by endothelin-3 and lower doses of endothelin-1 and endothelin-2, largely depends on the influx of Ca2+ ions [13].

Analytical, diagnostic and therapeutic context of EDN3

• The full-length cDNA of dog preproendothelin-3 (PPET3) was cloned from lung tissue using RT-PCR and rapid amplification of cDNA ends [9].
• The two peaks demonstrated on fast protein liquid chromatography co-eluted with endothelin 1 and endothelin 3 respectively [14].
• In addition, high-frequency RNS-induced decreases in the glomerular filtration rate (GFR) and the filtration fraction (FF) were suppressed by ET-3 infusion [15].

References