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Attenuated endothelin‐1 (ET‐1) vasoconstrictor responses in cardiometabolic syndrome are attributed to increased ET‐B receptors

Vascular dysfunction is an important complication linking cardiometabolic syndrome with cardiovascular diseases. The objective of the present study was to discover the effect of ET‐1 on mesenteric resistance arteries from a cardiometabolic syndrome disease model and assess the relative contribution of ET‐A and ET‐B receptors. Spontaneously hypertensive obese (SHROB) rats displayed increased blood pressure (154±3 vs. 123±2 mmHg) and body weight (417±7 vs. 270±5 g) compared to WKY rats. Mesenteric arteries were isolated and diameter responses to the vasoconstrictor peptide ET‐1 (0.01–10nM) were determined. Baseline mesenteric resistance artery diameters did not differ between WKY, SHR and SHROB. Mesenteric resistance artery responses to 10 nM ET‐1 were greatly attenuated in SHROB (26±9%) compared to SHR (44±13%) and WKY (69±2%). Addition of either ET‐A antagonist BQ123, or ET‐B agonist sarafotoxin 6c resulted in vasodilation in SHROB (105±2% and 104±2%, respectively) suggesting an enhanced ET‐B receptor mediated response in SHROB. Furthermore, ET‐B receptor protein expression was elevated 32 fold in SHROB compared to WKY, respectively. These results indicate that upregulation of the ET‐B receptor contributes to the greatly diminished ET‐1 vasoconstriction in cardiometabolic syndrome.