Effect of ENaC blockade on the myogenic response of rat juxtamedullary afferent arterioles

The mechanosensitive signal transduction pathway underlying the myogenic response is poorly understood. The role of epithelial sodium channels (ENaC) on the afferent arteriolar myogenic response was investigated in vitro using the blood‐perfused rat juxtamedullary nephron technique. Papillectomy was used to isolate myogenic influences by eliminating TGF signals. Pressure‐mediated autoregulatory responses were assessed by manipulating renal perfusion pressure in 30 mmHg steps. Under control (Con) conditions, the afferent arteriolar diameter increased 15% from 13.0±1.3 to 14.7±1.2μm (p<0.05) after decreasing pressure from 100 to 70 mmHg and then decreased to 11.3±1.1μm and 10.6±1.0μm after increasing pressure to 130 and 160 mmHg (88±1 and 81±2% of Con, p<0.05), respectively. Pressure‐mediated afferent arteriolar responses were inhibited by superfusion of 10 μμM amiloride (102±2, 97±4 and 94±3% of Con), 10 μM benzamil (106±5, 100±3 and 103±3% of Con) and when perfusing with blood containing 5 μμM amiloride (106±2, 97±4 and 97±4% of Con), while responses to 55mM KCl were preserved. Afferent arteriolar diameters declined by 66±7, 55±8 and 60±4% in each treatment group compared to 64±8% in Con (p>0.05). These results suggest that ENaC may be a component of the mechanosensitive ion channel complex eliciting myogenic responses in juxtamedullary afferent arterioles.