Targeting the Na+/H+ exchanger 1 (NHE1) protein produces significant coronary artery dilation, offering a novel therapeutic pathway for vasospastic angina—a condition where coronary vessels suddenly constrict and reduce blood flow to the heart muscle. The research demonstrates that NHE1 inhibitors can counteract the cellular mechanisms that trigger these dangerous arterial spasms. This discovery represents a meaningful advance in cardiovascular therapeutics, as vasospastic angina affects millions globally and current treatments often provide incomplete relief. Unlike traditional calcium channel blockers or nitrates that work downstream, NHE1 inhibition appears to address the fundamental ionic imbalances driving vessel constriction. The approach could prove especially valuable for patients who experience breakthrough episodes despite standard therapy, or those who cannot tolerate existing medications due to side effects like hypotension or peripheral edema. However, the transition from mechanistic discovery to clinical application requires extensive safety testing, particularly given NHE1's role in multiple organ systems. The finding aligns with growing recognition that ion transport dysregulation underlies many cardiovascular pathologies, suggesting this mechanism might extend beyond vasospastic angina to other forms of coronary artery disease characterized by abnormal vessel reactivity.