Puri and Saha (2003) found that in rats cadmium inhibited angiotensin-converting enzyme (ACE) at low, medium, and high doses without a dose–response effect yet paradoxically induced HTN; they postulated that cadmium’s vascular effects predominated over its central effects in HTN rats. Although cadmium’s central versus vascular effects in humans are unknown, it has been shown that the ACE inhibitor valsartan is more effective in preventing cardiac failure in HTN men than in HTN women (Zanchetti et al. 2006). Here, ACE is linked to hypertensive disorder.