Acute lead exposure stimulates the renin-angiotensin system, increasing renin and aldosterone levels through a calcium-dependent mechanism.
Suggests calcium-dependent RAS activation by lead in animals; leaves open translation to human hypertension risk.
Acute lead treatment of rabbits resulted in significant increases in both plasma renin activity and aldosterone concentration. No significant changes were observed in blood pressure, heart rate and plasma angiotensin-converting enzyme activity. The calcium channel-blocking drug verapamil attenuated the renin and aldosterone response in vivo. Lead increased renin release in a dose-dependent manner in a renal cortex slice preparation. Both verapamil and diltiazem attenuated the lead-induced renin release in vitro, but only with diltiazem did this attain statistical significance.
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Meredith et al. (1985) studied this question.
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