Different mechanisms for lead acetate, aluminum and cadmium sulfate in rat corpus cavernosum

Some heavy metals show adverse vascular and neurological effects, however, their effect on erection is underestimated. This study aims to investigate the effect of Pb, Cd and Al on erectile function and their potential mechanism of action in rats.

Measurement of intracavernosal pressure/mean arterial pressure (ICP/MAP) changes elicited by electrical stimulation of cavernous nerve in anesthetized rats treated with Pb-acetate, Al-sulfate, or Cd-sulfate acutely, and subacutely for 7 days. Serum creatinine, testosterone, TBARs, GSH levels and metal accumulation in corpus cavernosum were measured.

Pb, Al and Cd significantly reduced ICP/MAP in rats after acute (2,10-2,10 and 1,3 mg/kg respectively) and sub-acute (3, 3, and 1mg/kg/day respectively) treatments. They selectively accumulated in the corpus cavernosum reaching 25.107 ± 2.081 μg/g wet weight for Pb, 1.029 ± 0.193 for Cd, 31.343 ± 1.991 for Al, compared to 7.084 ± 1.517, 0.296 ± 0.067, and 8.86 ± 1.115 as controls respectively. Serum creatinine levels were not altered. Cd and Al significantly reduced testosterone level to 0.483 ± 0.059 and 0.419 ± 0.037 ng/ml respectively compared to 0.927 ± 0.105 ng/ml as control. Aluminum elevated TBARs significantly by 27.843%. The acute anti-erectile action of Pb was blocked by non-selective NOS and GC inhibitors and potassium channel blocker. Lead also masked the potentiatory effect of l-arginine and diazoxide on ICP/MAP. No interaction with muscarinic or nicotinic modulators was observed.

Pb, Cd and Al show anti-erectile effect independent on renal injury. They don not modulate cholinergic nor ganglionic transmission in corpus cavernosum. Pb may inhibit NO/cGMP/K+channel pathway. The effect of Cd and Al but not Pb seems to be hormonal dependent.