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Effects of some divalent cations on nitrergic relaxations in the mouse corpus cavernosum

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Acute effects of some divalent cations (Cd2+, Ni2+, Co2+, Zn2+, Mn2+ and Sn2+) were investigated on neurogenic and endothelium‐dependent relaxations in the isolated mouse corpus cavernosum. Neither neurogenic nor endothelium‐dependent relaxation was affected by cations at the concentrations used (up to 100 μM), except Cd2+. Although Cd2+ (20 and 40 μM) did not cause any significant alteration in the acetylcholine‐ (ACh) or sodium nitroprusside‐ (SNP) induced relaxation, it inhibited electrical field stimulation‐ (EFS) produced relaxation significantly. Zn2+ and selenium could not reverse this inhibitory action. Cd2+ did block the EFS‐evoked guanethidine‐sensitive contraction in the presence of NG‐nitro‐L‐arginine. Elevation of external Ca2+ content significantly reduced the inhibitions due to Cd2+ on the EFS‐induced relaxation and on the EFS‐evoked guanethidine‐sensitive contraction. In the Ca2+‐omitted medium, EFS‐induced relaxation disappeared, while acetylcholine‐elicited relaxation resisted. Verapamil was ineffective on the relaxation produced by EFS or acetylcholine. However, it significantly diminished phenylephrine‐induced contractions. These findings suggest that unlike other cations at the concentrations used in the present study, Cd2+ may have an effect on an external Ca2+‐dependent mechanism at the neuronal level, and this effect may be responsible for its acute inhibitory action on the neurogenic relaxation in the mouse corpus cavernosum.
Title: Effects of some divalent cations on nitrergic relaxations in the mouse corpus cavernosum
Description:
Acute effects of some divalent cations (Cd2+, Ni2+, Co2+, Zn2+, Mn2+ and Sn2+) were investigated on neurogenic and endothelium‐dependent relaxations in the isolated mouse corpus cavernosum.
Neither neurogenic nor endothelium‐dependent relaxation was affected by cations at the concentrations used (up to 100 μM), except Cd2+.
Although Cd2+ (20 and 40 μM) did not cause any significant alteration in the acetylcholine‐ (ACh) or sodium nitroprusside‐ (SNP) induced relaxation, it inhibited electrical field stimulation‐ (EFS) produced relaxation significantly.
Zn2+ and selenium could not reverse this inhibitory action.
Cd2+ did block the EFS‐evoked guanethidine‐sensitive contraction in the presence of NG‐nitro‐L‐arginine.
Elevation of external Ca2+ content significantly reduced the inhibitions due to Cd2+ on the EFS‐induced relaxation and on the EFS‐evoked guanethidine‐sensitive contraction.
In the Ca2+‐omitted medium, EFS‐induced relaxation disappeared, while acetylcholine‐elicited relaxation resisted.
Verapamil was ineffective on the relaxation produced by EFS or acetylcholine.
However, it significantly diminished phenylephrine‐induced contractions.
These findings suggest that unlike other cations at the concentrations used in the present study, Cd2+ may have an effect on an external Ca2+‐dependent mechanism at the neuronal level, and this effect may be responsible for its acute inhibitory action on the neurogenic relaxation in the mouse corpus cavernosum.

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