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. 1993 Mar;108(3):678–683. doi: 10.1111/j.1476-5381.1993.tb12860.x

Modulation of alpha 1-adrenoceptors and functional consequences in the bisected rat vas deferens following chronic inhibition of neuronal noradrenaline uptake.

J Sallés 1, A Badia 1
PMCID: PMC1908037  PMID: 8096783

Abstract

1. The adaptational changes induced after chronic inhibition of neuronal noradrenaline uptake on both functional responsiveness of alpha 1-adrenoceptor activation and [3H]-prazosin binding were investigated in prostatic and epididymal portions of the rat vas deferens. 2. Contractile concentration-response curves to phenylephrine and saturation isotherms of [3H]-prazosin binding to homogenates of each of the portions of the bisected rat vas deferens were determined 48 h after the last injection of desipramine, nomifensine or nisoxetine (10 mg kg-1; i.p. for 14 days). 3. Treatment with both nomifensine and nisoxetine decreased the potency (pD2) of phenylephrine by about 10 and 8 fold respectively in the epididymal portion. However, administration of desipramine only reduced the potency of the alpha 1-adrenoceptor agonist by about 1.8 fold. None of the treatments modified the maximal effect (Emax) elicited by phenylephrine in this portion of the vas deferens. In the prostatic portion only the treatment with nomifensine (1.4 fold) and nisoxetine (1.8 fold) decreased the potency of phenylephrine; the maximal contraction elicited by the agonist after the treatments was also reduced. 4. Chronic treatment with either nomifensine or nisoxetine did not change the KD for [3H]-prazosin binding in either epididymal or prostatic membranes. However, these two treatments resulted in a significant decrease in the [3H]-prazosin Bmax in membranes in both portions of rat vas deferens. The reduction in density of alpha 1-adrenoceptors was higher in the epididymal than the prostatic half. Desipramine reduced the Bmax only in the epididymal portion.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selected References

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