Sympathetic neurotransmission in the rat testicular capsule: Functional characterization and identification of mRNA encoding α1-adrenoceptor subtypes
Autor: | Aron Jurkiewicz, Luciana Ferreira Verde, Maria Christina W. Avellar, Neide H. Jurkiewicz, Afonso Caricati-Neto, Haydée Rezende Reuter |
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Rok vydání: | 2006 |
Předmět: |
Male
medicine.medical_specialty Spiperone Reserpine Sympathetic Nervous System Nifedipine Adrenergic Suramin Biology Synaptic Transmission Clonidine Dioxanes Norepinephrine chemistry.chemical_compound Adenosine Triphosphate Chloroethylclonidine Receptors Adrenergic alpha-1 Internal medicine Testis Purinergic P2 Receptor Antagonists medicine Prazosin Animals Channel blocker RNA Messenger Rats Wistar Adrenergic alpha-Antagonists Pharmacology Adrenergic Uptake Inhibitors Dose-Response Relationship Drug Receptors Purinergic P2 Reverse Transcriptase Polymerase Chain Reaction Antagonist Acetyl-CoA C-Acyltransferase Calcium Channel Blockers Electric Stimulation Rats Yohimbine Endocrinology chemistry Idazoxan Muscle Contraction medicine.drug |
Zdroj: | European Journal of Pharmacology. 543:141-150 |
ISSN: | 0014-2999 |
Popis: | The rat testicular capsule is a thin tissue surrounding the testis, whose precise function is still unknown. We have studied the contractile effects of electrical field stimulation, noradrenaline, and the blockade by antagonists of adrenergic receptors, in order to characterize sympathetic neurotransmission, and adrenoceptor subtypes. In addition, reverse transcription polymerase chain reaction (RT-PCR) assays were made to check for the expression of the three known subtypes of alpha(1)-adrenoceptors. The effects of electrical field stimulation (2 to 20 Hz, 1 ms, 60 V) were almost totally abolished by depletion of neuronal noradrenaline storage with reserpine (10 mg/Kg), but not by the purinergic receptor antagonist suramin (10(-5) M), indicating that noradrenaline, but not ATP, was involved in contractions. The selective alpha(1)-adrenoceptor antagonist prazosin (10(-7) M) was more effective than the selective alpha(2)-adrenoceptor antagonist idazoxan (10(-7) M) to inhibit contractions induced by electrical field stimulation, pointing out a major involvement of alpha(1)-adrenoceptor. When noradrenaline was used instead of electrical field stimulation, it showed a high potency (pD(2)=7.9). Noradrenaline-induced contractions were competitively blocked by the selective alpha(1A)-adrenoceptor antagonists WB 4101 (pA(2)=8.88), phentolamine (pA(2)=8.39) and by the alpha(1B)-adrenoceptor antagonist spiperone (pA(2)=8.57), indicating the presence of functional alpha(1A)- and alpha(1B)-adrenoceptors. In addition, contractions were not blocked by the selective alpha(1D)-adrenoceptor antagonist BMY 7378 (up to 10(-6) M), while selective alpha(2)-adrenoceptor antagonists showed low pA(2) values (yohimbine, 7.25 and idazoxan, 7.49), suggesting a minor role, if any, for alpha(1D)- and alpha(2)-adrenoceptors. To check the proportionate role of alpha(1A)- and alpha(1B)-adrenoceptors, we blocked alpha(1B)-adrenoceptors with chloroethylclonidine (CEC, 30 microM, 45 min), that reduced the maximal effect of noradrenaline by about 60%. The remnant CEC-insensitive noradrenaline contraction was assumed to be unrelated to alpha(1B)-adrenoceptor, and was inhibited by 5-methyl-urapidil (pA(2)=8.94) and by the Ca(2+) channel blocker nifedipine (3 microM), confirming the involvement of alpha(1A)-adrenoceptors. The presence of mRNA encoding alpha(1A)- and alpha(1B)-adrenoceptor was also shown on RT-PCR assays. Unexpectedly, alpha(1D)-transcripts were also detected in these assays. Taken together, our results show that ATP co-transmission could not be detected, and that neurotransmission involves the interaction of noradrenaline with both alpha(1A)- and alpha(1B)-, but not with alpha(1D)- or alpha(2)-adrenoceptor. The fact that the functional alpha(1D)-adrenoceptor could not be detected in spite of the presence of the corresponding mRNA, remains to be investigated. |
Databáze: | OpenAIRE |
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