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This Article Full Text Full Text (PDF) All Versions of this Article: 569/3/723    most recent jphysiol.2005.099309v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hashitani, H. Articles by Suzuki, H. Search for Related Content PubMed PubMed Citation Articles by Hashitani, H. Articles by Suzuki, H.

Departments of
¹ Regulatory Cell Physiology
² Nephrourology
³ Functional Morphology, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan
⁴ Department of Anatomy and Structural Science, Yamagata University Graduate School of Medical Science, Yamagata 990-9585, Japan

Interaction between spontaneous and neurally mediated regulation of tone in the corpus cavernosum smooth muscle (CCSM) of the rabbit was investigated. Changes in isometric muscle tension, intracellular Ca²⁺ concentration ([Ca²⁺]_i) and membrane potential were recorded. CCSM developed spontaneous contractions, transient increases in [Ca²⁺]_i (Ca²⁺ transients) and depolarizations. This spontaneous activity was abolished by blocking L-type Ca²⁺ channels (nicardipine, 1 µM), sarcoplasmic reticulum Ca²⁺ pump activity (cyclopiazonic acid, 10 µM), Ca²⁺-activated Cl^– channels (niflumic acid, 10 µM) or cyclooxygenase-2 (COX-2; NS-398, 1 µM). Transmural nerve stimulation initiated either -adrenergic contractions or nitrergic relaxations of CCSM depending on the level of muscle tone. NS-398 suppressed nerve-evoked contractions by about 70% but caused only a 40% reduction in the corresponding Ca²⁺ transient. Blocking nitric oxide synthase with N-nitro-L-arginine (LNA, 100 µM) reinforced nerve-evoked Ca²⁺ transients by about 150%, whilst increasing the corresponding Ca²⁺ transients by only 20%. In CCSM preparations that had been pre-contracted with either noradrenaline (0.3 µM) or prostaglandin F₂ (0.1 µM), nerve stimulation inhibited about 70% of the contraction and caused only a 20% decrease in [Ca²⁺]_i. Fluorescent immunohistochemistry with COX-2 antibodies and the reverse transcriptase-polymerase chain reaction (RT-PCR) method showed that the enzyme and its mRNA were highly expressed in the CCSM. These results suggest that spontaneously produced prostaglandins (PGs) not only contribute to the generation of spontaneous contractions but also facilitate nerve-evoked contractions. Conversely, spontaneously released nitric oxide (NO) suppresses excitation. Thus, interaction between spontaneous and neurally mediated regulation of CCSM tone may be fundamental to maintaining the muscle contractility. In addition, both PGs and NO appear to alter CCSM tone with only small changes in [Ca²⁺]_i.

(Received 26 September 2005; accepted after revision 18 October 2005; first published online 20 October 2005)
Corresponding author H. Hashitani: Department of Regulatory Cell Physiology & Nephrourology, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan. Email: hasitani{at}med.nagoya-cu.ac.jp

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