Altered Contractility of Rabbit Penile Corpus Cavernosum Smooth Muscle by Hypoxia

Kim, Noel N.; Kim, Je Jong; Hypolite, Joseph A.; García-Díaz, J. Fernando; Broderick, Gregory A.; Tornheim, Keith; Daley, Jennifer; Levin, Robert M.; Tejada, Iñigo Sáenz de

doi:10.1016/s0022-5347(01)66519-4

Cited by 52 publications

(47 citation statements)

References 20 publications

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“…These studies have investigated the effects of hypoxia, acidosis or glucopenia on cavernosal smooth muscle contraction. [4][5][6][7][8] The effects of acidosis and hypoxia have also been investigated using in vivo models. 9,10 As to which of these parameters is involved in irreversible smooth muscle dysfunction during low flow priapism has not yet been assessed.…”

Section: Introductionmentioning

confidence: 99%

“…Hypoxia has been shown to induce ATP depletion in the corpus cavernosum. 5 In other smooth muscle preparations, glucopenia or hypoxia either alone or in combination have been shown to cause loss of tone and depletion of ATP. [12][13][14] Whether intracellular ATP levels can be maintained during ischaemia and subsequently replenished following reperfusion in the corpus cavernosum is not entirely clear.…”

Section: Introductionmentioning

confidence: 99%

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Investigation of cavernosal smooth muscle dysfunction in low flow priapism using an in vitro model

et al. 2004

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The effects of hypoxia (pO 2 : 50 mmHg), acidosis (pH: 6.9) or glucopenia (absence of glucose) in vitro on the tone of the rabbit corpus cavernosum were investigated. The recovery of smooth muscle contractility following exposure to these conditions was also assessed. Hypoxia, acidosis or glucopenia alone or in combination showed a sustained reduction in the tone. Reperfusion of tissue strips showed complete recovery of smooth muscle tone for all conditions except when hypoxia and glucopenia were combined or when hypoxia, glucopenia and acidosis were used in combination. Incomplete recovery of tone was associated with a significant reduction in tissue ATP concentrations and an increase in the number of TUNEL (terminal deoxynucleotidyl transferasemediated dUTP nick-end labelling)-positive nuclei. This indicates that following reversal of hypoxia, acidosis and glucopenia, failure of conventional a-adrenergic agonists to produce tumescence in low flow priapism is associated with irreversible smooth muscle cell dysfunction, which is linked to ATP reduction and smooth muscle cell death.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Investigation of cavernosal smooth muscle dysfunction in low flow priapism using an in vitro model

et al. 2004

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“…However, it is known that in a rabbit model, hypoxia induced by prolonged erection and subsequent local acidosis impair contractility of trabecular smooth muscles. This phenomenon impedes the drainage of blood, perpetuates the ischemic state and may cause early ultrastructural changes (Kim et al 1996, Saenz de Tejada et al 1997, Moon et al 1999. Taking into account our findings, the risk that fibrotic alterations may begin early after acute hypoxia has occurred inside the corpora is quite elevated.…”

Section: Discussionmentioning

confidence: 64%

Platelet-derived growth factor (PDGF) and PDGF receptors in rat corpus cavernosum: changes in expression after transient in vivo hypoxia

Aversa

Basciani²,

Visca³

et al. 2001

Journal of Endocrinology

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Platelet-derived growth factor (PDGF) overactivity has been implicated in atherosclerosis and several fibrotic conditions including lung and kidney fibrosis, liver cirrhosis and myelofibrosis. Low oxygen tension (hypoxia) is a known stimulus for transcriptional induction of PDGF ligand and receptor genes in different tissues. We studied the expression and localization of PDGF-A, PDGF-B, and PDGF receptor (PDGFR)-and -subunits in adult rat isolated corpus cavernosum (CC) under generalized transient hypoxia (pO 2 10%) in comparison with normoxic conditions. Semi-quantitative RT-PCR analysis of mRNA extracted from rat penis showed higher amounts of PDGF-A, PDGF-B and PDGFR-mRNA transcripts in hypoxic versus normoxic animals. The immunohistochemical analysis showed that the localization of PDGF subunits and PDGFR-was confined to the cytoplasm of the perivascular smooth muscle cells, endothelium and trabecular fibroblasts. Our findings indicate that transient low oxygen tension induces PDGF overexpression in rat CC, which in the long term may lead to an increase of connective tissue production. We suggest that a local impairment of the PDGF/PDGFR system may contribute to CC fibrosis, which is an established cause of erectile dysfunction in man.

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“…In an in vitro study of rabbit erectile tissue under hypoxic conditions (pO2=10 mm Hg), contractions elicited by norepinephrine, endothelin-1 or potassium were attenuated. 18 The hypoxia-induced relaxation was not affected by the removal of the endothelium.…”

Section: The Role Of Hypoxiamentioning

confidence: 94%

Oxidative Stress and Molecular Reactions in Arteriogenic Erectile Dysfunction

Azadzoi

Siroky

2009

Chonnam Med J

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Vascular disorders are the leading causes of organic erectile dysfunction (ED). Most cases of arteriogenic ED are associated with vascular risk factors such as hypercholesterolemia, atherosclerosis, diabetes mellitus, hypertension, and smoking. These conditions impair vascular structure directly or indirectly by facilitating oxidative damage due to accumulation of reactive oxygen and nitrogen species such as superoxide (O 2 − ), hydrogen peroxide (H 2 O 2 ), hydroxyl radicals and peroxynitrite (O=NOO − ). Clinical studies have shown that the degree of arteriogenic ED cannot be predicted exclusively by the arterial integrity, suggesting that it involves local changes within penile smooth muscle cells, endothelium, nerves, and microvasculature. It is thought that arterial occlusion and subsequent lack of erectile tissue perfusion, nutrient deficiency, hypoxia, and accumulation of waste products constitute an environment hospitable to free radical formation and detrimental to nitric oxide (NO) bioavailability. Studies of animal and cell culture models have revealed that exposure to ischemia and hypoxia triggers a cascade of cellular and molecular changes in the erectile tissue with devastating impact on its structure and function. These alterations involve cytotoxic radicals, nitric oxide synthase (NOS), eicosanoids, neurotoxic elements, and growth factors and lead to impairment of NO/cGMP pathway, smooth muscle dysfunction, microvascular damage, and neurodegeneration. Ultimately, these events lead to erectile tissue fibrosis and the failure of penile veno-occlusive mechanism. These local changes in the hypoxic erectile tissue may explain the failure of revascularization surgery to completely cure arteriogenic ED and imply the need for newer therapeutic strategies to remove cytotoxic and neurotoxic elements from the chronically ischemic penis.

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Altered Contractility of Rabbit Penile Corpus Cavernosum Smooth Muscle by Hypoxia

Cited by 52 publications

References 20 publications

Investigation of cavernosal smooth muscle dysfunction in low flow priapism using an in vitro model

Investigation of cavernosal smooth muscle dysfunction in low flow priapism using an in vitro model

Platelet-derived growth factor (PDGF) and PDGF receptors in rat corpus cavernosum: changes in expression after transient in vivo hypoxia

Oxidative Stress and Molecular Reactions in Arteriogenic Erectile Dysfunction

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