Levels of nitric oxide metabolites do not increase during penile erection

Moriel, Evyatar Z.; González‐Cadavid, Néstor F.; Ignarro, Louis J.; Byrns, Russ; Rajfer, Jacob

doi:10.1016/0090-4295(93)90271-b

Cited by 17 publications

(7 citation statements)

References 11 publications

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“…A link between the pathogenesis of ED and decreased local NO activity has been suggested by De Tejada et al (1989), as in isolated corpus cavernosal strips from diabetic patients with ED, both neurogenic and endothelium-dependent relaxations were impaired. Contrary to our findings, Moriel et al (1993) could not find any difference between the cavernosal blood and serum nitrite and nitrate levels before and during erection in men with normal erectile function. A significant elevation of pentosidine was found in the penile tissue, but not in the serum, of diabetic patients in comparison with non-diabetic patients.…”

Section: Discussioncontrasting

confidence: 99%

“…Our findings could be explained with this mechanism. Contrary to our findings, Moriel et al (1993) could not find any difference between the cavernosal blood and serum nitrite and nitrate levels before and during erection in men with normal erectile function. The contradiction may, in part, be explained by measurement of NO metabolites in the serum.…”

Section: Discussioncontrasting

confidence: 99%

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Cavernosal tissue nitrite, nitrate, malondialdehyde and glutathione levels in diabetic and non‐diabetic erectile dysfunction

Tuncayengin¹,

Biri

Onaran

et al. 2003

Int J of Andrology

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The aim of this study is to investigate the role of nitric oxide (NO) stabile end products, membrane lipid peroxidation and antioxidant defensive mechanism in diabetic erectile dysfunction (ED) and compare these parameters with non-diabetic ED groups. We examined the penile cavernosal tissues, obtained from 22 patients who had undergone surgery of penile prostheses implantation, for the nitrite, nitrate, malondialdehyde (MDA) and glutathione (GSH) levels. Eight patients were suffering from diabetic erectile dysfunction (ED) and 14 patients had non-diabetic ED. Nitrite and nitrate levels were lower; MDA and GSH levels were higher in the diabetic group. There were statistically significant differences between diabetic and non-diabetic groups amongst the nitrite (p<0.001), nitrate (p<0.01), MDA (p<0.001) and GSH (p<0.01) levels. Our data provide evidence that NO deficiency, possibly due to the membrane lipid peroxidation and defective antioxidant defensive mechanism, may contribute to the development of diabetic ED and thus is involved in the pathogenesis of ED in diabetic patients.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussioncontrasting

confidence: 99%

Cavernosal tissue nitrite, nitrate, malondialdehyde and glutathione levels in diabetic and non‐diabetic erectile dysfunction

Tuncayengin¹,

Biri

Onaran

et al. 2003

Int J of Andrology

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“…In blood drawn from the cavernous bodies of human subjects undergoing erections, no changes were found in nitrite and nitrate levels [82]. Nitrite and nitrate in biological fluid derive from a variety of sources and can easily mask the contribution of locally produced NO.…”

Section: Penile Vasorelaxation and Erectionmentioning

confidence: 99%

Penile Arteries and Erection

Simonsen

García‐Sacristán²,

Prieto³

2002

J Vasc Res

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Alterations in the flow of blood to and from the penis are thought to be the most frequent causes of male erectile dysfunction and, therefore, the present review focuses on the penile vasculature. In the flaccid state, tonic noradrenaline release from the sympathetic nerves contracts penile arterial and corporal smooth muscle through activation of postjunctional α₁-adrenoceptors, both by increasing intracellular calcium and by enhancing the sensitivity of the contractile apparatus for calcium. In addition, noradrenaline inhibits vasodilatatory neurotransmitter release by prejunctional α₂-adrenoceptors. The exact role of the sympathetic neurotransmitters, neuropeptide Y and adenosine 5′-triphosphate, in erection is largely unknown. Penile vasodilatation during erection is mediated by nitric oxide (NO) through activation of guanylyl cyclase in the smooth muscle layer, followed by increases in cyclic guanosine monophosphate lowering of intracellular calcium and desensitisation of the contractile apparatus for calcium. Acetylcholine, vasoactive intestinal peptide as well as peptides in sensory nerves probably also play a role in penile vasodilation. Increased flow through the penile arteries stimulates the endothelium leading to release of NO, prostanoids and a non-NO non-prostanoid factor, and as such enhances the vasodilatation, while the role of endothelium-derived contractile factors in penile vasoconstriction is not clear. Erectile dysfunction shares arterial risk factors with ischaemic heart disease, and diabetes, age, and hypercholesterolaemia are associated with impairment of both neurogenic and endothelium-dependent vasodilator mechanisms in corpus cavernosum. Only few studies have investigated the impact of these risk factors on the penile vasculature, although recent evidence suggests that arterial insufficiency precedes changes in corpus cavernosum leading to erectile dysfunction.

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“…In the pithed rat, L-NNA attenuated the corporeal response to spinal stimulation [59, 60], and in the intact rat, i.v. On the other hand, erection in male volunteers was not associated with any measurable level of nitric oxide metabolites in cavernous or peripheral blood [139]; however, this observation may have been due to methodological difficulties involved in measuring such drug levels. In dogs, L-NNA blocked pelvic nerve-stimulated erections.…”

Section: Nitric Oxidementioning

confidence: 75%

Regulation of tone in penile cavernous smooth muscle

Andersson

Holmquist

1994

World J Urol

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Since Benson, in 1983, reported on a potent nonadrenergic, noncholinergic (NANC) transmitter postulated to relax penile vessels and the corpus cavernosum, much new information on the mechanisms of contraction and relaxation of corporeal smooth muscle and penile vasculature has been obtained. The information currently available suggests that NANC transmitters may be involved in both contractile and relaxant responses of penile erectile tissues. There is good experimental evidence to allow the assumption that neurogenic nitric oxide (NO) is a mediator of penile erection, but even if NO probably is the most important factor for relaxation of penile vessels and the corpus cavernosum, this does not exclude the possibility that other agents released from nerves m a y have a modulatory function in this process. However, the roles of, for example, vasoactive intestinal polypeptide and related peptides as neurotransmitters and/or neuromodulators in the nervous control of penile erection have yet to be established. The restricted availability of human penile erectile tissues has led to the use of cavernous tissue and penile vessels from animals, both for screening and for detailed analysis of mechanisms previously demonstrated to exist also in human tissues. When interpreting the results obtained, it is important to stress that there may be important differences between human and animal tissues, that each of the tissues only gives a piece of information on the complex process of penile erection, and that the physiological and clinical importance of results from such experiments may be limited. The differing responses in different parts of the vasculature within the penis and the multiplicity of putative transmitters present in the corpus cavernosum and in perivascular nerves make further investigations necessary, as do the interactions between transmitters and neuromodulators at the neuromuscular junction, and between the neural and endothelial control of vascular tone. matter has increased markedly, mainly as a consequence of the now widely used principle of treating impotence by intracavernous injections of vasoactive agents. To fulfill better the needs of each individual patient and to treat impotence on the basis of the underlying pathological disorder, it is essential to gain detailed knowledge about the mechanisms controlling tumescence and detumescence under normal conditions and to characterize the possible factors influencing this finely tuned system.It has long been believed that the contraction of penile smooth muscle, necessary for keeping the penis in the flaccid state, is maintained mainly, but probably not solely, by the release of noradrenaline acting on postjunctional o~adrenoceptors, and several reviews discussing this issue have recently been published (e.g., [7, 8, 51,121]). It is also known that parasympathetic activity is of importance for penile erection, possibly through release of factors causing inhibition and thereby decreasing the effects of contractile factors. However, because of the quite var...

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Levels of nitric oxide metabolites do not increase during penile erection

Cited by 17 publications

References 11 publications

Cavernosal tissue nitrite, nitrate, malondialdehyde and glutathione levels in diabetic and non‐diabetic erectile dysfunction

Cavernosal tissue nitrite, nitrate, malondialdehyde and glutathione levels in diabetic and non‐diabetic erectile dysfunction

Penile Arteries and Erection

Regulation of tone in penile cavernous smooth muscle

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