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NO from Flaxseed Enhances Sexual Function
Published in Robert Fried, Richard M. Carlton, Flaxseed, 2023
Robert Fried, Richard M. Carlton
While a great many American men—said to exceed 30 million—suffer varying degrees of erectile dysfunction (ED), their problem is rarely low or absent sexual desire. American men would not resort to, and pay the high cost of prescription meds such as Viagra® and Cialis® for instance, if they had no desire for sex. The millions of such prescriptions filled by consumers tell us clearly that their problem is weak or absent sexual performance—absent or unreliable penile erection—not lack of desire: they want to do it …but somehow, they can’t.
The twentieth century
Published in Michael J. O’Dowd, The History of Medications for Women, 2020
By the end of the 1980s the drug armamentarium for the treatment of impotence included imipramine, naftidrofuryl, papaverine, phenoxybenzamine, phenotolamine, prostaglandin El, thyroxamine, and verapamil. The mid–1990s saw the introduction of new drugs that worked by enhancing nitric oxide-mediated relaxation of the smooth muscle of the corpus cavernosal (Boolell et al., 1996; Gingell et al., 1996; Eardley et al., 1996). Trials on one such drug, sildenafil (Viagra) showed a response rate of almost 90% in men with erectile dysfunction of no organic cause. Sildenafil is a type 5 phosphodiesterase inhibitor that causes the release of nitric oxide, an essential part of the erectile process. Early reports suggested that it could produce an effective response in almost 90% of patients who presented with psychological erectile dysfunction. Although there were a number of side-effects, priapism (a problem with intracavernosal injections) was not reported with Viagra. (Priapism, is penile erection sustained for more than six hours, and requires expert attention.)
Regulation of Reproduction by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Successful reproduction depends on the male’s ability to achieve and maintain penile erection, enabling the delivery of sperm to the female reproductive tract. Penile erection begins with sensory and mental stimulation (arousal). The male sexual response reflects a dynamic balance between exciting and inhibiting forces of the autonomic nervous system within the penis and throughout the central nervous system (CNS). The sympathetic component tends to inhibit erections, whereas the parasympathetic system is one of several excitatory pathways.
Impact of COVID 19 on erectile function
Published in The Aging Male, 2022
D. H. Adeyemi, A. F. Odetayo, M. A. Hamed, R. E. Akhigbe
The process that culminates in penile erection entails a mix of several physiological conditions that border on the input from both central and peripheral nervous systems. Besides, there are a series of the interplay between several biological mediators, vasoactive agents, neurotransmitters, and endocrine agents to achieve the optimal erection necessary for sexual intercourse [48]. The central processing unit in response to tactile, visual, and imaginative stimuli enhances penile erection. In other words, the central and peripheral control systems remain the two major established pathways that regulate or control penile erection. Stimulations of the peripheral tissues involved in erection elicit the response that is controlled by spinal and somatic activities. In addition, evidence from animal studies has suggested that the central control of sexual arousal or erection is predominantly localized in the limbic system structures. The medial preoptic area, paraventricular nucleus, medial amygdala, nucleus acumens, ventral tegmental area, and hippocampus are primary structures in the regulation of male sexual response [49]. Subsequently, a spinal network consisting of primary afferent signals emanating from the genitals, spinal interneurons, sympathetic, parasympathetic, and somatic nuclei are responsible for integrating signals from the periphery thus eliciting reflexive erections [50].
Application of dual-energy CT angiography in diagnosis of arterial erectile dysfunction: new scanning technology, new scanning area
Published in The Aging Male, 2022
Ming Wang, Yutian Dai, Hui Jiang, Andrea Sansone, Emmanuele A. Jannini, Xiansheng Zhang
Penile erection depends on synergistic mechanisms between psychologic, neural, endocrine and vascular systems, and therefore ED can be caused by any defect in these systems [39]. Decreased perfusion of penile arteries caused by arterial lesions is an important cause of vasculogenic ED. Currently, penile duplex Doppler ultrasound (PDDU) is treated as the gold standard for diagnosis of vascular ED because of the high sensitivity in the assessment of penial hemodynamics and significant correlation with arteriography [16,17]. However, there are some obvious limitations to ultrasonography. First, the diagnosis is highly susceptible to the skill and experience of operator, and the value relies on Doppler cursor angle and anatomic location [40]. Second, the result is considered to be affected by psychological disturbance such as anxiety and nervousness, especially in young patients [41]. Finally, it is unable to fully evaluate penile arteries, focusing only on selected vessels [36]. Additional diagnostic tests, such as cavernosometry and cavernosography, have also been used in the investigation of ED, but are considered “third line” options in the clinical setting, being invasive and complicated procedures [42].
Potential mechanism of Achyranthis bidentatae radix plus semen vaccariae granules in the treatment of diabetes mellitus-induced erectile dysfunction in rats utilizing combined experimental model and network pharmacology
Published in Pharmaceutical Biology, 2021
Ji-Sheng Wang, Jun-Long Feng, Heng-Heng Dai, Zi-Long Chen, Xiao Li, Bing-Hao Bao, Sheng Deng, Fan-Chao Meng, Qi Zhao, Hong-Sheng Xu, Bin Wang, Hai-Song Li
DMED has become a research “hotspot” in recent years (Qiu et al. 2021). Penile erection is caused first by the body accepting conduction of a nerve impulse, which leads to relaxation of smooth muscle in the cavernous tissue of the penis, inflow of arterial blood, occlusion of venous vessels, increased blood volume in the penis, and then erection (Thorve et al. 2011). Any factors leading to decreased blood flow to the penis can lead to ED. Hyperglycaemia in DM patients can produce peripheral vascular lesions by affecting vascular walls and endothelial factors. These actions lead to the glycosylation of elastic fibres in vascular walls, which limits vasodilation in cavernous sinusoids, reduces blood flow in the cavernous body and, thus, affects penile erection (Richards and Vinik 2002; De Young et al. 2004). DMED pathogenesis may also be related to oxidative-stress injury caused by a long-term hyperglycaemic environment in DM patients. The products of oxidative stress (e.g., reactive oxygen species, malondialdehyde, 8-oxo-2′-deoxyguanosine) damage vascular endothelial cells (VECs), affect the release of nitric oxide (NO) and other factors released by endothelial cells, and can even cause VEC apoptosis (Cui et al. 2018).