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Early improvement in SHIM scores with Revactin®

International Journal of Impotence Research volume 32, pages 255–256 (2020)Cite this article

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Regardless of age, the majority of men with erectile dysfunction (ED) seem to have some degree of cavernosal veno-occlusive dysfunction (CVOD). For those under 40 years of age, CVOD or venous leakage appears to be the primary cause for their ED [1]. It has been proposed that venous leakage becomes clinically apparent when ~15% of the corporal smooth muscle cells (CSMC) have become dysfunctional [1]. This dysfunction is believed to be due primarily to the onset of an apoptotic process associated simply with normal aging. According to the free radical theory of Harman [2], our cells begin to “age” sometime around the end of our third decade of life, coinciding with the onset of intracellular oxidative stress. In men, this time period is associated with the clinically recognizable progressive increase in the refractory period that all men experience as they transition from their teenage years to middle age. This refractory period definitely continues to increase at a genetically predetermined rate that is specific for each individual as they journey through middle age into senescence [1]. Even though arterial disease becomes manifest during middle age and senescence, in many men who complain of the onset or worsening of their ED at this stage of their lives, a diminished arterial inflow into the corpora is not always identified. This suggests that the progressive aging-related apoptotic process within the CSMC could be one of the major reasons why men who are at that time on phosphodiesterase inhibitors (PDE5i) for their ED will ultimately require progressively higher doses of the drug or may even become non-responsive to the PDE5i as they continue to age.

In its effort to combat this aging-related oxidative stress and apoptotic process, the CSMC cells themselves begin to activate the normally inactive inducible nitric oxide synthase (iNOS) enzyme [3]. This iNOS enzyme typically produces high levels of intracellular nitric oxide (NO), and acts locally in an anti-apoptotic and anti-oxidative manner. For example, it has been shown experimentally in the aged rat corpora that upregulation of this iNOS–NO–cGMP pathway, e.g. by the use of chronic and long-term PDE5i, can result in an inhibition of this apoptotic activity within the CSMC; from a functional point of view, this can translate clinically into an improvement in CVOD and resultant erectile function [3]. These experimental observations in the rat suggested the possibility that direct stimulation of this iNOS–NO–cGMP pathway in the human CSMC could potentially slow down or even inhibit the apoptosis and resultant dysfunction of the CSMC even before men become clinically aware of this ongoing aging process within the CSMC.

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Acknowledgements

Bottles of Revactin® capsules were provided gratis by KLRM, LLC, which receives royalty from Revactin® sales.

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Authors and Affiliations

  1. Department of Health and Life Sciences, Charles R. Drew University of Medicine and Science, Los Angeles, CA, USA

    Sabine Nguyen

  2. Department of Surgery, College of Medicine, Charles R Drew University, Los Angeles, CA, USA

    Magda Shaheen

  3. David Geffen School of Medicine at UCLA, Los Angeles, CA, USA

    Magda Shaheen

  4. LA Biomed Institute at Harbor-UCLA Medical Center, Torrance, CA, USA

    Youngju Pak

  5. Department of Urology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA

    Jacob Rajfer

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  1. Sabine Nguyen
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  2. Magda Shaheen
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  3. Youngju Pak
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  4. Jacob Rajfer
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Correspondence to Jacob Rajfer.

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JR is a 25% equity partner in KLRM, LLC.

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Nguyen, S., Shaheen, M., Pak, Y. et al. Early improvement in SHIM scores with Revactin®. Int J Impot Res 32, 255–256 (2020). https://doi.org/10.1038/s41443-019-0123-1

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