Ultrastructural comparison of penile cavernous tissue between hypertensive and normotensive rats

Abstract

Our aim was to compare the ultrastructure of penile cavernous tissue in the spontaneous hypertensive rat (SHR) and normotensive rat, and study the relation of blood pressure with erectile function. After injection of apomorphine (APO), penile erectile frequency in 16-week-old SHR (group A) and Wistar-Kyoto rat (WKY) (group B) was observed and noted. The ultrastructure of the penile cavernous tissue was studied by scanning electron microscope and transmission electron microscope. The mean blood pressures were significantly higher in group A than in group B (P ¼ 0; 171.20710.94 and 117.60712.38, n ¼ 5, for group A and group B, respectively). After treatment of the two groups with APO, the erectile frequency in group A was significantly less than in group B (P ¼ 0.007; 0.4070.55 and 2.4071.14, n ¼ 5, for group A and group B, respectively). Significant ultrastructural pathological changes were observed in the tunica albuginea and penile cavernous tissue of SHR. The elastic fibers were decreased and the collagen fibers of the sinusoid were increased in group A. The tunica albuginea thickness (mean7s.d.) was 100.2077.22 lm and 126.0077.65 lm in group A and group B, respectively. The tunica albuginea of group A was significantly thinner than that in B (P ¼ 0.001). Some endothelial cells and smooth muscle cells exhibited damaged mitochondria, and endoplasmic reticulums and Schwann cells were degenerated in group A. Although the function of penile erection might be affected by a secondary effect related to endothelial dysfunction of hypertension, these ultrastructural pathological changes of the penile cavernous tissue might also be one of the important mechanisms of erectile dysfunction caused by hypertension.

Energy restriction ameliorates metabolic syndrome-induced cavernous tissue structural modifications in aged rats

“…This condition leads to vascular stiffness, compromises cavernous SM vasodilatation, and modifies the cell-cell communication. The sinusoidal spaces will become narrower, less able to retain blood, and thus the inflow of blood into cavernous spaces to elevate the pressure within the penis decreases (Jiang et al 2005) contributing to veno-occlusive ED (Shen et al 2001).…”

Effect of muscle‐derived stem cells on the restoration of corpora cavernosa smooth muscle and erectile function in the aged rat

“…Ageing-related erectile dysfunction (ED) is primarily due to corporal veno-occlusive dysfunction (CVOD) [1,2], as a result of a loss of the corporal smooth muscle cells (SMCs) together with excessive collagen deposition within the corpora, as shown both in man [3][4][5] and rat models [6][7][8][9][10][11][12][13][14]. It has been hypothesized that this histological alteration is due to oxidative stress triggered by the release of profibrotic factors such as reactive oxygen species, TGF-β 1 , plasminogen activator inhibitor-1, and others, that not only lead to collagen accumulation but also to an increase in apoptosis and a reduction in corporal SMC proliferation [6][7][8][9][10][11][12][13][14].…”

“…It has been hypothesized that this histological alteration is due to oxidative stress triggered by the release of profibrotic factors such as reactive oxygen species, TGF-β 1 , plasminogen activator inhibitor-1, and others, that not only lead to collagen accumulation but also to an increase in apoptosis and a reduction in corporal SMC proliferation [6][7][8][9][10][11][12][13][14]. As such, it appears as if the ideal way to treat this ageing-related ED would be to reverse or prevent these changes, because such an approach has the potential to become a curative rather than a palliative intervention for this form of ED.…”

Daily use of phosphodiesterase 5 inhibitors for erectile dysfunction and lower urinary tract symptoms

“…This second study also found that the elastic tissue within the corporeal bodies showed an inverse relationship with blood pressure. 14 Although changes in collagen content have been found in animal models of ED, human studies do not show such a clear relationship. 15 Fibrosis and increased collagen content do not appear to be as strong a predictor of erectile function as smooth muscle function or smooth muscle content.…”