Erectile Dysfunction in Hypertensive Subjects

Abstract

Hypertension is often cited as a risk factor for erectile dysfunction. To clarify the relation between hypertension and erectile dysfunction, we evaluated 32 consecutive hypertensive and 78 normotensive impotent men with respect to multiple potential determinants and parameters of erectile function, including medical and sexual history, depression, hormonal profile, penile nocturnal tumescence, penile vascular supply, and pudendal nerve conduction. The hypertensive men were older, had higher body mass index, and used more medications than the normotensive men. The groups were not different with respect to the prevalence of smoking and peripheral vascular disease, but the hypertensive men had a marginally higher rate of ischemic heart disease (P = .06). The prevalence of depression, abnormal nocturnal penile tumescence, anomalous pudendal nerve conduction, and impairment in arterial supply as determined by penile brachial index were similar in the two groups. Testosterone and bioavailable testosterone levels were lower in the hypertensive men. After stratification by age and body mass index, hypertensive men younger than 50 years with body mass index less than 30 kg/m2 had significantly lower testosterone levels (12.0 +/- 1.7 versus 21.3 +/- 1.4 nmol/L, P < .02) but not bioavailable testosterone levels (3.9 +/- 0.7 versus 6.4 +/- 0.7 nmol/L, P < .17) than the corresponding normotensive group. Prolactin, follicle-stimulating hormone, and luteinizing hormone levels of the two groups were not significantly different. Contrary to common belief and with the exception of lower circulating testosterone levels, the overall analysis showed little difference between hypertensive and normotensive men with respect to a wide range of classic determinants of erectile function. Direct study of the local vascular erectile apparatus appears necessary for further elucidation of the mechanisms underlying erectile dysfunction in hypertensive men.

A new surrogate variable for erectile dysfunction status in the Massachusetts male aging study

“…All of these factors have been identified in previous research as possible risk factors for ED [18][19][20][21][22]. For two of the six items, age and smoking, the MMAS method generated a substantially stronger association than the clinic method.…”

Phosphodiesterase-5 inhibition synergizes rho-kinase antagonism and enhances erectile response in male hypertensive rats

“…The impact of hypertension on male sexual function has been the focus of several clinical previous investigations. 2,3,24 Animal behavioral studies employing the well-recognized genetic model (SHR) of hypertension have demonstrated a significant impairment of erectile reflexes in hypertensive animals. 25 Hemodynamic studies in SHR species have shown that hypertension in these animals leads to structural changes in penile vasculature similar to those in other vascular beds, characterized by a narrow vascular lumen and increased medial smooth muscle bulk.…”

“…[1][2][3] Endothelial dysfunction, hormonal abnormalities, and vascular factors are considered possible etiologic factors. 2 Clinical studies suggest that antihypertensive drugs per se could affect the compliance of the erectile tissue.…”

“…[1][2][3] Endothelial dysfunction, hormonal abnormalities, and vascular factors are considered possible etiologic factors. 2 Clinical studies suggest that antihypertensive drugs per se could affect the compliance of the erectile tissue. 3,4 Normal erectile function is characterized by a delicate in vivo balance between the effects of vasoconstricting and vasorelaxing neurotransmitters/hormones on the level of corporal smooth muscle tone.…”

Cardiovascular effects of sildenafil in hypertensive men with erectile dysfunction and different alleles of the type 5 cGMP-specific phosphodiesterase (PDE5)

“…[1][2][3][4][5] Many common risk factors are involved in both ED and EH (eg age, diabetes, dyslipidemia, obesity), but it is not clear if a common mechanism could be responsible for the association between EH and ED. [6][7][8] A likely common pathogenetic pathway could be a reduced ability of arteriolar vascular smooth muscle (VSM) to relax. 9,10 One of the main regulators of VSM contractile tone is cGMP: 11 increasing intracellular levels of cGMP reduce the contractile status of VSM and induce vasodilation with systemic and local effects (eg blood pressure (BP) decrease, erection).…”