Table 1.
Cause | Effect | Probable mechanism |
---|---|---|
Medication | ||
Antidepressants | ED, ↓sexual desire, retarded ejaculation | Descending inhibitory input to sacral serotonergic ‘sex center’ + peripheral anticholinergic effects; potentially reversed by cyproheptadine (serotonin antagonist) or bethanechol (cholinergic) |
Antihypertensives (e.g. α-methyldopa, reserpine) | ↓Sexual desire, ED, retarded ejaculation | Deplete central dopamine, which mediates neural input related to sexuality (in hypothalamus/paraventricular nucleus); lower blood pressure; direct actions in corpus cavernosum (e.g. intracellular calcium regulation); effects on neurotransmitters/hormones (e.g. ↑prolactin) |
Other cardiovascular agents (e.g. digoxin, disopyramide, antihyperlipidemics, propranolol) | ED, ↓sexual desire | Digoxin ↓testosterone and ↑oestrogen levels because of similar structure to sex steroids; digoxin also blocks Na-K-ATPase pump with net increase in intracellular calcium and increased corporeal smooth-muscle tone (anti-erectile effects) |
Diuretics | ED (thiazide), ↓sexual desire, gynaecomastia and/or mastodynia (spironolactone, bendrofluazide, HCTZ) | Spironolactone blocks testosterone synthesis and competitively binds to androgen receptors |
Antipsychotics (neuroleptics) | ↓Sexual desire, ED, retarded ejaculation (with or without priapism) | Block pituitary/hypothalamic dopamine receptors; ↑prolactin levels; anticholinergic activity + α-adrenergic activity; indirect effects secondary to weight gain, CNS sedation, parkinsonism, psychomotor retardation |
Drugs of abuse (e.g. cocaine, amphetamines) | ED | Diffuse atherosclerotic changes/endothelial toxicity + ↑α-adrenergic activity on chronic use |
Histamine (H2) blockers | ↓Sexual desire (cimetidine), ED, gynaecomastia | Anti-androgen activities/blockade of androgen receptors; ↑prolactin; direct corporeal effects |
Anti-androgens (e.g. finasteride) | ED, reduced sexual desire | Block androgen synthesis; oestrogen, ketoconazole and digoxin may lower serum testosterone and/or competitively bind to androgen receptors |
Surgery/radiation/brachytherapy (e.g. for prostate cancer) | ED | Effects on neurovascular structures |
Adapted from Rehman and Melman (34) with permission. ED, erectile dysfunction; HCTZ, hydrochlorothiazide; CNS, central nervous system. Adapted from (CMG and Atlas of Clinical Urology: Impotence and Infertility. Vol 1. Philadelphia, PA: Current Medicine Inc; 1999:1.1–1.16, Figure 1–17, page 1.14, Rehman J, Melman A. Pathophysiology of erectile dysfunction.) with kind permission of Current Medicine Group, LLC. © 1999 All rights reserved