How do Viagra and Cialis work to treat erectile dysfunction?
Executive summary
Viagra (sildenafil) and Cialis (tadalafil) are oral phosphodiesterase type 5 (PDE5) inhibitors that increase blood flow to the penis during sexual stimulation by blocking the enzyme that normally helps “turn off” an erection; sildenafil typically acts faster and lasts hours while tadalafil can last up to 36 hours and is also approved for benign prostatic hyperplasia (BPH) [1] [2] [3]. Both drugs require sexual stimulation because they amplify the natural nitric-oxide → cGMP pathway, and combining them is not recommended because they share the same mechanism and raise the risk of side effects without added benefit [3] [4].
1. How the drugs hijack a natural erection switch
Viagra and Cialis amplify the body’s normal erection pathway: sexual stimulation triggers nitric oxide (NO) release, NO raises cyclic GMP (cGMP) in penile tissue, cGMP causes smooth-muscle relaxation and increased blood flow, and PDE5 is the enzyme that degrades cGMP. Sildenafil and tadalafil inhibit PDE5, prolonging cGMP’s effect so an erection is easier to achieve and maintain during sexual arousal [3] [1].
2. Why sexual stimulation is still required
Neither pill forces an erection on its own; they potentiate the NO–cGMP signal that only begins with sexual stimulation. Clinical summaries and drug guides note explicitly that PDE5 inhibitors “work only in the presence of sexual stimulation” because NO is released during arousal, which is the substrate the drugs enhance [3].
3. Key practical differences that shape patient choice
Sildenafil (Viagra) usually takes effect in about 30–60 minutes and wears off in a few hours; tadalafil (Cialis) has a slower onset (roughly 1–2 hours to peak) but a much longer window of effect—up to about 36 hours—leading to different lifestyle uses (scheduled “on-demand” vs. greater spontaneity or daily low-dose use) [2] [5] [6].
4. Safety, interactions and why you shouldn’t mix them
Because both drugs relax blood vessels, they lower blood pressure modestly and can interact dangerously with nitrates or certain vasodilators. Taking sildenafil and tadalafil together or switching too soon increases side-effect risk without improving efficacy; guidance from pharmacists and drug information sources advises against combined use and recommends medical supervision for any regimen changes [7] [4].
5. Side-effect profiles and additional uses
Common side effects relate to vasodilation—headache, flushing, nasal congestion and dizziness—and rare but serious events (e.g., vision changes, sudden hearing loss, or nonarteritic anterior ischemic optic neuropathy) prompt stopping the drug and seeking care per prescribing guidance (available sources do not give a comprehensive adverse-event list in these snippets; see [13] for safety alerts and [9] for side-effect discussion). Tadalafil additionally has an FDA indication for BPH and is sometimes used as a daily therapy for both ED and lower urinary tract symptoms [8] [9].
6. Evidence, preferences and prescribing trade-offs
Clinical and market reporting emphasize similar efficacy between the two as PDE5 inhibitors, with differences in duration, onset, dosing flexibility and food interactions shaping preference: sildenafil may be slower after a fatty meal, whereas tadalafil’s activity is less affected by food [2] [5] [10]. Real-world preference data cited in reporting find many men favor tadalafil for spontaneity, while others prefer sildenafil’s predictability [11] [6].
7. Misuse, counterfeit risks and regulatory context
Because sildenafil and tadalafil are effective, they are also manufactured generically and appear in illicit or misbranded products; law enforcement cases have alleged smuggling and mislabeling of pills containing these active ingredients, underscoring risks of buying ED drugs from unverified sources [12]. Formularies and payer policies also regulate coverage—some policies explicitly address tadalafil use and exclusions [13].
Limitations and final note on sources
This analysis relies solely on the provided patient guides, drug-information sites, clinical summaries and news reports. The sources consistently describe PDE5 inhibition, the need for sexual stimulation, differences in onset/duration, and safety cautions [1] [3] [2] [7]. Available sources do not mention certain granular pharmacokinetic numbers (e.g., exact half-lives across populations) beyond onset/duration comparisons, nor do they provide head‑to‑head randomized trial data in the snippets provided—those details are not found in current reporting excerpts supplied here.