Influence of sildenafil on esophageal motor function in humans: Studies using high-resolution manometry

Sildenafil induces smooth muscle relaxation of the esophagus by blocking type 5 phosphodiesterase that degrades cyclic guanine monophosphate. We aimed to characterize the effects of sildenafil on esophageal peristalsis and contraction reserve using high-resolution manometry (HRM).

Fifteen healthy adults (12 men, age 21-39, mean 27 years) participated in this study using HRM following either sildenafil 50 mg or placebo. HRM with ten wet swallows and five multiple rapid swallows was performed in all participants. HRM metrics included esophagogastric junction contractile integral (EGJ-CI), basal lower esophageal sphincter (LES) pressure, 4-second integrated relaxation pressure (IRP-4s), distal contractile integral (DCI), distal latency, resting upper esophageal sphincter pressure (UESP), and the response to MRS.

Sildenafil significantly lowered EGJ-CI (P < .001), LES pressure (P = .04), IRP-4s (P = .02), and DCI (P < .001). There was no difference in UESP (P = .87) between sildenafil and placebo. Sildenafil significantly decreased peristaltic vigor, inducing absent peristalsis in 12 subjects and ineffective esophageal motility in 3 subjects. Peristaltic response and augmentation following MRS were significantly inhibited following sildenafil (7% vs 100%, P < .001, and none vs 73%, P < .001).

Sildenafil attenuates EGJ barrier function, resting LES pressure, and LES relaxation. Both esophageal body contractility and contraction reserve are inhibited by sildenafil in healthy adults.