Johns Hopkins researchers have recently discovered that Viagra has a few "other talents" (as they described it in their press release). It turns out that this drug also helps a 'signaling' protein shield the heart from high blood pressure damage. This is interesting because Viagra had been seen more and more frequently as a "lifestyle" drug, and not something with a genuine healthcare benefit.
These researchers report what is believed to be the first direct evidence in lab animals that the erectile dysfunction drug sildenafil amplifies the effects of a heart-protective protein, in a new article published in the Journal of Clinical Investigation Jan. 5. Their work helps explain why sildenafil, more widely known as Viagra, has already been shown to improve heart function and may one day have value in either treating or preventing heart damage due to chronic high blood pressure.
The key, investigators say, is sildenafil's effects on a single protein, RGS2, newly identified in the latest study as an essential link in the chain reactions that initially protect the body's main blood-pumping organ from spiraling into heart failure.
Experimenting in mice, the team of heart experts first established that after a week of induced high blood pressure, the hearts of animals engineered to lack RGS2, or regulator of G-protein signaling 2, quickly expanded in weight by 90 percent. Almost half the mice died of heart failure. In mice with RGS2, by contrast, the dangerous muscle expansion, known as hypertrophy, was delayed, growing only 30 percent, and no mice died.
Subsequent tests treating hypertensive mice that had RGS2 with sildenafil showed enhanced buffering, with less hypertrophy, stronger heart muscle contraction and relaxation, and as much as 10 times lower stress-related enzyme activity compared to their untreated counterparts. In mice lacking RGS2, sildenafil had no effect.
"Sildenafil (Viagra) clearly prolongs the protective effects of RGS2 in mouse hearts," says study senior investigator and cardiologist David Kass, M.D.