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Researchers from University of Montreal and Montreal Heart Institute have suggested that Viagra may protect the hearts of patients with muscular dystrophy.

Muscular dystrophy is characterized by weakness and progressive degeneration of the muscles, including the heart muscle. It is caused by a genetic mutation of dystrophin, a protein that acts as the backbone of muscular cells.

The study conducted using a mouse model showed that sildenafil protected the heart in mice with Duchenne muscular dystrophy.

This achievement was a true team initiative and is the culmination of sustained efforts on the part of Dr. Maya Khairallah, who was a doctoral student at the time, and all of the researchers from participating centres, said Dr. Christine Des Rosiers, lead researcher from the Universite de Montreal and the Montreal Heart Institute.

Im pleased that my work has sparked interest in an eventual application for humans, says Dr. Khairallah

The researchers explain that the choice of sildenafil was based on their previous studies indicating that the hearts of dystrophic mice do not function as effectively and are more susceptible to stress-induced cell death.

These studies suggested that this might be due to a decrease in the formation of a molecule named cGMP (cyclic guanosine monophosphate).

For the new study, researchers used two different approaches to increase cGMP production in the heart, with the result that the hearts were able to function more effectively and were less susceptible to cell death.

One of these approaches involved the use of sildenafil, which increased cGMP concentration by preventing its degradation by the phosphodiesterase 5 enzyme, said Dr. Basil Petrof of the Research Institute of the McGill University Health Centre (MUHC)

Our work had shown for many years the benefits of cGMP on the heart and the present study confirms the therapeutic potential of this molecule, said Dr. Christian Deschepper of the Institut de recherches cliniques de Montreal.

The researchers also made reference of another study showing the beneficial effects of a medication similar to sildenafil on the other muscles of dystrophic mice. Thus, the benefits of this approach may not be limited to the heart.

The study findings are published in the online edition of the Proceedings of the National Academy of Sciences.

Experiments on animals conducted by Johns Hopkins and other researchers have confirmed that the erectile dysfunction drug called Viagra amplifies the effects of a heart-protective protein.
Reporting their findings in the online edition of the Journal of Clinical Investigation, the researchers have said that their study helps explain why Viagra, scientifically known as sildenafil, has already been shown to improve heart function.
They said that their findings also went to suggest that one day Viagra might have value in either treating or preventing heart damage due to chronic high blood pressure.
The researchers revealed that the key is Viagras effects on a single protein called RGS2, which is an essential link in the chain reactions that initially protect the body’’s main blood-pumping organ from spiralling into heart failure.
While experimenting with mice, the researchers first observed 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.
The researchers revealed that about 50 percent of the mice died of heart failure.
In mice with RGS2, by contrast, the dangerous muscle expansion called hypertrophy was delayed, growing only 30 percent, and no mice died.
When hypertensive mice with RGS2 were treated with Viagra in subsequent tests, they 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, Viagra had no effect.
“Sildenafil clearly prolongs the protective effects of RGS2 in mouse hearts,” says study senior investigator and cardiologist Dr. David Kass, a professor at the Johns Hopkins University School of Medicine and its Heart and Vascular Institute.
According to Kass, RGS2 is stimulated by an enzyme, protein kinase G, whose action is, in turn, raised by countering the activity of another enzyme, phosphodiesterase 5 (PDE5A).
He and his team has already shown in 2005 that Viagras ability to block PDE5A is responsible for blunting hypertrophy due to high blood pressure in mice and offsetting similar, adrenaline-stimulated heart stress in people.
Kass says that RGS2 “acts like a short-term reset mechanism in the heart,” recoupling G proteins that if left alone stimulate the heart’’s response to high blood pressure. And without the “reset,” a cascade of reactions known as Gq signalling leads to scar tissue formation, hypertrophy and heart failure.
“The evidence is piling up that unbridled Gq signaling is driving a central biological chain reaction in heart failure, and that by extending the protective effects of RGS2 or by developing a test for its presence, researchers can develop new therapies or improve existing ones, including ACE inhibitors and possibly sildenafil, for people with heart failure who will benefit most,” says Kass.