Grow Taller with Viagra

After promising height increase findings with other male enhancement formulas like Tribulus Terristris and Horny Goat Weed, I thought I might see if the big one(Viagra) had height increasing effects.  A number of male enhancement formulas exert their height increasing effects by Nitric Oxide mediated increase of Guanyl Cyclase and in turn cGMP.  C-type Natruiretic peptides are available for sale(for researchers) as CNP-22 and CNP-53 but not really for the public.  Nitric Oxide stimulators are readily available and Guanyl Cyclase interacts with CNP.  Viagra acts by reducing PDE5 expression which inhibits cGMP.

cGMP-dependent protein kinases and cGMP phosphodiesterases in nitric oxide and cGMP action.

"Biological signaling by nitric oxide (NO) is primarily mediated by cGMP, which is synthesized by NO-activated guanylyl cyclases and broken down by cyclic nucleotide phosphodiesterases (PDEs). Effects of cGMP occur through three main groups of cellular targets: cGMP-dependent protein kinases (PKGs), cGMP-gated cation channels, and PDEs. cGMP binding activates PKG, which phosphorylates serines and threonines on many cellular proteins, frequently resulting in changes in activity or function, subcellular localization, or regulatory features. The proteins that are so modified by PKG commonly regulate calcium homeostasis, calcium sensitivity of cellular proteins, platelet activation and adhesion, smooth muscle contraction, cardiac function, gene expression, feedback of the NO-signaling pathway, and other processes. Current therapies that have successfully targeted the NO-signaling pathway include nitrovasodilators (nitroglycerin), PDE5 inhibitors [sildenafil (Viagra and Revatio), vardenafil (Levitra), and tadalafil (Cialis and Adcirca)] for treatment of a number of vascular diseases including angina pectoris, erectile dysfunction, and pulmonary hypertension; the PDE3 inhibitors [cilostazol (Pletal) and milrinone (Primacor)] are used for treatment of intermittent claudication and acute heart failure, respectively. Potential for use of these medications in the treatment of other maladies continues to emerge."

PDE5 inhibits cGMP and Viagra inhibits PDE5.  cGMP encourages hypertrophic differentiation of the growth plate.

Phosphorylation of GSK-3beta by cGMP-dependent protein kinase II promotes hypertrophic differentiation of murine chondrocytes.

"cGMP-dependent protein kinase II (cGKII; encoded by PRKG2) is a serine/threonine kinase that is critical for skeletal growth in mammals; in mice, cGKII deficiency results in dwarfism. Using radiographic analysis, we determined that this growth defect was a consequence of an elongated growth plate and impaired chondrocyte hypertrophy. To investigate the mechanism of cGKII-mediated chondrocyte hypertrophy, we performed a kinase substrate array and identified glycogen synthase kinase-3beta (GSK-3beta; encoded by Gsk3b) as a principal phosphorylation target of cGKII. In cultured mouse chondrocytes, phosphorylation-mediated inhibition of GSK-3beta was associated with enhanced hypertrophic differentiation. Furthermore, cGKII induction of chondrocyte hypertrophy was suppressed by cotransfection with a phosphorylation-deficient mutant of GSK-3beta. Analyses of mice with compound deficiencies in both protein kinases (Prkg2(-/-)Gsk3b(+/-)) demonstrated that the growth retardation and elongated growth plate associated with cGKII deficiency were partially rescued by haploinsufficiency of Gsk3b. We found that beta-catenin levels decreased in Prkg2(-/-) mice, while overexpression of cGKII increased the accumulation and transactivation function of beta-catenin in mouse chondroprogenitor ATDC5 cells. This effect was blocked by coexpression of phosphorylation-deficient GSK-3beta. These data indicate that hypertrophic differentiation of growth plate chondrocytes during skeletal growth is promoted by phosphorylation and inactivation of GSK-3beta by cGKII."

Nitric oxide, C-type natriuretic peptide and cGMP as regulators of endochondral ossification.

"A well studied model of NO action involves its binding to the heme-containing soluble protein guanylate cyclase, causing increased enzymatic activity and formation of cGMP. Depending on the cell type, the increase in cGMP concentration may lead to activation of phosphodiesterases, cGMP-regulated ion channels and cGMP-dependent kinases (cGKs)"

"Furthermore, cartilage-specific overexpression of CNP rescued the phenotype of CNP-deficient mice, strongly suggesting that CNP stimulates bone growth through direct effects on chondrocytes (rather than systemically). In agreement with this phenotype, organ culture studies of endochondral bones showed that exogenous CNP is a potent stimulator of longitudinal bone growth"

"CNP induces synthesis of cGMP and thus activation of several downstream pathways, namely cGMP-dependent kinases, phosphodiesterases and specific ion channels. Since NO also induces cGMP synthesis, it is likely that it shares many of the biological activities of CNP"

CNP overexpression increased height.  Both NO and CNP cause the upregulation of cGMP.  cGMP increases hypertrophic differentiation.  Unfortunately, I can't find any studies with cGMP or cGKII trasgenic mice so we don't if an increase in serum levels of cGMP will increase height.  But we do have the fact that CNP overexpression increases height and that CNP results in an increase in cGMP.

But if cGMP can increase height then Viagra can increase height by inhibiting PDE5 which inhibits cGMP.