Hippiekinkster
Posts: 5512
Joined: 11/20/2007
From: Liechtenstein
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quote:
ORIGINAL: DarqueMirror
quote:
ORIGINAL: Hippiekinkster
She's a lot more "quite" than you are, Doctor.
Nitric Oxide and Erections
How do you think blue diamonds work?
You should read your own sources more carefully.
"Once blood starts flowing into the penis, the source of nitric oxide in the blood vessels is continuously activated so that more nitric oxide is released, more tissue relaxes, more blood comes in and a sustained erection is achieved," Burnett says."
You should investigate a little more thoroughly before telling people to read more carefully.
"All these results suggest that not only may NO precursor or donor induce penile erection, but also non-NO donors or precursors are also able to induce penile erection via the common mediator of NO."
http://www.nature.com/ijir/journal/v14/n3/full/3900825a.html
"For approximately a decade now, substantial evidence has accrued supporting nitric oxide (NO) as the central component of a major signal transduction system that acts in the penis to mediate the erectile response. This molecule subserves a unique biochemical cascade involving production of the potent second-messenger molecule, 3', 5'-cyclic guanosine monophosphate (cGMP), and its activation of protein kinase G (PKG), which induces physiologic penile erection by regulating the state of penile smooth muscle contractility (Burnett, 1997). In fact, current data support the notion that this NO-based biochemical cascade represents a convergence of cellular, biochemical, and molecular inputs, which, on the signal transduction regulatory level, is indispensable for the mechanism of penile erection (Hedlund et al, 2000a). Consistent with the importance of NO mediation of penile erection, its biology in the penis is quite complex, involving multiple regulatory interactions: the molecule itself may target several biochemical mechanisms that achieve erectile tissue relaxation, but it is also the target of a host of modulatory influences that determine its release and mode of action in erectile tissue. "
http://www.andrologyjournal.org/cgi/content/full/23/5/S20
"The NO–sGC–cGMP pathway plays a crucial role in the initiation and maintenance of cavernosal relaxation. It would appear to achieve this predominantly through the actions of PKGs. Cyclic GMP can alter cell function through protein phosphorylation or through mechanisms not directly related to protein phosphorylation. It is also becoming clear that the localization of these cGMP receptor proteins in the cell is an important factor in the regulation of cell function by cGMP. Soluble GC plays an important role in the transduction of inter- and intracellular signals conveyed by NO. To fulfill this role, sGC has evolved a unique heme-coordination, which customizes it for NO sensitivity and its product, cGMP, regulates a plethora of biological functions depending on location and cell type. It is crucial that the NO–sGC–cGMP transduction system is understood in its entirety, to provide the greatest opportunity for the design and development of therapeutics."
http://www.nature.com/ijir/journal/v16/n6/full/3901256a.html
And while I'm at it, NO is associated with the isomeric form of cyclooxygenase, COX-2, which is an enzyme responsible for increased prostaglandin synthesis, which leads to inflammation, which leads to pain (the COX-2 inhibitory effects of NSAIDS relieve pain)
"The biosynthesis and release of nitric oxide (NO) and prostaglandins (PGs) share a number of similarities. Two major forms of nitric-oxide synthase (NOS) and cyclooxygenase (COX) enzymes have been identified to date. Under normal circumstances, the constitutive isoforms of these enzymes (constitutive NOS and COX-1) are found in virtually all organs. Their presence accounts for the regulation of several important physiological effects (e.g. antiplatelet activity, vasodilation, and cytoprotection). On the other hand, in inflammatory setting, the inducible isoforms of these enzymes (inducible NOS and COX-2) are detected in a variety of cells, resulting in the production of large amounts of proinflammatory and cytotoxic NO and PGs. The release of NO and PGs by the inducible isoforms of NOS and COX has been associated with the pathological roles of these mediators in disease states as evidenced by the use of selective inhibitors. An important link between the NOS and COX pathways was made in 1993 by Salvemini and coworkers when they demonstrated that the enhanced release of PGs, which follows inflammatory mechanisms, was nearly entirely driven by NO. Such studies raised the possibility that COX enzymes represent important endogenous “receptor” targets for modulating the multifaceted roles of NO."
http://pharmrev.aspetjournals.org/content/57/2/217.full
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