Although this decline is gradual for most women, those who have undergone bilateral oophorectomy experience a sudden drop in testosterone levels, as the ovaries produce 40% of the bodys circulating testosterone.Sexual desire has been related to three separate components: drive, beliefs and values, and motivation. Particularly in postmenopausal women, drive fades and is no longer the initial step in a womans sexual response. Diagnosis
List of disorders
DSM
The fourth edition of the Diagnostic and Statistical Manual of Mental Disorders lists the following sexual dysfunctions:

Hypoactive sexual desire disorder (see also asexuality, which is not classified as a disorder)
Sexual aversion disorder (avoidance of or lack of desire for sexual intercourse)
Female sexual arousal disorder (failure of normal lubricating arousal response)
Male erectile disorder
Female orgasmic disorder (see anorgasmia)
Male orgasmic disorder (see anorgasmia)
Premature ejaculation
Dyspareunia
VaginismusAdditional DSM sexual disorders that are not sexual dysfunctions include:

Paraphilias
PTSD due to genital mutilation or childhood sexual abuse

Other sexual problems
Sexual dissatisfaction (non-specific)
Lack of sexual desire
Anorgasmia
Impotence
Sexually transmitted diseases
Delay or absence of ejaculation, despite adequate stimulation
Inability to control timing of ejaculation
Inability to relax vaginal muscles enough to allow intercourse
Inadequate vaginal lubrication preceding and during intercourse
Burning pain on the vulva or in the vagina with contact to those areas
Unhappiness or confusion related to sexual orientation
Transsexual and transgender people may have sexual problems before or after surgery. Persistent sexual arousal syndrome
Sexual addiction
Hypersexuality
All forms of female genital cutting
Post-orgasmic diseases, such as Dhat syndrome, PCT, POIS, and sexual headacheS. Treatment
Males
Several decades ago, the medical community believed most sexual dysfunction cases were related to psychological issues.
Enzymatic production of adenosine can be anti-inflammatory or immunosuppressive. Adenosine receptors
All adenosine receptor subtypes (A1, A2A, A2B, and A3) are G-protein-coupled receptors. The four receptor subtypes are further classified based on their ability to either stimulate or inhibit adenylate cyclase activity. The A1 receptors couple to Gi/o and decreases cAMP levels, while the A2 adenosine receptors couple to Gs, which stimulates adenylate cyclase activity. In addition, A1 receptors couple to Go, which has been reported to mediate adenosine inhibition of Ca2+ conductance, whereas A2B and A3 receptors also couple to Gq and stimulate phospholipase activity. Researchers at Cornell University have recently shown adenosine receptors to be key in opening the blood-brain barrier (BBB). Mice dosed with adenosine have shown increased transport across the BBB of amyloid plaque antibodies and prodrugs associated with Parkinsons disease, Alzheimers, multiple sclerosis, and cancers of the central nervous system. Ghrelin/growth hormone secretagogue receptor
Adenosine is an endogenous agonist of the ghrelin/growth hormone secretagogue receptor. However, while it is able to increase appetite, unlike other agonists of this receptor, adenosine is unable to induce the secretion of growth hormone and increase its plasma levels. Mechanism of action
When it is administered intravenously, adenosine causes transient heart block in the atrioventricular (AV) node. This is mediated via the A1 receptor, inhibiting adenylyl cyclase, reducing cAMP and so causing cell hyperpolarization by increasing K+ efflux via inward rectifier K+ channels, subsequently inhibiting Ca2+ current. It also causes endothelial-dependent relaxation of smooth muscle as is found inside the artery walls.