.

[golf]

If i were you I wouldnt mess with urologist anymore and look on a site like vitals.com for the best endo in your area, or if your situation is bad visit one of the suggested ones on this website. Personally i would suggest Jacobs or Mariano. if your not happy with your current endo, go to a new one that will listen. simple as that.

also it is very confusing to read stuff that you are pasting from some medical source like:

balance between contractile and relaxant factors governs flaccidity/rigidity within the penis. Drugs that raise cytosolic calcium either prevent or abort erection. Conversely, drugs that lower cytosolic calcium relax smooth muscle and can initiate penile erection. Efficacy in treating erectile dysfunction (ED) with phosphodiesterase inhibitors, especially type 5; α-adrenergic-receptor antagonists; and dopamine agonists exploit these mechanisms within the penis or CNS. So his saying its my medication because of its actions on dopamine but my medication depresses dopamine, then if he knows that why not test for levels of CA2+ and soluble guanylate cyclase (sGC), facilitating the conversion of GTP to cGMP.

then going into what your actually writing, such as

What would you do if you was me

Please use the quote button when citing medical literature.

[bluejaysfan]

Kind of interesting…

Smooth muscle apoptosis is a major contributing factor to erectile dysfunction (ED) development in prostatectomy and diabetic patients and animal models. A critical regulator of penile smooth muscle and apoptosis is Sonic hedgehog (SHH). The SHH protein is decreased in ED models and SHH treatment of cavernous nerve (CN) injured rats prevents smooth muscle apoptosis. A close association between androgen deficiency and ED has been suggested in the literature, but few studies have examined the molecular effects on penile smooth muscle and on known signaling mechanisms that regulate morphology. Aim.

Examine testosterone and SHH interaction in eugonadal adult, adolescent and juvenile rats by performing castration studies and treatment with supraphysiological testosterone. Methods.

The eugonadal adult Sprague Dawley rats were either treated with testosterone for 7 or 14 days (N = 14) or were castrated for 4 or 7 days (N = 12). The juvenile rats were treated with testosterone for 8 days (N = 7). The adolescent rats were castrated and sacrificed at P88 (N = 8). The control rats had empty vehicle (N = 22) or sham surgery (N = 20). Main Outcome Measures.

The active form of SHH protein and mRNA were quantified by semi-quantitative immunohistochemical analysis and real-time reverse transcriptase polymerase chain reaction (RT-PCR). Results.

Testosterone treatment did not alter SHH signaling in juvenile rats. Shh mRNA increased 3.2-fold and SHH protein increased 1.2-fold in rats castrated during puberty. In adult rats, castration decreased Shh mRNA 3.2-fold but did not alter SHH protein. Testosterone supplement in adult rats increased Shh mRNA 2.3-fold and decreased SHH protein 1.3-fold.

Conclusions.

SHH signaling is independent of testosterone in normal juvenile rats and is sensitive to testosterone during adolescence, while testosterone supplement in the adult adversely impacts SHH signaling in a very similar manner to that observed with CN injury.
Bond CW, Angeloni NL, and Podlasek CA. Analysis of testosterone effects on sonic hedgehog signaling in juvenile, adolescent and adult Sprague Dawley rat penis. J Sex Med 2010;7:1116-1125.

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