Agmatine looks interesting. What really strikes me as strange is that Agmatine has a positive effect on Testosterone, while Nitric Oxide in general is negative.
Agmatine, a novel hypothalamic amine, stimulates pituitary luteinizing hormone release in vivo and hypothalamic luteinizing hormone-releasing hormone release in vitro.Kalra SP, Pearson E, Sahu A, Kalra PS.
Department of Neuroscience, University of Florida College of Medicine, Gainesville 32610-0244, USA.
Agmatine, a clonidine displacing substance and imidazoline receptor agonist, was recently isolated from bovine brain and shown to be present in the rat hypothalamus. Since clonidine can stimulate the release of pituitary luteinizing hormone (LH), we tested the hypothesis that agmatine may similarly act in the rat to stimulate the hypothalamic luteinizing hormone-releasing hormone (LHRH)-pituitary LH axis. Administration of agmatine intracerebroventricularly rapidly augmented the release of LH in a dose-related fashion in ovariectomized, ovarian steroid-primed rats. Additionally, agmatine enhanced the in vitro efflux of LH releasing hormone from the median eminence-arcuate nucleus of the hypothalami of rats similarly pretreated with steroids. These studies imply that the endogenous imidazoline receptor agonist, agmatine, may serve as an excitatory neurotransmitter/neuromodulator in the hypothalamic control of LH release and we suggest that the previously reported excitatory effects of clonidine on LH release may be attributed to stimulation by clonidine of imidazoline receptors.
PMID: 7478229 [PubMed - indexed for MEDLINE]
Here is one on Nitric Oxide
Nitric oxide inhibits Leydig cell steroidogenesis
K Del Punta, EH Charreau and OP Pignataro
Instituto de Biologia y Medicina Experimental-Consejo Nacional de Investigaciones Cientificas y Tecnicas and Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina.
Testicular macrophages as well as endothelial cells, which are intimately associated with Leydig cells, constitute a potential source of paracrine nitric oxide (NO) in the testis. In the present study, we investigated the effect of NO donors on MA-10 murine Leydig tumor cell line and rat Leydig cell steroidogenesis. We show that NO donors inhibit human CG-induced steroidogenesis in both type of cells. We also studied NO mechanism of action. Contrary to what is observed in many other systems, NO inhibitory effect on Leydig cell steroidogenesis is not mediated by cyclic GMP (cGMP) because NO fails to increase cGMP production, and cGMP analogs do not reproduce NO effect. NO does not modify the production of cAMP, the main second messenger that mediates gonadotropin action. When we studied NO effect over the steroidogenic pathway in MA-10 cells, we found that NO was inhibiting the conversion of cholesterol to pregnenolone. Taken together these results show an inhibitory effect of NO donors on Leydig cell steroidogenesis, and suggest that NO can be directly inhibiting cholesterol side-chain cleavage enzyme (cytochrome P450scc) as it does with other heme proteins, including different cytochromes P450.
