Three months of daily sc injections of adult male dogs with the gonadotropin-releasing hormone agonist (GnRH-A) [D-Trp6, des-Gly-NH210]GnRH ethylamide produced significant decrease in the diameter of seminiferous tubules and conspicuously altered the ultrastructure of testicular microvasculature. In contrast to capillaries and venules in untreated controls, which had typical continuous endothelial layers surrounded by a basal lamina, in testes of dogs chronically treated with GnRH-A, 14.3% of the capillaries and 21.2% of the venules showed wide (30\p=n-\500nm) endothelial gaps. In a few capillaries (1.7%) and venules (4%) endothelial fenestrations were found. A high percentage of capillaries (59.3%) and venules (32.8%), with endothelial gaps or continuous endothelium were surrounded by multiple layers of basal lamina. All arterioles, 24.7% of the capillaries and 42.6% of the venules showed the normal features as found in the controls. Superfluous basal laminae, not associated with cells were present in the testes of the chronically treated dogs, but were also found after 4 months of recovery from the GnRH-A treatment. However, within 4 months after cessation of the GnRH-A treatment, the diameters of the seminiferous tubules were comparable to those in untreated controls. Capillaries and venules with endothelial gaps or fenestrations were completely absent. All arterioles, 43.6% of the capillaries and 65.6% of the venules revealed the normal features of continuous endothelium. However, 56.4% of the capillaries and 34.4% of the venules were characterized by superfluous layers of basal lamina. Thus, impaired spermatogenesis, as reflected by significantly decreased tubular diameters, owing to chronic administration of this GnRH-A in the dog is accompanied by major alterations of the testicular microvasculature. Although the mechanism(s) of these vascular changes are unclear, we propose that testicular microvessels could be a factor involved in the inhibition of spermatogenesis by chronic GnRH-A treatment.The inhibitory effects of the gonadotropin-releasing hormone agonist (GnRH-A) [D-Trp1', des-Gly-NH2"']GnRH ethylamide on spermatogenesis in the dog have recently been described by Dubé et al. (1987). After 16 weeks of daily treatment, the semi¬ niferous tubules contained only type A and spermatogonia, a few spermatocytes, and Sertoli cells with increased numbers of phagosomes and lipid droplets. These alterations as well as the accumula¬ tion of lipid droplets and the presence of mito¬ chondria with lamellar cristae in the Leydig cells were reversible within 16 weeks after cessation of the treatment.There is increasing evidence that GnRH-A has additional effects on the testicular microvasculature: in the rat severe vasodilatation, hyperemia, accumulation of leucocytes and interstitial edema have been reported by Habenicht et al. (1985Habenicht et al. ( , 1987 and Sandow (1985) to occur within a few hours after a single injection with a GnRH-A. Similar ef¬ fects were described by Habenicht & Müller (1988) in another ...