To investigate the role of cholinergic neurotransmission in erection, human penile corpus cavernosum tissue was studied. Electrical stimulation of strips of corpus cavernosum suspended in an organ chamber induced contractions and relaxations that were blocked by tetrodotoxin. The contractions also were blocked by bretylium and prazosin. Norepinephrine and phenylephrine contracted the isolated strips and this response was prevented by prazosin. Electrical stimulation-induced relaxations were enhanced by bretylium and physostigmine and partially blocked by atropine. The effect of atropine, but not that of physostigmine, was prevented by bretylium. Corporal strips contracted with norepinephrine relaxed to acetylcholine; this effect was blocked by atropine and enhanced by physostigmine. Strips lacking endothelium contracted normally with norepinephrine, but the relaxation caused by acetylcholine was virtually abolished. Thus endothelium lining the lacunar spaces within human corpus cavernosum is required for the relaxation caused by exogenous acetylcholine. There may be three neurotransmitter effector systems that control corpus cavernosum smooth muscle tone: adrenergic (excitatory), cholinergic (inhibitory), and nonadrenergic noncholinergic (inhibitory). Cholinergic nerves do not dilate or constrict directly the smooth muscle but may modulate other neuroeffector systems and/or the endothelium.

We investigated the therapeutic effect of antilnphocyte serum (ALS) on clinically overt diabetes by using a nonobese diabetic (NOD) Immunotherapy with ALS. ALS was obtained by immunizing rabbits with a pool of lymph node cells prepared from NOD, C3H/He, DBA/2, and (C57BL/6 x A)F1 mice (11). A 0.4-ml injection of ALS was given intraperitoneally to diabetic NOD mice on days 0 (the first day of treatment regardless of the duration of diabetes) and +2. Control mice were given 0.4 ml ofnormal rabbit serum (NRS) on days 0 and +2. Blood glucose levels were monitored every 2-3 days initially and once a week thereafter. Achievement of euglycemia (<11 mM) and independence from exogenous insulin treatment after immunotherapy was defined as clinical remission.Immunotherapy with Monoclonal Antibodis (mAbs). Hybridoma cells producing anti-CD4 (anti-L3T4, clone GK 1.5) mAb were kindly provided by Kevin J. Lafferty (Barbara Davis Center for Juvenile Diabetes, Denver). Hybridomas producing anti-CD8 (anti-Lyt 2.1, clone 116-13.1, and antiLyt 2.2, clone 41-3.48) mAb were obtained from American Type Culture Collection. Ascites fluid that contained mAbs at -5 mg/ml was used. Diabetic NOD mice were treated with anti-CD4 mAb at 0.2 ml on days 0, 7, 14, and 21 and/or 0.1 ml of anti-CD8 (anti-Lyt 2.1) mAb on days 0 and 14. This treatment protocol has been shown (12) to achieve long-term removal of CD4' and/or CD8+ T lymphocytes from peripheral lymphoid organs in other inbred mouse strains. Control diabetic NOD mice were treated with 0.2 ml of anti-Lyt 2.2 mAb on days 0, 7, 14, and 21.Flow Cytometric Analysis. Peripheral lymph node cells were stained with fluorescein isothiocyanate conjugates of mAb 53-6.7 (anti-CD8) and phycoerythrin-conjugates of mAb GK1.5 (anti-CD4), both of which were obtained from Becton Dickinson. Two-color analysis was performed with a singlebeam flow cytometer, FACScan (Becton Dickinson) and the FACSCAN Research Software (Becton Dickinson).Islet Isolation and Transplantation. Because insulitis generally starts at 4 weeks of age (1), NOD islet donors were Abbreviations: NOD, nonobese diabetic; ALS, anti-lymphocyte serum; NRS, normal rabbit serum; mAb, monoclonal antibody.tTo whom reprint requests should be addressed at: CRI, New