Notes: Summary 1. There is a gradual proximo-distal increase in the thickness of the muscle coat of the human ductuli efferentes, duetus epididymidis and ductus deferens. Circularly arranged smooth muscle bundles predominate in the ductuli efferentes and ductus epididymidis of the caput section. Scanty strands of longitudinally and obliquely oriented smooth muscle bundles form an additional, incomplete outer muscle layer around the ductus epididymidis of the corpus. Small smooth muscle-like cells constitute the muscle elements of the upper sections of the excretory ducts (from the ductuli efferentes to the midcauda). At the transition of the corpus and cauda epididymidis ordinary large smooth muscle cells join the small contractile cells to form—in more distal sections of the cauda—a composed, thick subepithelial muscle coat. In most distal portions of the cauda, the two-layered muscle coat of the ductus epididymidis is transformed into a three-layered coat, a pattern of construction which is retained in the vas deferens. 2. Electron microscopically, three types of contractile cells are distinguished in the human ductuli efferentes and ductus epididymidis: a) contractile cells of medium transparency containing exclusively thin myofilaments (60 Å in diameter), b) dark contractile cells containing bundles of thin myofilaments (60 Å in diameter) and single coarse filaments (140 Å in diameter), c) light contractile cells with loosely dispersed, interweaving thin and thick myofilaments. Commutual diameter changes at regular intervals are seen in individual myofilaments, giving the impression of structural periodicity not unlike that of filaments of striated muscle. Ordinary smooth muscle cells of the cauda epididymidis and vas deferens are characterized by uniformly sized, closely packed but evenly distributed thin myofilaments with numerous dense patches. 3. Fluorescence microscopy performed on formaldehyde treated freeze dried tissues reveals that the contractile cells of the ductuli efferentes in man and monkey receive a low number of single adrenergic terminal fibres penetrating the depth of the muscle coat. The adrenergic innervation of the ductus epididymidis is restricted to small peritubular nerve fascicles running contiguous to the most superficially located bundles of smooth muscle-like cells. The adrenergic ground plexus is rather wide-meshed in the proximal cauda, becomes increasingly dense in more distal cauda sections and in initial, funicular portions of the vas deferens, and reaches maximum density in abdominal parts of the ductus. Perivascular and adventitial adrenergic plexuses are well developed at arteries of the caput and corpus epididymidis in man, monkey, rabbit, guinea-pig and rat. 4. Electron microscopically, noradrenergic nerves have been identified by the presence of small granular vesicles in preterminal varicose axon dilatations. Nerve fibre swellings filled with small empty spherical vesicles have been considered to belong to “cholinergic” neurons whereas occasional varicosities equipped with some large membrane bound granules and abundant mitochondria may represent local expansions of sensory axons. 5. Neuromuscular relationships in the upper sections of excretory ducts comprise adrenergic synapses by distance (more than 1000 Å), and a few intimate, ensheated close contacts, whereas the main type of contact of nerves to ordinary smooth muscle cells in the lower duct section is by means of close but not intimate approach (500–2000 Å). 6. Adrenergic synapses in the ductus epididymidis and ductus deferens of the monkey resemble—what concerns their morphology, relationship to effectors and distribution pattern—those of man. 7. In accordance with the total number of vascular and non-vascular adrenergic nerves, visualized by fluorescence microscopy, the amount of noradrenaline varied considerably in different sections of the human male internal genital organs: The lowest amounts were estimated in the testis (0.12±0.03 μg/g). Medium to high concentrations were detected in various sections of the caput and corpus epididymidis (ductuli efferentes 0.60±0.09 μg/g; ductuli efferentes and caput 0.72±0.13 μg/g; corpus epididymidis 1.04±0.25 μg/g; proximal cauda 0.95±0.17 μg/g; distal cauda 0.97±0.19 μg/g). The highest noradrenaline content was found in the human vas deferens (prox. vas deferens 1.11±0.21 μg/g; interm. vas deferens 1.20±0.42 μg/g; distal portion 1.43±0.39 μg/g). 8. For comparison, the noradrenaline content of the testis and epididymis of the rhesus monkey, the epididymis of the rabbit and the vas deferens of the rabbit, mouse, guinea-pig and rat has been determined. 9. Adrenaline of exogenous origin was detected in the vas deferens, cauda epididymidis and plexus pampiniformis of two cases who received this catecholamine as part of the local anaesthetic drug mixture. Due to methodological reasons, the presence of small amounts of adrenaline of endogenous source in adrenergic nerves of the human and monkey internal male genital organs cannot be excluded. 10. The differences in motility behaviour of the ductus epididymidis (spontaneous, rhythmic contractions) and ductus deferens (absence of any spontaneous movements under conditions at rest) in vivo and in vitro have been correlated with the occurrence of specialized contractile cells in the upper segment (ductuli efferentes, ductus epididymidis of the caput, corpus and initial cauda) and ordinary large smooth muscle cells in the lower segment (ductus epididymidis of the distal cauda and the vas deferens) and furthermore correlated with differences in the pattern of the adrenergic innervation; the concept is advanced that progressive cytological differentiation of smooth muscle cells and the development of a dense direct adrenergic innervation suppresses autocontractility and, that the reverse condition may favour spontaneous motility of smooth muscle elements.

Notes: Summary The effect of different doses of 5.6-dihydroxytryptamine—a serotonin analogue which produces a degeneration of serotonin containing nerve terminals in the rat brain—on the noradrenaline (NA) content and—storage sites of peripheral sympathetic nerves in the mouse and rat heart, spleen, rectum and vas deferens has been investigated by fluorescence—, electron microscopical and chemical methods. Moderate doses of 5.6-dihydroxytryptamine (5.6-DHT) (10–45 mg/kg ip.) cause a temporary, reversible displacement of noradrenaline from the adrenergic nerves concomitant with a significant increase in the number and opacity of small and especially large granular vesicles. The recovery of the neuronal NA concentration is, however, retarded after doses higher than 45 mg/kg (60 or 100 mg/kg ip.); a partial degeneration of varicose NA terminals is verified fluorescence- and electron microscopically. A combined treatment of animals with tyrosine hydroxylase inhibitors (α-methyl-paratyrosine or α-propyl-dopacetamide) and 5.6-DHT, in some instances also followed by reserpine, potentiates the destructive properties of 5.6-DHT; a similar potentiation is accomplished by reserpine posttreatment or by an additional pretreatment of animals with reserpine and nialamide. The results suggest that 5.6-DHT when given in moderate doses (up to 45 mg/kg) may be handled by sympathetic adrenergic nerves like a false neurotransmitter which displaces noradrenaline from the stores, but that it causes a “chemical degeneration” of noradrenaline containing nerve terminals when applied either in single high doses (60 or 100 mg/kg ip.), or when administered in moderate non-degenerative doses together with drugs that impair the neuronal inactivation mechanisms for 5.6-DHT (granular uptake and storage mechanism and/or monoamine oxidase activity) and thus provoke a temporary increase in the amount of free 5.6-DHT in the neuron's cytoplasm. The molar efficiency of 5.6-DHT in causing a chemical sympathectomy is clearly inferior to that caused by 6-hydroxydopamine. The differences are probably mainly due to differences in the affinity of both drugs to the amine uptake system located at the cell membrane and the membrane of the intraneuronal storage vesicles of the adrenergic nerve terminals.