The Sympathetic Innervation of the Urinary Bladder and Urethra in the Normal State and After Parasympathetic Denervation at the Spinal Root Level: An Experimental Study in Cats

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Abstract
The innervation of the feline bladder and urethra was studied by a histochemical fluorescence technique and the use of peripheral nerve stimulations in combination with different blocking agents. The studies were performed in the normal state and at various times after parasympathetic denervation, achieved by sectioning of appropriate ventral roots. After parasympathetic denervation the bladder response following hypogastric nerve stimulation was changed from a normal response of initial contraction and subsequent relaxation into a sustained bladder contraction. This altered response, first observed after 6 weeks, was composed of two phases; a weak and brief contraction followed immediately by a strong and long-lasting contraction. The second phase was adrenergic (blocked by an adrenergic aL-blocking agent) and presumably effected via intramural ganglia (blocked by a ganglionic blocking agent). Consistent with this was the histochemical observation of a change in adrenergic innervation. About 6 weeks after parasympathetic denervation, adrenergic sprouts with growth cones were observed in the bladder; later there was an increasing number of adrenergic terminals in the detrusor muscle. These terminals probably originated in adrenergic cell bodies of intramural ganglia, since the number of such terminals was not notably reduced by hypogastric nerve sectioning. It is suggested that this increase in adrenergic innervation and in aL-receptor activity, which implies that the hypogastric nerves mediate excitatory instead of inhibitory impulses to the bladder, might be responsible for the “autonomous» contractions and the hypertrophy seen in long-term parasympathetically denervated bladders.