[Pharmacologic modification of ureteral activity].

The renal pelvis and the ureter represent a functional system with myogenic excitation generation and conduction. The activity of this system is modulated by the autonomic nervous system: alpha-adrenergic and cholinergic substances stimulate, beta-adrenergic drugs inhibit the pyeloureteral activity. Besides the sympathetic nervous system with adrenergic postganglionic excitation conduction and the parasympathetic nervous system with cholinergic transmission, non-adrenergic, non-cholinergic systems appear to exist. Vasoactive intestinal peptide (VIP), e.g., markably decreases the frequency and amplitude of the ureteral activity. Calcium antagonists (e.g. nifedipin) lead to a direct inhibition of the ureteral activity: the quick phasic contractions are selectively oppressed without any influence on the tonic activity of the pyeloureter. A direct therapeutic modulation of the ureteral activity, however, e.g. to treat a colic or to accelerate the spontaneous discharge of stones, seems to be only rarely possible: Glucagone shows a markable decrease of ureteral peristalsis in animal experiments. Antagonists of prostaglandine proved to have not only an antiinflammatory and central analgetic effect but they also influence the pyeloureter directly by relaxing the muscular layer.