Action of clonidine on micturitional reflexes in decerebrate cats.

We explored the urodynamic action of clonidine (preferential alpha 2-agonist) and yohimbine (preferential alpha 2-blocker) in decerebrate cats. These animals retain catecholaminergic fibers from the complex of the locus coeruleus to the spinal cord and have synergic and faster micturition cycles than normal cats. Twenty-nine male cats were made decerebrate at intercollicular level under ether anesthesia. Voiding, vesical, urethral and blood pressures, and the EMG of the external sphincter-pelvic floor and leg muscles were studied. Preparations with the urethrovesical junction opened and closed were used. Control activity was characterized by two types of vesical pressure waves: (1) low frequency, high intensity, and (2) high frequency, low intensity. Type-2 preceded Type-1 waves. Clonidine caused: (A) reduction of Type-1 and enhancement of Type-2 Pves waves; (B) diminution of vesical capacity; (C) facilitation of external sphincter relaxation; (D) inhibition of skeletal muscle activity; (E) systemic hypotension and bradycardia. Yohimbine inhibited clonidine's actions. When injected alone, it inhibited vesical and increased sphincteric activities. It also produced systemic hypertension and enhanced crisis of autonomic dysreflexia. The overall effect of clonidine on urodynamics in acute decerebrate cats was to bring about an active, small (normotonic) bladder with urinary frequencies. We suggest that clonidine: (1) inhibited Type-1 waves by inhibiting cellular activity in the locus coeruleus. As a result, the vesico-vesical contraction long loop reflex was abolished; (2) facilitated Type-2 waves by inhibiting inhibitory interneurons in the sacral parasympathetic center. As a result, the vesicovesical contraction short loop reflex was facilitated.