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Effects of prostaglandins on the field-stimulated rat isolated urinary bladder
PROSTAGLANDINS
measured PGE2 -LI depending upon the characteristics of the particular antiserum employed. Therefore, RIA reliably measures PGE2 and PGF2?J in human urine only after adequate purification and with the use of highly specific antisera or complete separation of the PG-LI. EZCTS QF.PRGSTAGLAND1N.S ON THE FIELD-STIMULATED RAT ISOLATED URINARY BLADDER, Carin Larsson, Ph.D., Department of Pharmacology, AB KABI, Stockholm, Sweden. ABSTRACT Recent findings indicate that the contraction of the rat detrusor muscle is induced only partly by cholinergic neurotransmission. Non-cholinergic meurotransmission contributes about 70% to the response at 2Hz (field-stimulated isolated strips of detrusor muscle). The present study was undertaken to evaluate the contribution of PGs. Rat urinary bladder was cut into a longitudinal strip, and suspended in lo-ml organ baths containing Krebs solution at 35oC, bubbled with 95% oxygen and 5% carbon dioxide. Resting tension was adjusted to 0.8g. Isometric responses were measured with Grass FT 03 force-displacement transducers coupled to a Grass polygraph. Submaximal field-stimulation was induced by electrical stimulation of two platinum ring electrodes, placed in the bath at the upper and lower ends of the tissue by a Grass S 88 stimulator (2 set trains of biphasic pulses, 2H2, O-5-0.8 ms duration every 90 set). Arachidonic tcid (C20:4) (lo-12M - 10W5M), PGE2 (lo-l2 - 10s6M), PGEl (lo-l2 - lo- M) or PGF2b (lo-l2 -10W6M) increased the spontaneous activity and tone and potentiated, in a concentration-dependent manner, the contractions induced by field stimulation: maximum response wi;q C20:4 10s5M, 203 + 36% of control, n=9; the responses with PG 10 M were: PGE2 233 + 25, n=2; PGE 199 + 18, n=3; PGF 125, n=l. The PG synthesis-inhibitors inaomethacin (ind.) an 3 naproxen (napr.), and the thromboxane synthesis inhibitor L-8027, reduced the spontaneous activity and tone and also the contractions induced by field stimulation (% of control contraction at 10N6M: for ind. 113. n=l; napr. 64 + 7.6, n=4; L-8027, 77 + 3.2, n=3; at 10s5M: for ind: 26.6 _ + 23, n=37 napr. 36 + 4.6, n=3; c-8027, 45.2 + 10, n=5. Responses-to acetycholine remzined unchanged. The resrdual response _ induced by transmural stimulation in the presence of atropine was also reduced by PG-synthesis inhibitors. Potassium-induced contraction of the detrusor muscle was not changed by pretreatment with atropine or naproxen. Treatment with tetrodotoxin did not abolish the response to C20:4. Thus, the influence of PGs on the detrusor muscle seems at least partly non-neuronal. In conclusion, PGs may have a local role in the detrusor muscle for the maintenance of myogenic tone and spontaneous activity, and in a possible neuronal relationship the PGs may contribute to the atropine-insensitive contraction of the detrusor muscle.
APRIL 1978 VOL. 15 NO. 4
701
measured PGE2 -LI depending upon the characteristics of the particular antiserum employed. Therefore, RIA reliably measures PGE2 and PGF2?J in human urine only after adequate purification and with the use of highly specific antisera or complete separation of the PG-LI. EZCTS QF.PRGSTAGLAND1N.S ON THE FIELD-STIMULATED RAT ISOLATED URINARY BLADDER, Carin Larsson, Ph.D., Department of Pharmacology, AB KABI, Stockholm, Sweden. ABSTRACT Recent findings indicate that the contraction of the rat detrusor muscle is induced only partly by cholinergic neurotransmission. Non-cholinergic meurotransmission contributes about 70% to the response at 2Hz (field-stimulated isolated strips of detrusor muscle). The present study was undertaken to evaluate the contribution of PGs. Rat urinary bladder was cut into a longitudinal strip, and suspended in lo-ml organ baths containing Krebs solution at 35oC, bubbled with 95% oxygen and 5% carbon dioxide. Resting tension was adjusted to 0.8g. Isometric responses were measured with Grass FT 03 force-displacement transducers coupled to a Grass polygraph. Submaximal field-stimulation was induced by electrical stimulation of two platinum ring electrodes, placed in the bath at the upper and lower ends of the tissue by a Grass S 88 stimulator (2 set trains of biphasic pulses, 2H2, O-5-0.8 ms duration every 90 set). Arachidonic tcid (C20:4) (lo-12M - 10W5M), PGE2 (lo-l2 - 10s6M), PGEl (lo-l2 - lo- M) or PGF2b (lo-l2 -10W6M) increased the spontaneous activity and tone and potentiated, in a concentration-dependent manner, the contractions induced by field stimulation: maximum response wi;q C20:4 10s5M, 203 + 36% of control, n=9; the responses with PG 10 M were: PGE2 233 + 25, n=2; PGE 199 + 18, n=3; PGF 125, n=l. The PG synthesis-inhibitors inaomethacin (ind.) an 3 naproxen (napr.), and the thromboxane synthesis inhibitor L-8027, reduced the spontaneous activity and tone and also the contractions induced by field stimulation (% of control contraction at 10N6M: for ind. 113. n=l; napr. 64 + 7.6, n=4; L-8027, 77 + 3.2, n=3; at 10s5M: for ind: 26.6 _ + 23, n=37 napr. 36 + 4.6, n=3; c-8027, 45.2 + 10, n=5. Responses-to acetycholine remzined unchanged. The resrdual response _ induced by transmural stimulation in the presence of atropine was also reduced by PG-synthesis inhibitors. Potassium-induced contraction of the detrusor muscle was not changed by pretreatment with atropine or naproxen. Treatment with tetrodotoxin did not abolish the response to C20:4. Thus, the influence of PGs on the detrusor muscle seems at least partly non-neuronal. In conclusion, PGs may have a local role in the detrusor muscle for the maintenance of myogenic tone and spontaneous activity, and in a possible neuronal relationship the PGs may contribute to the atropine-insensitive contraction of the detrusor muscle.
APRIL 1978 VOL. 15 NO. 4
701