It is generally accepted that the agonists, full agonist and partial agonist, interact with the same receptors according to the classical receptor mechanisms. We tried to modify the drug receptor mechanisms in muscarinic cholinoceptors, α₁-adrenoceptors and β-adrenoceptors. In the muscarinic cholinoceptor, there are two subtypes of M₃-cholinoceptors, propylbenzilylcholine mustard (PrBCM)-sensitive receptors and PrBCM-resistant ones. The full agonists contract the longitudinal muscle through the interaction of two cholinoceptors, PrBCM-sensitive and-resistant ones, while the partial agonists produce the contrac-tion through only the activation of PrBCM-sensitive ones. Upon activation PrBCM-sensi-tive receptors may use cytosolic Ca²⁺ more effectively than PrBCM-resistant receptors. In the α₁-adrenoceptor, the full agonist induces contraction through both ai A and α_1B, subtypes and the partial agonist through only α_1A, subtype. The adrenoceptors activated by full agonist may be partly different from that by partial agonist in the arteries. In both the common iliac artery and thoracic aorta treated with the irreversible antagonist, phenoxybenzamine the slopes of schild plots of the results obtained from an antagonism between full agonist (phenylephrine) and α_1A-selective competitive antagonist (WB4101) equal to 1, suggesting that phenoxybenzamine preferably interacts with α_1B, subtype. In the β-adrenoceptor, the pD₂-values of the partial agonists obtained from the concentration-response curves are significantly different from their pA₂-values against full agonist (isoprenaline). The Scatchard plot of the specific [³H] befunolol (the partial agonist) binding showed two affinity sites of the receptors in the absence of Gpp (NH) p but the low affinity site was reduced while the high affinity site was not affected in the presence of Gpp (NH) p.The β-adrenergic partial agonists are able to discriminate these two different binding sites of the β-adrenoceptors. Our results suggest that the receptors activated by full agonists are partly different from those by partial agonists in muscarinic cholinoceptors, α₁-and β-adrenoceptors, and that the irreversible antagonist can discriminate between the sites interact with full agonists and those with partial agonists in muscarinic cholinoceptors and α₁-adrenoceptors.

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The effect of terazosin on the lower urinary tract function was studied by combined recording of bladder and urethral pressures and external sphincter electromyogram in 8 male decerebrate dogs. Reflex micturitions were induced by bladder filling before and after terazosin. The statistical analysis was carried out on the urodynamic parameters.
During the collecting phase, terazosin at doses of 10, 30 and 100 μg/kg produced a significant decrease in maximum urethral pressure in the dose dependent manner. Threshold pressure was significantly shown to decrease at doses of 30 and 100 μg/kg. In the urodynamic parameters of the emptying phase there was a significant decrease in maximum contraction pressure at 10 and 30 μg/kg, and in voided volume at 100 μg/kg. Terazosin seems to facilitate an initiation of the bladder contraction with a decrease in threshold pressure.
It concludes that α1 adrenergic activity seems to take an important role for the maintenance of the urethral pressure and to control the initiation of bladder contraction in modulation with threshold pressure.

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Effect of ageing on α_1A adrenoceptor mechanisms in rabbit bronchial preparations was studied. The potency (pD₂ value) of norepinephrine increased with age from 5 to 13 weeks and thereafter did not alter with age from 13 to 180 weeks. The affinity of norepinephrine (PK_A value) and of a selective α_1A-adrenoceptor blocker, 5-methylurapidil (pA₂ value) did not alter with age. Efficacy of norepinephrine was proportional to receptor reserve (pD₂-pK_A). These results suggest that age-related changes in α_1A-adrenoceptor mechanisms are due to changes in receptor reserve or total concentration of receptors, but not to changes in affinity of drugs to α_1A-adrenoceptors and in contraction mechanisms.

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Gastrointestinal motility and plasma PYY levels were investigated under chronic progressive large bowel obstruction in dogs. The obstruction device was applied arround the descending colon at a laparotomy and gastrointestinal motility was recorded with strain gauge force transducers in the conscious state. Complete obstruction occured at 26 days (21-33 days). The duration of postprandial interruption of motor complex (DIMC) in the antrum and duodenum were prolonged progressively, at partial obstruction (17.7±2.7 hr; p<0.05) and complete obstruction (23.O ± 4.0 hr: p<0.01) vs in control (13.7 ± 1.9 hr), while DIMC in the smal bowel showed no significant changes. Progressive obstruction caused hypermotility in the proximal colon to the obstrution and hypomotility in the distal colon. These dysmotility were improved after resection of the obstructed segment and anastomosis. Plasma PYY levels in the fasting state showed no significant increase at complete obstruction (42.6±14.5 pmol/l) vs in control (32.9±10.2 pmol/l)

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