duction path. Without such an elaborate chemical modification, some progress might be possible by using regular enzymes, with required coenzymes, in a mixed conducting suspension of a material such as NMPTCNQ. Progress might include long lifetime, freedom from covering membrane, and possible increased amplification, compared with the now conventional enzyme-catalyzed amperometric sensors. ConclusionsPlasticizing NMPTCNQ with DIBP reduces its electronic conduction linearly, with an extrapolated specific conductivity of 0.1 S/cm at zero plasticizer content. At very high DIBP levels, the electronic conductivity is so low that it is comparable with the apparent ionic component, estimated experimentally at 10-6-10 -7 S/cm. NMPTCNQ/DIBP mixtures are quite stable and ohmic at low voltages, using electronic contacts, except for very high DIBP contents when electric fields may change the orientation of NMPTCNQ particles.Simple redox reagents: copper(II, I, 0) and ferro-/ferricyanide retain electroactivity on plasticized NMPTCNQ coatings on glassy carbon electrodes, and demonstrated the possibility of using suspensions to mediate and promote enzyme/substrate/surface reactions.

The effect of bradykinin (BK) on the release of β-endorphin-like immunoreactivity (β-EpLI) in rats was studied in vivo and in vitro. Intraperitoneal injection of BK at 5 µg/100g body weight resulted in significant increase in the plasma β-EpLI level after 15 min. BK at concentrations of 10^–12–10^–7M also caused dose-dependent stimulation of β-EpLI release from dispersed cells of rat anterior pituitary. On gel chromatography, the β-EpLI released by incubation of the cells with 10^–7M BK separated into two components, eluted in the same positions as human β-lipotropin and human β-endorphin, respectively. BK did not stimulate β-EpLI release in Ca⁺⁺-free medium. Addition of 10^–3 M verapamil or 10^–6M dexamethasone to the incubation medium inhibited BK-induced β-EpLI release from the cells. Quabain (10^–5M) also stimulated β-EpLI release, but its effect was not additive with that of BK. These results indicate that BK stimulates β-EpLI release and that calcium ion is involved in the mechanism of this effect.

The effects of various ingested materials on plasma neurotensin-like immunoreactivity (NTLI) in humans were investigated using a newly developed, specific radioimmunoassay. Plasma NTLI was determined after its extraction with acid/acetone (recovery 77 +/- 4%). The intraassay and interassay coefficients of variation were 3.6% and 8.9%, respectively. The plasma concentration of human NTLI in normal subjects was 5.6 +/- 2.9 pmol/l and showed no significant sex difference. Ingestion of a test meal (150 g of Campbell's condensed meat soup) caused a biphasic rise in plasma NTLI from a basal level of 5.7 +/- 1.0 pmol/l to 10.8 +/- 1.2 pmol/l after 30 min and 9.6 +/- 1.1 pmol/l after 120 min. Ingestion of 5.5 g fat resulted in a biphasic rise in plasma NTLI from a basal level of 4.8 +/- 0.3 pmol/l to 8.9 +/- 0.3 pmol/l after 15 min and 11.9 +/- 0.4 pmol/l after 90 min. When 100-150 mg of ileal mucosa was perfused with a solution of 2 mEq/l fatty acids, 1 mM or 5 mM sodium taurocholate or 154 mM sodium bicarbonate (NaHCO3), the release of NTLI from the mucosa into the perfusate was 2.3-fold, 4.3-fold and 7.5-fold, respectively, over the base level. These results indicate that NTLI release is stimulated by ingestions of meat soup and fat and that NTLI present in the human ileum is released by the direct actions of solutions of fatty acid, sodium taurocholate, and NaHCO3 on the ileal mucosa. These findings strongly suggest that neurotensin (NT) has a physiological role in gut physiology.

The effects of bile salts on the release of beta-endorphin-like immunoreactivity (beta-END-LI) were investigated in men using a specific radioimmunoassay developed by the authors. Plasma beta-END-LI was determined after extraction by the acid-acetone method (recovery: 73 +/- 5%). Oral administration of 400 mg of sodium taurocholate caused a rise in plasma beta-END-LI from 9.9 +/- 0.5 pmol/liter to 21.3 +/- 1.2 pmol/liter after 30 min and 18.1 +/- 0.5 pmol/liter after 60 min, with return to the initial value after 90 min. Oral administration of chenodeoxycholic acid (CDCA) also increased plasma beta-END-LI from a basal level of 8.4 +/- 0.7 pmol/liter to 18.7 +/- 0.8 pmol/liter after 30 min. Oral administration of ursodeoxycholic acid (UDCA) increased plasma beta-END-LI from 7.3 +/- 0.3 pmol/liter to 30.6 +/- 0.2 pmol/liter after 30 min. In gel chromatography, the beta-END-LI released after UDCA administration separated into two components, which eluted in the same positions as human beta-lipotropin and human beta-endorphin, respectively. These results suggested that bile salts may participate the release of beta-END-LI.