In pulmonary circulation, small muscular resistance arteries are known to have different receptor properties and sensitivity to neurotransmitters from those of large elastic conduit arteries. It is, however, not yet certain whether the different properties are primarily due to the diameter or the location of arteries. In the present study, we compared the contractile responses to various agonists among large extralobar (ELPA, diameter: 2-3 mm), large intralobar (ILPA, diameter: 2-3 mm), and small intralobar pulmonary arteries (SPA, diameter: 300-500μm) of the rabbit.
There were no differences in normalized dose-response curves to KCl among three groups. Half maximum doses (EC₅₀ in mM) were 38.0±2.0 (n=8, mean±SEM) in ELPA, 36.9±2.4 (n=10) in ILPA, and 39.0±0.9 (n=12) in SPA. Responses to phenylephrine, epinephrine, histamine, serotonin, and PGF_2α were normalized and expressed as a relativecontraction against maximum tension to KCl. In ELPA, the contractile responses tovarious agents showed the following sequence: KCl>epinephrine>phenylephrine>serotonin>PGF_2α>histamine. In ILPA and SPA, the sequence was: KCl>histamine>PGF_2α>serotonin. There was little response to phenylephrine and epinephrine in ILPA and SPA.
These results demonstrate that the difference of contractile responses between ELPA and ILPA was more prominent than that between ILPA and SPA, suggesting that the location is more important than the diameter itself in determining the characteristic contractile responses of pulmonary arteries.

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The relaxing effects of the adenosine 5'-triphosphate (ATP)-sensitive K⁺ channel openers (K_ATP openers ; diazoxide, minoxidil, pinacidil, (±)-cromakalim, (+)-cromakalim and (-)-cromakalim) were investigated on the resting tone of pig proximal urethra. In addition, patch-clamp techniques were utilized for recording cromakalim-induced ionic currents in cells dispersed from the same urethral region. The (-)-cromakalim-induced relaxation of urethral muscle strips was stable, reversible and reproducible. The rank order of potency regarding of K_ATP openers in lowering the resting urethral tone was (-)-cromakalim > pinacidil> diazoxide > minoxidil. K_ATP opener-induced urethral relaxation was suppressed by subsequent application of glibenclamide (1μM).(+)-Cromakalim (>10μM) did not relax the urethra nor antagonize the (-)-cromakalim-induced urethral relaxation.However, at higher concentrations, (+)-cromakalim (>30μM) caused a small but significant urethral relaxation. In accordance with these observations, the relaxation induced by 5μM (-)-cromakalim was identical to that induced by 10μM (±)-cromakalim, as expected from a theoretical half potency for (±)-cromakalim. In whole-cell recording, (-)-cromakalim and (+)-cromakalim (100μM) activated a glibenclamide-sensitive outward current which was due to the activation of the glibenclamide-sensitive 43 pS K⁺ channel (K_GS-43 pS). The potency of (+)-cromakalim to activate K_GS-43 pS was much weaker than that of (-)-cromakalim. These results indicate that the ability of K_ATP openers to relax pig urethral smooth muscle can be accounted for by activation of glibenclamide-sensitive K⁺ channels.

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