No abstract

1 In rabbit isolated pulmonary artery previously incubated with [3H]-noradrenaline, isoprenaline (0.3 riM) had no effect on the stimulation-induced outflow of radioactivity. However, if the phosphodiesterase inhibitor ICI 63,197 (30 gM) or the a-adrenoceptor blocker phentolamine (1 gM) was present, then isoprenaline significantly enhanced the stimulation-induced outflow, an effect blocked by propranolol (0.1 tIM). ICI 63,197 (30 tM) but not phentolamine significantly enhanced the stimulation-induced outflow of radioactivity.2 In mouse isolated atria previously incubated with [3H]-noradrenaline and stimulated at a frequency of 10 Hz, isoprenaline had no effect on the stimulation-induced outflow of radioactivity; this is in contrast to its release-enhancing effects at stimulation frequencies of 4 Hz and 2 Hz. The facilitation of stimulation-induced outflow by isoprenaline at 4 Hz was blocked by propranolol (0.08 ILM) which, by itself, had no effect on the stimulation-induced outflow. 3 At a stimulation frequency of 2 Hz in mouse atria thefacilitatory effect of isoprenaline (0.01 tM) was significantly greater in the presence of ICI 63,197 (30 jM) which, by itself, had no effect on the stimulation-induced outflow. Similarly, the facilitatory effect of isoprenaline was significantly greater in the presence of phentolamine (I 4M) but, in this case, phentolamine significantly enhanced the stimulation-induced outflow.4 These results suggest that facilitatory prejunctional P-adrenoceptors are present in both rabbit pulmonary artery and mouse atria. The effects of the phosphodiesterase inhibitor ICI 63,197 suggest that they are linked to adenylate cyclase in both tissues and we propose that the ability ofphentolamine to facilitate the release and enhance the effect of isoprenaline may be due to the blockade of aadrenoceptor inhibition of adenylate cyclase. This latter proposition needs further investigation.

3 The inhibition of the stimulation-induced outflow produced by clonidine (0.031M) and its facilitation produced by phentolamine (1 I1M) were unaltered in the presence of 8-bromo-cyclic AMP (90JM). However, in the presence of 8-bromo-cyclic AMP (270 AM), the facilitatory effect of phentolamine was enhanced, but the inhibitory effect of clonidine (0.03 gM) was unaltered. In the presence of ICI 63197 (30 LM) the inhibitory effect of clonidine (0.03 tM) was unaltered, but the facilitatory effect of phentolamine (1 gM) was slightly enhanced. 4 Isoprenaline (0.003-0.1;tM) enhanced the fractional stimulation-induced outflow, an effect blocked by propranolol (0.1 M). In the presence of 8-bromo-cyclic AMP (901M), the facilitatory effect of isoprenaline (0.01 gIM) was blocked. In the presence of ICI 63197 (30 gM) the facilitatory effect of isoprenaline (0.003 gIM) was potentiated.5 These results suggest that whereas P-adrenoceptor-mediated enhancement ofnoradrenaline release is linked to the stimulation of adenylate cyclase and enhanced formation of cyclic AMP, OCadrenoceptor-mediated inhibition of noradrenaline release is not linked to inhibition of adenylate cyclase activity.

We compare the chlorophyll fluorescence decay kinetics of the wild type and the D2-H117N mutant photosystem II reaction centers isolated from Chlamydomonas reinhardtii. The histidine residue located at site 117 on the D2 polypeptide of photosystem II is a proposed binding site for one of two peripheral accessory chlorophylls located in the reaction center complex. The peripheral accessory chlorophylls are thought to be coupled with the primary electron donor, P680, and thus involved in energy transfer with P680. The conservative replacement of the histidine residue with an asparagine residue allows the chlorophyll to remain bound to the reaction center. However, slight changes in the structural organization of the reaction center may exist that can affect the energy transfer kinetics. We show that the D2-H117N mutation causes a shift in the 20−30 ps lifetime component that has been associated with energy equilibration among coupled chlorophylls in the photosystem II reaction center.