ABSTRACT
A recent controversial report suggests that the nocturnal inhibitor of Rubisco, 2-carboxy-D-arabinitol 1-phosphate (CAIP), does not bind to Rubisco in vivo and therefore that CA1P has no physiological relevance to photosynthetic regulation. It is now proved that a direct rapid assay can be used to distinguish between Rubisco-bound and free CA1P, as postulated in the controversial report. Application of this direct assay demonstrates that CA1P is bound to Rubisco in vivo in dark-adapted leaves. Furthermore, CA1P is shown to be in the chloroplasts of mesophyll cells. Thus, CA1P does play a physiological role in the regulation of Rubisco.
Subject(s)
Fabaceae/enzymology , Pentosephosphates/metabolism , Plant Leaves/metabolism , Plants, Medicinal , Ribulose-Bisphosphate Carboxylase/antagonists & inhibitors , Binding Sites , Chlorophyll/analysis , Chloroplasts/chemistry , Chloroplasts/enzymology , Chloroplasts/metabolism , Enzyme Inhibitors/metabolism , Fabaceae/metabolism , Freeze Drying , Light , Photoperiod , Plant Leaves/enzymology , Ribulose-Bisphosphate Carboxylase/metabolism , Sulfates/pharmacology , Time FactorsABSTRACT
Bradycardia occurring during coronary angiography may be due to the direct effect of dye or to reflex vagal effects on pacemaker centers. Fifteen patients were classified according to the origin of the sinus nodal and atrioventricular nodal arteries. In patients with type A anatomy, both the sinus and the atrioventricular nodal arteries arose from the right coronary artery. In those with type B anatomy, only the atrioventricular nodal artery arose from the right coronary artery. Heart rate recordings were made during coronary angiography before and after selective infusion of atropine (0.2mg) into the right coronary artery. In type A patients, the sinus bradycardia observed during right coronary dye injection was caused by a combination of both direct and reflex effects on pacemaker tissue. Sinus bradycardia occurring with left coronary dye injections was entirely reflex in nature and was completely blocked with right coronary arterial injection of atropine. In type B patients, sinus bradycardia with right coronary dye injections was produced by reflex suppression of the sinus pacemaker. A junctional rhythm was consistently produced after administration of atropine. Junctional bradycardia in type B patients was caused by direct suppression of the junctional pacemaker. Thus, angiographic dye appears to decrease heart rate by a direct effect on pacemaker tissue and by reflex vagal suppression of the sinus pacemaker.
