Phosphorylation of cardiac troponin by guanosine 3':5'-monophosphate-dependent protein kinase.

Journal ArticleHomogeneous cGMP-dependent protein kinase catalyzes the rapid incorporation of phosphate, specifically into the inhibitory subunit of purified cardiac troponin with a maximal incorporation of 1 mol of phosphate/mol of troponin. When troponin was incubated in the presence of both cGMP- and cAMP-dependent protein kinases, a maximal incorporation of 1 mol of phosphate/mol of troponin was observed which suggested phosphorylation of the same site by the two kinases. Both cyclic nucleotide-dependent kinases had similar Km values for troponin, but the Vmax value for the phosphorylation reaction catalyzed by cAMP-dependent protein kinase was 12-fold greater than the value obtained for cGMP-dependent protein kinase

Impaired Endothelial Function in Coronary Heart Disease Patients With Depressive Symptomatology

OBJECTIVES The purpose of this study was to assess whether depressive symptomatology was associated with vascular endothelial dysfunction in patients with coronary heart disease (CHD). BACKGROUND In patients with CHD, the presence of depression is associated with a two to four times increased risk of mortality, but the disease pathways involved are uncertain. Endothelial dysfunction is an established risk factor for cardiovascular events in patients with CHD. METHODS Flow-mediated dilation (FMD) of the brachial artery, a measure of endothelial function, was assessed in 143 patients (99 men, 44 women), ages 40 to 84 years (mean age, 63 ± 10 years), with documented CHD. RESULTS Patients with significant depressive symptomatology, as indicated by a Beck Depression Inventory (BDI) score ≥10 (n = 47) showed attenuated FMD (p = 0.001) compared with patients that were not depressed (BDI <10 n = 96). The use of antidepressant medication was associated with improved FMD (p < 0.05). CONCLUSIONS The increased risk of cardiovascular events in CHD patients with elevated symptoms of depression may be mediated, in part, by endothelial dysfunction