Do aCE inhibitors promote nitric oxide accumulation to modulate myocardial oxygen consumption?
Our data indicate that stimulation of local kinin formation by use of a precursor for kinin formation or inhibition of kinin degradation by use of ACE inhibitors increases NO formation and is important in the control of cardiac O2 consumption. Vasodilation and control of myocardial O2 consumption by NO may contribute importantly to the therapeutic actions of ACE inhibitors in cardiac disease states.
Our results suggest that 5-FU mediates apoptosis and G1/S cell cycle phase arrest in laryngeal carcinoma via a p53-independent but p21WAF1/CIP1-dependent or p21WAF1/CIP1-Rb-dependent pathway. While p53 does not seem to be involved in 5-FU induced apoptosis and cell cycle arrest in laryngeal carcinoma, further studies are needed to examine the roles of retinoblastoma protein and p21WAF1/CIP1 in laryngeal carcinoma receiving chemotherapy.