Disease relevance of CD-349

• The increase in HR associated with the hypotension induced by CD-349 at 1 mg/kg was relatively transient in comparison with that induced by nifedipine at the same dose in both types of hypertensive rat [1].

High impact information on CD-349

• Scatchard plot analysis of the binding of CD-349 to CaM revealed that the apparent dissociation constant (Kapp) of CD-349 was 2.1 microM and the maximal number of binding sites (Bmax) of CD-349 was 1.0 nmol/nmol CaM [2].
• Comparison of a calcium antagonist, CD-349, with nifedipine, diltiazem, and verapamil in rabbit spontaneously beating sinoatrial node cells [3].
• CD-349 10(-8) M significantly decreased the maximum rate of depolarization and prolonged action potential duration (APD) and the cycle length (CL) without affecting action potential (AP) amplitude (APA) and maximum diastolic potential (MDP) [3].
• Effects of CD-349, a novel 1,4-dihydropyridine, and other calcium antagonists on membrane potentials in spontaneously beating and the membrane currents in voltage-clamped rabbit sinoatrial (SA) node cells were examined [3].
• Electrophysiological effects of CD-349, a dihydropyridine-type calcium antagonist, on goat cardiac Purkinje fibers [4].

Biological context of CD-349

• The effects of a Ca2+ entry blocker CD-349 and an intracellular Ca2+ release inhibitor TMB-8 on renal vasoconstriction induced by angiotensin II (ANG II) and arg-vasopressin (AVP) were examined in anesthetized dogs [5].
• CD-349 of 10 micrograms/kg infused into the carotid artery produced a remarkable and long-lasting decrease in systemic blood pressure, whereas BrPO2, BrPCO2 and BrpH did not change significantly [6].

Anatomical context of CD-349

• We examined the calcium antagonistic action of CD-349, a dihydropyridine derivative, on goat cardiac Purkinje fibers using the two-microelectrode voltage-clamp method [4].
• This inhibitory effect of CD-349 was independent of the existence of endothelium [7].
• A new Ca-antagonist, CD-349, binding to the Ca-channel of rat myocardium and brain and hog coronary artery [8].
• Form these results it is suggested that CD-349 exerts direct vasodilatory action via inhibition of calcium influx across vascular cell membranes into cerebral vessels [9].
• The pial vein (101 +/- 20 micron) was also dilated with the percent increase of the diameter being 11.4 +/- 4.0% (p less than 0.01) 1 min and 11.3 +/- 4.9% (p less than 0.05) 5 min after the CD-349 administration [9].

Associations of CD-349 with other chemical compounds

• 1. CD-349 inhibited the noradrenaline (NA)-induced contraction of aortas in Ca2(+)-free medium [10].
• Early treatment with CD-349 (1 or 2mg/kg/day, i.m.) for 1 week reversed not only the enhanced contraction of the basilar artery in response to 5-HT but also the impairment of endothelium-dependent relaxation in response to substance-P in SAH [11].

References