Cardiovascular Effects of Nifedipine and Bay K 8644 in Hypertensive Rats

BACKGROUND: Calcium plays a key role in vascular contraction and regulates receptor sensitivity to certain neurotransmitters. Calcium channel blockers are useful in the treatment of both clinical and experimental hypertension. The present study was designed to examine whether there is an alteration of the activity of calcium channels in association with the development of hypertension. METHODS: Deoxycorticosterone acetate(DOCA)-salt hypertension was made by subcutaneous implantation of DOCA(200mg/kg)strip plus saline drinking(1%) and 2-kidney, 1 clip(2KIC)hypertension by clipping the left renal artery with a silver clip(internal gap of 0.2mm). They were used 4 weeks later. Age-matched normal rats served as a control. Mean arterial pressure(MAP) and heart rate(HR) were continuously recorded from the right femoral artery. The drugs were administered intravenously. RESULTS: Vehicle alone was without effect on MAP or HR. In normotensive rats, nifedipine infusion(5 and 10ug/kg/min)caused a dose-dependent decrease in MAP without significant changes in HR, while Bay k 8644(Bay K, 5 and 10 ug/kg/min) increased MAP transiently. Both the depressor response to nifedipine and the pressor response to Bay k were more marked in DOCA-salt hypetensive rats than in normotensive rats. The maximal changes in MAP indced by nifedipine(5 and 50 ug/kg) or Bay K(5 and 50 ug/kg) were also enhanced in 2KIC hypertensive rats as compared with control rats. CONCLUSION: These results indicate that calcium channel inhibitors and activators can affect on the regulation of blood pressure in an opposite fashion. It is also suggested that the activity of calcium channels might be altered in the developement of experimental hypertension.

Circardian Variation of Premature Ventricular Complex in Dilated Cardiomyopathy

BACKGROUND: Circardian variation in the onset of cardiovascular events includig sudden cardiac death, myocardial infarction and ventricular arrhythmias has been discribed. The frequency of ventricular premature complexes has also been reported to demonstrate a pattern consisting of a daytime peak and nightime nadir. We tried to see if the same circardian pattern is found in dilated cardiomyopathy patients. We have also studed how various modifying factors such as left ventricular ejection fration and ACE inhibitor use may affect the circardian pattern. METHOD: 24-hour ambulatory electrocaridiographic monitorings were performed in 50 dilated cardiomyopathy patients and 20 control subjects. Patients were prospectively divided in 2 groups based on LVEF and ACE inhibitor use. RESULTS: In dilated cardiomyopathy patients, the expected morning increase in VPC frequency is absent and show a peak in evening. This pattern is not correlated with heart rate. Evening peak is more prominent in low LVEF group and ACE inhibitor non-user group. CONCLUSION: In dilated cardiomyopathy patients, VPC frequency show a peak in the evening.