Cardiovascular Effects of Nifedipine and Bay K 8644 in Hypertensive Rats.
10.4070/kcj.1997.27.12.1310
- Author:
Tai Myoung CHOI
;
Jong Seung KIM
;
Sung Ho MOON
;
Hyeong Kyun OH
;
Jeong Hoe LIEE
;
Jae Yeoul JUN
;
Cheol Ho YEUM
;
Pyung Jin YOON
;
Soon Pyo HONG
- Publication Type:Original Article
- Keywords:
Cardiovascular;
Nifedipine;
Bay K 8644;
Hypertension
- MeSH:
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester*;
Animals;
Bays*;
Blood Pressure;
Calcium;
Calcium Channel Blockers;
Calcium Channels;
Desoxycorticosterone;
Femoral Artery;
Heart;
Hypertension;
Neurotransmitter Agents;
Nifedipine*;
Rats*;
Renal Artery;
Silver
- From:Korean Circulation Journal
1997;27(12):1310-1317
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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.
