Interaction of calcium channel blockers with different agonists in aorta from normal and diseased rats

The interactions of calcium channel blockers (CCBs) with noradrenaline (NA), phenylephrine (PE), dopamine (DA) and KCl have been investigated in rat isolated aortic strip. In preparations from control and hypertensive (DOCA-saline) rats chronically treated with verapamil, nifedipine and diltiazem, t...

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Bibliographic Details
Published in:Indian journal of physiology and pharmacology 1996-04, Vol.40 (2), p.109
Main Authors: Bhugra, P, Gulati, O D
Format: Article
Language:English
Subjects:
Adrenergic alpha-Agonists - pharmacology
Animals
Aorta, Thoracic - drug effects
Calcium Channel Agonists - pharmacology
Calcium Channel Blockers - pharmacology
Dopamine - pharmacology
Drug Interactions
Hypertension - physiopathology
Hyperthyroidism - physiopathology
In Vitro Techniques
Male
Muscle Contraction - drug effects
Norepinephrine - pharmacology
Phenylephrine - pharmacology
Potassium Chloride - pharmacology
Rats
Rats, Wistar
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Summary:The interactions of calcium channel blockers (CCBs) with noradrenaline (NA), phenylephrine (PE), dopamine (DA) and KCl have been investigated in rat isolated aortic strip. In preparations from control and hypertensive (DOCA-saline) rats chronically treated with verapamil, nifedipine and diltiazem, there was partial inhibition of contractions to NA, PE and DA. However, with nimodipine, there was potentiation of responses. This could be related to the occurrence of different isoforms of L-type calcium channels. In preparations obtained from hyperthyroid rats the concentration-response curves of NA, PE and KCl were shifted to the right with depressed maximal response which could be secondary to the primary effect exerted on the heart. In preparations from L-thyroxine + nimodipine/nifedipine treated rats the concentration-response curves of NA, PE and KCl were shifted to the right and the maxima was depressed suggesting that this may be due to decreased alpha receptor density (NA and PE) and down-regulation of voltage operated channels (KCl).
ISSN:0019-5499