ABSTRACT
This study was conducted to declare the effect of calcium channel blockers [nifedipine and isradipine] on the vasoconstrictor responseophenylephrine and norepinephrine.Mongrel dogs were used to study this interaction on the blood pressure, nifedipine and isradipine attenuated the effect of vasopressors on the blood pressure. The degree of attenuation was in the following order: norepinephrine > phenylephrine. When dogs were subjected to bleeding, it was found that nifedipine and isradipine also attenuated the effect of vasopressors on the blood pressure of dogs. The degree of attenuation was in the following order: norepinephrine > phenylephrine. Using Albino rat hind quarter preparations, it was found that nifedipine and isradipine produced significant increase in the vascular outflow rate. The effect of isradipine was more significant than that of nifedipine. Phenyleprine and norepinephrine significantly decreased the vascular outflow rate. Nifedipine and isradipine did not attenuate the vasoconstrictor response of phenylephrine and non significant attenuation to the vasoconstrictor response of norepinephrine was observed. In conclusion, and 2 -mediated vasoconstriction is mostly dependent upon the influx of calcium through calcium channels. This effect is almost totally blocked by nifedipine and isradipine. and1 -mediated vasoconstriction is mediated, by the previously mentioned mechanism and other mechanisms e.g. intracellular release of calcium. The vasopressor effect mediated by and 1-stimulant is resistant to total blockade by nifedipine or isradipine. Blockade of the vasoconstrictor effect mediated by and 1 or and 2 stimulants should be taken in consideration if a subject under nifedipine or isradipine treatment needs and 1 or and 2 stimulant for treatment of emergency hypotensive states