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Ismelin (guanethidine monosulfate) acts at the sympathetic neuroeffector junction by inhibiting or interfering with the release and/or distribution of the chemical mediator (presumably the catecholamine norepinephrine), rather than acting at the effector cell by inhibiting the association of the transmitter with its receptors. In contrast to ganglionic blocking agents, Ismelin (guanethidine monosulfate) suppresses equally the responses mediated by alpha-and beta-adrenergic receptors but does not produce parasympathetic blockade. Since sympathetic blockade results in modest decreases in peripheral resistance and cardiac output, Ismelin (guanethidine monosulfate) lowers blood pressure in the supine position. It further reduces blood pressure by decreasing the degree of vasoconstriction that normally results from reflex sympathetic nervous activity upon assumption of the upright posture, thus reducing venous return and cardiac output more. The inhibition of sympathetic venoconstrictive mechanisms results in venous pooling of blood. Therefore, the effect of Ismelin (guanethidine monosulfate) is especially pronounced when the patient is standing. Both the systolic and diastolic pressures are reduced.
Other actions at the sympathetic nerve terminal include depletion of norepinephrine. Once it gains access to the neuron, Ismelin (guanethidine monosulfate) accumulates within the intraneuronal storage vesicles and causes depletion of norepinephrine stores within the nerve terminal. Prolonged oral administration of Ismelin (guanethidine monosulfate) produces a denervation sensitivity of the neuroeffector junction, probably resulting from the chronic reduction in norepinephrine released by the sympathetic nerve endings. Systemic responses to catecholamines released from the adrenal medulla are not prevented and may even be augmented as a result of this denervation sensitivity. A paradoxical hypertensive crisis may occur if Ismelin (guanethidine monosulfate) is given to patients with pheochromocytoma or if norepinephrine is given to a patient receiving the drug.
Due to its poor lipid solubility, Ismelin (guanethidine monosulfate) does not readily cross the blood-brain barrier. In contrast to most neural blocking agents, Ismelin (guanethidine monosulfate) does not appear to suppress plasma renin activity in many patients.
The pharmacokinetics of Ismelin (guanethidine monosulfate) are complex. The amount of drug in plasma and in urine is linearly related to dose, although large differences occur between individuals because of variation in absorption and metabolism. Adrenergic blockade occurs with a minimum concentration in plasma of 8 ng/ml; this concentration is achieved in different individuals with dosages of 10-50 mg/day at steady state. Ismelin (guanethidine monosulfate) is eliminated slowly because of extensive tissue binding. After chronic oral administration, the initial phase of elimination with a half-life of 1.5 days is followed by a second phase of elimination with a half-life of 4-8 days. The renal clearance of Ismelin (guanethidine monosulfate) is 56 ml/min. Ismelin (guanethidine monosulfate) is converted by the liver to three metabolites, which are excreted in the urine. The metabolites are pharmacologically less active than Ismelin (guanethidine monosulfate) .
Last reviewed on RxList: 12/8/2004
This monograph has been modified to include the generic and brand name in many instances.
Additional Ismelin Information
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