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Prior reports by Dr. Bond [1] have described the occurrence of an initial compensatory vasoconstriction followed by a decompensatory vasodilation response in animals that progress to irreversible shock induced by blood loss. Further analysis suggests that the secondary vascular decompensation is the result of sympathetic inhibition of adrenergic neurotransmission.

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Tiodazosin, a new antihypertensive, resembles prazosin in structure and alpha-adrenergic-blocking activity, and it also exerts a direct vasodilator effect. We evaluated its long-term hemodynamic and systemic effects in patients with essential hypertension. Our data show that after 10 wk of therapy with tiodazosin, 7 of our 10 patients had significant reduction in intra-arterial mean blood pressure as a result of a fall in systemic vascular resistance.

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Tiodazosin is a recently developed compound that is currently undergoing investigation for use in hypertension. It is structurally and pharmacologically similar to prazosin, the prototype of the aminoquinazoline class of vasodilators. Lacking an intravenous dosage form for use in human subjects, our study concentrated on the determination of the bioavailability and disposition parameters of tiodazosin in dogs, with a comparison to those parameters for prazosin, obtained from previous work in our laboratory.

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