The use of pharmacologic agents in the treatment of pulmonary hypertension has not proved to be uniformly successful or predictable. One possible reason for the vagaries in response is that the pulmonary vascular lesions are not consistent. We examined the relation between the structure of the pulmonary resistance vessels in unexplained (primary) pulmonary hypertension and the response to pulmo...

RUDOLPH, ABRAHAM M., M. DAVID KURLAND, PETER A. M. AULD AND MILTON EL PAUL. Effects of vasodilator d ugs on normal and serotonin-constricted pulmonary vessels of the dog. Am. J. Physiol. I g7(3) : 6 I 7-623. I gsg.---Previous studies of the action of vasodilator drugs on the pulmonary blood vessels have yielded inconclusive results. Studies on the effects of continuous infusion of vasodilator a...

Raynaud phenomenon (RP) in connective tissue disease (CTD) can be resistant to oral vasodilator therapy, resulting uncontrollable digital ischemia. Intravenous (IV) prostanoids are often used, but the benefit transient and not all patients respond. Selexipag is an orally active selective IP-type prostanoid receptor agonist used pulmonary arterial hypertension. We describe 2 where selexipag sig...

Cardiac phosphodiesterase III (PDE) inhibitors derived from pyridinone, imidazolone, pyridazinone and related structures form a new class of positive inotropic vasodilator agents (e.g. milrinone) that are beneficial in the treatment of acute and chronic heart failure. These agents inhibit the intracellular hydrolysis of cyclic AMP, thereby promoting cyclic AMP-catalysed phosphorylation of sarco...

A cytochrome P450-derived metabolite of arachidonic acid, namely an epoxyeicosatrienoic acid (EET), has many of the properties of a hyperpolarizing factor that mediates endothelium-dependent, nitric oxide-independent vasodilation. As there are four EET regioisomers, we used pharmacological criteria, based on previous observations with bradykinin (BK), to evaluate which, if any, of the EETs coul...

Vasodilator substances act either directly on vascular smooth muscle (e.g., adenosine) or indirectly (e.g., acetylcholine) on endothelial cells that respond by releasing an unknown powerful, short-lived relaxing factor. To determine whether chronic hypertension or hypercholesterolemia or both would alter the release of the endothelium-derived relaxing factor, experiments were performed in hyper...

n the 1960s, when we initially introduced the concept of asodilator therapy for the failing heart (1), we had to vercome skepticism about the safety and efficacy of this pproach. Health care workers were focused on ausculatory lood pressure (BP), which often was falsely reduced in sick atients (2), and vasoconstrictor drugs frequently were dministered to restore perceived low pressure, which wa...