The Effect of "Sympatholytic Drugs on the Cardiovascular Responses to Epinephrine and Norepinephrine in Man

Abstract

Under controlled conditions the effects of various "sympatholytic" agents on the cardiovascular responses to epinephrine and norepinephrine were compared in man. The dosages of the sympatholytic drugs administered approximated those usually employed clinically. Such basic data are given for the following agents: Dibenamine, the imidazoline derivatives [Priscoline and Regitine (C-7337)], the dihydrogenated alkaloids of ergot (D.H.K. and C.C.K.), L-hydrazinophthalazine (C-5968), tetraethylammonium, and hexamethonium (C6).

Mechanism of the Altered Blood Pressure Responsiveness Produced by Chlorothiazide *

“…Both agents were diluted in 5 per cent dextrose in water to make up final concentrations of 4 mg levarterenol in 1,000 ml and 500 mg trimethaphan in 500 ml. These were given intravenously by the method previously described (9). Control titrations were carried out on the day prior to chlorothiazide administration and the experimental infusions on the third day following chlorothiazide.…”

Cardiovascular and Renal Adjustments to a Hypotensive Agent

“…It has been shown that this drug antagonizes the pressor action of epinephrine and to a lesser extent that of nor-epinephrine (14,(17)(18)(19)(20). It abolishes the pressor effect brought about by centripetal vagus stimulation and thought due to serotonin (21), and it has an inhibitory effect against the National Heart Institute, U the pressor action of angiotonin and possibly other factors causally related to hypertension (22)(23)(24).…”

Inhibitory Effects of Polyphenol-Rich Fraction Extracted from Rubus coreanum M on Thoracic Aortic Contractility of Spontaneously Hypertensive Rats

“…However, in the presence of adrenergic α-receptor blockade, the peripheral β 2 -agonist properties of epinephrine predominate and a fall in arterial pressure or reversal of the pressor response is observed. In contrast, the pressor responses to norepinephrine are impaired by adrenergic α-receptor blockade, but are not reversed (Freis et al, 1951) as this agent processes little β 2 -agonist activity (Ablad et al, 1975). Based on these fi ndings, our results that PCRC strongly depressed phenylephrineevoked contractile response and norepinephrine-induced hypertensive response suggest the possibility that the vasorelaxant activity of PCRC may be medated through the adrenergic α-receptor blockade.…”