Pressor Response to Intravenous Tyramine Is a Marker of Cardiac, but Not Vascular, Adrenergic Function

Abstract

Intravenous injections of the indirect sympathetic amine, tyramine, are used as a test of peripheral adrenergic function. The authors measured the time course of increases in ejection fraction, heart rate, systolic and diastolic pressure, popliteal artery flow, and greater saphenous vein diameter before and after an injection of 4.0 mg/m(2) body surface area of tyramine in normal human subjects. The tyramine caused moderate, significant increases in systolic pressure and significant decreases in total peripheral resistance. The earliest changes were a 30% increase in ejection fraction and a 16% increase in systolic pressure, followed by a 60% increase in popliteal artery flow and a later 11% increase in greater saphenous vein diameter. There were no changes in diastolic pressure or heart rate. These results suggest that pressor responses during tyramine injections are primarily due to an inotropic response that increases cardiac output and pressure and causes a reflex decrease in vascular resistance. Thus, tyramine pressor tests are a measure of cardiac, but not vascular, sympathetic function.

Functional effects of cardiac sympathetic denervation in neurogenic orthostatic hypotension

“…Dopamine contamination of infused tyramine probably confounded the previously published results [19,21]; however, even infusion of uncontaminated tyramine seems to increase blood pressure via an increase in cardiac output. [20] The findings of the present study lead us to propose that failure to augment delivery of norepinephrine to its receptors may explain complaints such as fatigue and exercise intolerance in patients with cardiac sympathetic denervation in the setting of neurogenic orthostatic hypotension. [22,23] The second finding of the study was that to attain the target increment in heart rate (about 25 bpm), patients with cardiac sympathetic denervation required lower doses of infused isoproterenol and had lower plasma isoproterenol concentrations than did patients with intact cardiac innervation.…”

“…[16][17][18][19][20] Sympathetic nerves take up tyramine via the cell membrane norepinephrine transporter. Tyramine in the axoplasm is then taken up into vesicles via the vesicular monoamine transporter, and in the vesicles tyramine displaces norepinephrine.…”

“…Although one might presume that tyramine increases blood pressure via generalized vasoconstriction and increased total peripheral resistance, it appears that most of the pressor response to tyramine depends on increased cardiac output, from increased stroke volume, in turn from increased myocardial contractility or increased venous return to the heart. [18,20] Others have reported forearm vasodilation in response to systemic tyramine administration, which would tend to decrease total peripheral resistance. Dopamine contamination of infused tyramine probably confounded the previously published results [19,21]; however, even infusion of uncontaminated tyramine seems to increase blood pressure via an increase in cardiac output.…”

Modulation of Resistance Artery Tone by the Trace Amine β-Phenylethylamine: Dual Indirect Sympathomimetic and α1-Adrenoceptor Blocking Actions

“…Furthermore, block of a 1 -adrenoceptors by prazosin abolished nerve-evoked vasoconstriction in the presence of PEA, confirming that enhancement of responses was due to the release of noradrenaline and not to some other contractile factor. Although an indirect sympathomimetic action has been implicated in the pressor effect of trace amines on blood pressure in vivo (Meck et al, 2003) and in conduit arteries such as rabbit pulmonary and ear artery (Knoll et al, 1996), these data provide the first direct demonstration that PEA can significantly enhance nerve-mediated vasoconstriction and increase noradrenaline release in resistance arteries.…”

Antianxiety effects of riparin I fromAniba riparia (Nees) Mez (Lauraceae) in mice

“…As far as is known, there are no studies in the literature on the central actions of riparin I. However, riparin I is a methyl ether of N-benzoyl tyramine, and previous data showed that the action of tyramine increased the release of norepinephrine (Meck et al, 2003). Some reports cited that individuals in treatment with antidepressive drugs, such as monoaminoxidase inhibitors, presented a prolonged increase in blood pressure when ingesting tyramine-rich foods (Potter and Hollister, 1998).…”