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The Journal of Clinical Endocrinology & Metabolism 92(1):250 254

Copyright 2007 by The Endocrine Society
doi: 10.1210/jc.2006-1552

Acute Effects of Triiodothyronine on Endothelial

Function in Human Subjects
Raffaele Napoli, Vincenzo Guardasole, Valentina Angelini, Emanuela Zarra, Daniela Terracciano,
Carolina DAnna, Margherita Matarazzo, Ugo Oliviero, Vincenzo Macchia, and Luigi Sacca`
Departments of Internal Medicine and Cardiovascular Sciences (R.N., V.G., V.A., E.Z., C.D., M.M., U.O., L.S.) and Clinical
Pathology (D.T., V.M.), University Federico II, 80131 Naples, Italy
Results: FBF response to the endothelium-dependent vasodilator
acetylcholine was enhanced by T3 (P 0.002 for the interaction
between T3 and acetylcholine). The slopes of the dose-response curves
were 0.41 0.06 and 0.23 0.04 ml/dlmin/g in the T3 and placebo
study, respectively (P 0.03). T3 infusion had no effect on the FBF
response to sodium nitroprusside. T3 potentiated the vasoconstrictor
response to norepinephrine (P 0.006 for the interaction). Also, the
slopes of the dose-response curves were affected by T3 (1.95 0.77 and
3.83 0.35 ml/dlmin/mg in the placebo and T3 study, respectively;
P 0.05). The increase in basal FBF induced by T3 was inhibited by
NG-monomethyl-L-arginine.

Context: Thyroid hormone regulates several cardiovascular functions, and low T3 levels are frequently associated with cardiovascular
diseases. Whether T3 exerts any acute and direct effect on endothelial
function in humans is unknown.
Objective: Our objective was to clarify whether acute changes in
serum T3 concentration affect endothelial function.
Design, Setting, and Subjects: Ten healthy subjects (age, 24 1
yr) participated in a double-blind, placebo-controlled trial at a university hospital.
Interventions: T3 (or placebo) was infused for 7 h into the brachial
artery to raise local T3 to levels observed in moderate hyperthyroidism. Vascular reactivity was tested by intraarterial infusion of vasoactive agents.

Conclusions: T3 exerts direct and acute effects on the resistance

vessels by enhancing endothelial function and norepinephrine-induced vasoconstriction. The data may help clarify the vascular impact
of the low T3 syndrome and point to potential therapeutic strategies.
(J Clin Endocrinol Metab 92: 250 254, 2007)

Main Outcome Measures: We assessed changes in forearm blood

flow (FBF) measured by plethysmography.

HE CARDIOVASCULAR SYSTEM is a specific target of

thyroid hormone (TH), and when TH secretion is
chronically altered, this is accompanied by profound changes
in cardiovascular hemodynamics (1, 2). In particular, hyperthyroidism induces a high-output state, with a marked fall in
systemic vascular resistance (SVR), whereas hypothyroidism
causes opposite changes. More recent studies demonstrate
that vascular reactivity is exaggerated in patients with hyperthyroidism because of enhanced sensitivity of the endothelial component (3). Conversely, impaired endothelial
function is associated with hypothyroidism, even if the disease is present only at a subclinical level (4 6). Overall, the
data available support a physiological role for TH in the
long-term control of endothelial function and vascular
homeostasis.
A low-T3 syndrome may occur in acute diseases and is
characterized by depressed cardiac function and elevated
SVR (711). It was hypothesized that acute correction of the
low T3 levels might be beneficial to the cardiovascular hemodynamics (1218). However, the precise link between T3

and the altered hemodynamics remains elusive because the

effects of acute elevations in serum T3 concentration on human vascular physiology have never been explored in depth.
In particular, there is no information as to whether acute
changes in circulating T3 are able to exert any effect on
endothelial function and the vascular sensitivity to vasoactive agents. The present study was thus designed to address
this specific question.
Subjects and Methods
Subjects
The study was performed on 10 healthy volunteers, recruited from
the medical population of the medical school (six male, four female,
23.9 0.6 yr of age; body mass index, 23.6 1.6 kg/m2; arterial blood
pressure, 119 6/74 5 mm Hg). Informed consent was obtained from
all subjects, and the study protocol was approved by the Ethics Committee of the Federico II University School of Medicine.

Experimental procedures
The study design was double blinded and placebo controlled, with
each subject serving as his/her own control. The test (T3) and control
study were performed in random order and separated by a 3- to 4-wk
interval. In the test study, T3 was infused into the brachial artery and
forearm hemodynamics were monitored for 240 min. Then the responses
of forearm blood flow (FBF) to vasoactive test substances were measured
while keeping the infusion of T3 going. In the control study, the protocol
was the same except that placebo was infused instead of T3. The dose
of T3 was 40 ng/min. This dose was chosen in pilot experiments as the
one able to raise free T3 (fT3) concentration in the forearm circulation to

First Published Online October 17, 2006

Abbreviations: Ach, Acetylcholine; FBF, forearm blood flow; fT3, free
T3; FVR, forearm vascular resistance; l-NMMA, NG-monomethyl-larginine; NP, nitroprusside; SVR, systemic vascular resistance; TH, thyroid hormone; VSMC, vascular smooth muscle cell.
JCEM is published monthly by The Endocrine Society (http://www.
endo-society.org), the foremost professional society serving the endocrine community.

250
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Napoli et al. Acute T3 Effects on Endothelial Function

J Clin Endocrinol Metab, January 2007, 92(1):250 254 251

moderate hyperthyroidism values. T3 vials for human use (Thyrotardin)

were provided by Henning GMBH, Sanofi-Synthelabo, Berlin, Germany.
All the experiments were performed in the morning in a quiet room
kept at 2224 C. A plastic cannula (20 gauge) was inserted into the
brachial artery of the nondominant arm under local anesthesia and used
for the infusion of the test substances and the monitoring of arterial
blood pressure. Systolic and diastolic blood pressure and heart rate were
recorded by a transducer connected to the arterial cannula. FBF was
measured by a strain-gauge plethysmograph (Hokanson 045 EC4; PMS
Instruments, Maidenhead, UK). The data were monitored continuously
with McLab software. Additional details of the procedure have been
previously published (3, 19). Each subject underwent the following
stepwise infusions into the brachial artery in this order: 1) acetylcholine
(Ach) infused at a rate of 15, 30, and 45 g per liter of forearm per min
(g/litermin) to assess endothelium-mediated vasodilation; 2) sodium
nitroprusside (NP), a direct nitric oxide donor, infused at the rate of 1,
3, and 9 g/litermin to assess non-endothelium-mediated vasodilation;
3) norepinephrine infused at a rate of 140, 280, and 560 g/litermin to
assess the vascular sensitivity to sympathetic stimulation; and 4) NGmonomethyl-l-arginine (L-NMMA), a competitive inactive analog of
l-arginine, infused at the rate of 1 mg/litermin to assess the role of
endothelial NO release in the maintenance of the basal vascular tone.
Test substances were infused in the same order in all the subjects and
the infusion of each substance started only when the effect on FBF of the
previous infusion was dissolved and baseline FBF restored. Each dose
of the test substances was infused for 5.5 min, and FBF was measured
during the last 1.5 min of infusion. At least 30 min of washout time was
allowed between each substance. The infusion rates were adjusted according to the forearm volume of each subject, measured by water
displacement. FBF was measured simultaneously in both arms to ensure
that no systemic effects occurred during the experiment. Each FBF value
represents the mean of six consecutive measurements performed at
10-sec intervals.

Assays and calculations

T3 plasma level was measured by RIA. Forearm vascular resistance
(FVR) was measured as the ratio of mean arterial blood pressure to FBF.
Comparison between placebo and T3 was performed by a two-way
ANOVA for repeated measures (version 12.0; SPSS Inc., Chicago, IL).
Comparison between the slopes of the dose-response curves was performed by paired t test. Results are expressed as the mean sem.

Results

The study was well tolerated by all subjects without any

systemic reaction. In particular, arterial systolic and diastolic
blood pressure and heart rate did not change from their basal
values (Table 1).
Local, intrabrachial T3 infusion raised the plasma venous
concentration of fT3 in the ipsilateral forearm from 3.23

0.19 to 10.42 0.88 pg/ml. The systemic fT3 concentration,

as measured in the control arm, was not affected by local T3
infusion (3.24 0.2 and 3.92 0.23 pg/ml at baseline and
at the end of the infusion period, respectively). In the placebo
study, the fT3 concentration in the venous plasma of the
infused forearm was 3.24 0.2 pg/ml basally and remained
unchanged throughout the study. Similarly, TSH plasma
levels remained unchanged during T3 infusion (1.17 0.12
and 1.41 0.22 U/ml, at 240 min in controls and during T3
infusion, respectively, P value was nonsignificant).
FBF was very similar in the T3 and placebo studies in the
basal state (Table 1). During intraarterial T3 infusion, FBF
increased progressively and reached values that were significantly higher than those in the placebo study at 120 min
and thereafter. This was due to a significant fall in SVR,
because arterial blood pressure remained totally unchanged.
Figure 1 depicts the dose-response curve to the endothelium-dependent vasodilator Ach. The increment of FBF observed in the T3 study was much more pronounced as compared with placebo (P 0.014 for the treatment effect by
ANOVA for repeated measures). The values reached at the
highest Ach level were 17.5 2.7 and 10.2 1.7 ml/100
mmin in the test and placebo study, respectively (P 0.04).
The dynamics of the response was also profoundly affected
by T3, as evidenced by the significant interaction between T3
and Ach (P 0.002) and the markedly steeper slope of the
T3 dose response compared with that in the placebo study
(0.41 0.06 and 0.23 0.04 ml/dlmin/g, respectively, P
0.03).
Figure 2 depicts the response of FBF to NP, an endothelium-independent vasodilator. The dose-response curves
were virtually identical in the T3 and placebo studies (P value
nonsignificant for both the treatment effect and the interaction). Consistently, the calculated slopes of the two curves
were almost identical (1.59 0.19 and 1.66 0.15 ml/
dlmin/g in the placebo and T3 study, respectively).
As shown in Fig. 3, T3 also affected the response of FBF to
norepinephrine. In the control study, norepinephrine induced a progressive but moderate decrease in FBF. In contrast, the fall in FBF was 2-fold greater in the subjects receiving T3 than in the placebo study (P 0.019 for the
treatment effect, and P 0.006 for the interaction). Accord-

TABLE 1. Effects of intrabrachial T3 infusion on FBF, mean blood pressure, heart rate, and vascular resistance

FBF (ml/100 mlmin)

Placebo
T3
Mean blood pressure (mm Hg)
Placebo
T3
Heart rate (bpm)
Placebo
T3
FVR (resistance units)
Placebo
T3
Results are shown as mean
a
P 0.05 vs. 0 min.
b
P 0.01 vs. 0 min.
c
P 0.05 vs. placebo.

0 min

60 min

120 min

180 min

240 min

1.71 0.17
1.93 0.17

1.74 0.17
2.14 0.22

2.16 0.33
2.56 0.33a

2.11 0.34
3.06 0.47b,c

2.02 0.30
2,82 0.25b,c

92 4
86 3

92 4
88 2

92 4
87 2

93 5
88 2

93 5
90 3

71 8
65 2

68 7
65 2

72 7
65 2

69 7
65 3

72 6
66 4

61.6 10
49.2 5.6

56.4 5.0
45.7 4.4

52.5 5.9
44.0 9.6

54.1 8.7
34.3 4.2b,c

SE.

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55.3 7.4
35.1 3.8b,c

252

J Clin Endocrinol Metab, January 2007, 92(1):250 254

FIG. 1. FBF response to infusion of Ach into brachial artery in placebo- and T3-treated subjects (n 10). T3 or placebo was infused for
4 h, and then vascular reactivity was tested while keeping the infusion
going. Data (mean SE) were analyzed by ANOVA for repeated
measures. P 0.014 for the effect of T3, and P 0.002 for the
interaction between T3 and Ach. Comparison between slopes was
performed by the paired t test. The units of the slopes are ml/dlmin/
g.

ingly, the slopes of the dose-response curves were 1.95 0.77

and 3.83 0.35 ml/dlmin/mg in the placebo and T3 groups,
respectively (P 0.05).
Inhibition of basal NO bioavailability by intraarterial administration of l-NMMA caused FBF to rapidly fall. However, the decrease of FBF was more marked during T3 infusion than in the placebo study (1.47 0.2 and 2.43 0.5
ml/dlmin in the placebo and T3 study, respectively; P
0.05).
The intrabrachial T3 infusion did not affect systemic he-

FIG. 2. Response of FBF to infusion of NP in placebo- and T3-treated

subjects (n 10). The response to NP was assessed 30 min after the
end of the Ach test. Data (mean SE) were analyzed by ANOVA for
repeated measures. P 0.21 for the effect of T3, and P 0.81 for the
interaction between T3 and NP. Comparison between slopes was performed by the paired t test. The units of the slopes are ml/dlmin/g.

Napoli et al. Acute T3 Effects on Endothelial Function

FIG. 3. Response of FBF to infusion of norepinephrine in placebo- and

T3-treated subjects (n 10). The response to norepinephrine was
assessed 30 min after the end of the NP test. Data were analyzed by
ANOVA for repeated measures. P 0.019 for the effect of norepinephrine, and P 0.006 for the interaction between norepinephrine
and T3. Comparison between slopes was performed by the paired t
test. The units of the slopes are ml/dlmin/mg.

modynamics, as demonstrated by the unchanged heart rate

and arterial blood pressure. In addition, FBF and FVR in the
contralateral arm did not change from their basal values
throughout the study period.
Discussion

Current knowledge about the cardiovascular actions of T3

is mainly deduced from studies of disease states of altered
TH secretion or from animal models of chronic TH excess or
deficiency. No attempt was made before the present study to
explore the impact on vascular physiology of an acute elevation of T3 concentration in human subjects. We tried to
answer the question by using the forearm perfusion technique. T3 concentration was acutely raised to levels comparable to those seen in patients with hyperthyroidism of intermediate severity. In addition, T3 concentration was raised
only locally, in the forearm circulation, and this allows assessment of the direct effect of T3 on vascular function, without the intervention of systemic factors, either chemical or
hemodynamic in nature, potentially able to affect vascular
reactivity. The main findings of our study are 1) T3 increments to hyperthyroid values cause a significant fall in FVR
by an endothelium-dependent mechanism; 2) T3 markedly
potentiates Ach-induced vasodilation but is without effect on
the vasodilatory response to NP, which indicates that T3
effects are entirely mediated by the endothelium and do
not involve the vascular smooth muscle cell (VSMC) component; and 3) the sensitivity of the resistance vessels to
the vasoconstrictory effect of norepinephrine is enhanced
by T3.
Previous experiments using mesenteric resistance vessels
showed that the vasorelaxing effect of TH was impaired by
pretreatment with an arginine analog that prevented endo-

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Napoli et al. Acute T3 Effects on Endothelial Function

thelial nitric oxide production (20). Similarly, in another

study on renal artery rings, endothelium-dependent relaxation to Ach was enhanced 36 h after T3 treatment (21). The
present data are consistent with those in vitro observations
regarding the role played by the endothelium in mediating
the vascular effects of TH. At variance with these data, other
studies have supported a role for VSMCs in mediating the
vasodilating effect of T3. For instance, the vasorelaxing effect
of T3 in isolated resistance vessels was attenuated but not
abolished by endothelial denudation of the arteries (22), suggesting activation by T3 of both the endothelial and the nonendothelial component of vasodilation. In another study performed in isolated VSMCs, it was reported that TH was able
to cause vasorelaxation (23). The reasons for the difference
between our findings and some of the previous studies indicating also a role of VSMC is not clearly apparent and may
entail differences among species and in vitro vs. in vivo data.
However, taking the data altogether, one thing that emerges
clearly is that whenever the vascular effects of TH were
tested in human models (normal subjects, hyperthyroidism,
overt hypothyroidism, or subclinical hypothyroidism), the
changes in vascular reactivity always involved exclusively
the endothelial component (3, 4, 6, 24). The current study
documents the ability of acute T3 increments to enhance
the activity of endothelial NO synthase, as evidenced by
the attenuation of FBF after exposure to the arginine antagonistic agent l-NMMA. This finding is consistent with
previous studies in chronically hyperthyroid patients as
well as experimental studies in various animal models
(3, 25).
T3 mainly acts by binding to specific nuclear receptors, so
regulating transcription of target genes. In addition, T3 may
also activate extranuclear, nongenomic mechanisms, by
which it regulates the activity of plasma membrane ion channels. Examples are provided by the well-known T3 effects to
enhance myocardial contractility, to regulate the contractile
state of VSMCs, and to stimulate glucose uptake (26 28). The
current study was not intended to clarify whether T3 affects
vascular function through genomic or extranuclear mechanisms. However, the examination of the time course of FBF
response to T3 infusion suggests that T3 acted through the
activation of genomic mechanisms. This interpretation is also
supported by the fact that by using the local infusion approach, the desired T3 concentration in the forearm is reached
almost immediately, whereas the first demonstrable increment in FBF occurred after 2 h.
In a previous study in normal volunteers, T3 was able to
reduce SVR as early as 3 min after the start of the infusion
(29). This clearly speaks in favor of T3 ability to activate very
rapidly nongenomic mechanisms. The data, however, are not
in contrast with the present study, because we infused relatively low doses of T3, whereas in previous studies, T3 was
used in big doses that raised the hormone concentration to
more than 40 pg/ml (four times the values achieved in our
study).
In conclusion, the present data demonstrate that T3 is a
strong modulator of the resistance vessel response to vasoactive agents, as a consequence of an acute and direct
interaction.

J Clin Endocrinol Metab, January 2007, 92(1):250 254 253

Acknowledgments
We thank Dr. Emidio Botta, Dr. Michael Haring, and Henning GMBH,
Sanofi-Synthelabo, Berlin, Germany, for the generous supply of Thyrotardin vials.
Received July 17, 2006. Accepted October 10, 2006.
Address all correspondence and requests for reprints to: Dr. R.
Napoli, Department of Internal Medicine, Via Pansini, 80131 Napoli,
Italy. E-mail: napoli@unina.it.
This study was supported by a grant provided by the Centro di
Competenza GEAR of Regione Campania.
Disclosure Summary: All the authors have nothing to declare.

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JCEM is published monthly by The Endocrine Society (http://www.endo-society.org), the foremost professional society serving the
endocrine community.

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