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1-
and 2-adrenoceptor activation
Division of Pulmonary and Critical Care Medicine, Mount Sinai Medical Center, University of Miami School of Medicine, Miami Beach, Florida 33140
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Zschauer, A. O. A., M. W. Sielczak, D. A. S. Smith, and A. Wanner. Norepinephrine-induced contraction of isolated rabbit bronchial artery: role of 
1-
and 2-adrenoceptor activation. J. Appl. Physiol. 82(6):
1918-1925, 1997.
The contractile effect of norepinephrine (NE) on
isolated rabbit bronchial artery rings (150-300 µm in diameter)
and the role of 1- and
2-adrenoceptors (AR) on smooth
muscle and endothelium were studied. In intact arteries, NE increased
tension in a dose-dependent manner, and the sensitivity for NE was
further increased in the absence of endothelium. In intact but not in
endothelium-denuded arteries, the response to NE was increased in the
presence of both indomethacin (Indo; cyclooxygenase inhibitor) and
NG-nitro-L-arginine
methyl ester [L-NAME;
nitric oxide (NO) synthase inhibitor], indicating that two
endothelium-derived factors, NO and a prostanoid, modulate the
NE-induced contraction. The
1-AR antagonist prazosin
shifted the NE dose-response curve to the right, and phenylephrine
(1-AR agonist) induced a
dose-dependent contraction that was potentiated by
L-NAME or removal of the
endothelium. The sensitivity to NE was increased slightly by the
2-AR antagonists yohimbine and
idazoxan, and this effect was abolished by Indo or removal of the
endothelium. Similarly, contractions induced by UK-14304
(2-AR agonist) were potentiated
by Indo or removal of the endothelium. These results suggest that
NE-induced contraction is mediated through activation of
1- and
2-ARs on both smooth muscle and
endothelium. Activation of the
1- and
2-ARs on the smooth muscle
causes contraction, whereas activation of the endothelial 1- and
2-ARs induces relaxation
through release of NO (1-ARs) and a prostanoid (2-ARs).
endothelium-derived relaxing factors; nitric oxide; prostanoid; vasoconstriction
INTRODUCTION ADRENERGIC NEURONS, the major source of physiologically
active norepinephrine (NE), have been shown to innervate the bronchial arteries in several species (5, 25). In most blood vessels innervated
by sympathetic neurons, NE activates postjunctional The decrease of bronchial arterial blood flow by In the present study we therefore isolated the main bronchial branches
of the bronchoesophageal artery in rabbits and characterized the role
of smooth muscle and endothelial MATERIALS AND METHODS
-adrenoceptors
(-ARs), thereby causing contraction of the vascular smooth muscle.
Vascular -ARs are divided into two major subtypes, 1- and
2. In contrast to larger
arteries, which generally have only
1-ARs mediating contraction,
both 1- and
2-ARs are involved in the
constrictor response of resistance arteries (i.e., arteries with
diameters <500 µM) to NE (18).
-adrenergic
agonists and increase in bronchovascular resistance have been demonstrated (1, 22), and recently the contractile effect of NE has
been described in isolated bronchial arteries of dogs, pigs, and cows
(23). However, information on the roles of
1- and
2-ARs and the endothelium in
bronchial arterial responsiveness to NE is lacking.
-ARs in NE-induced contractions of
these resistance vessels. Our study showed evidence for
1- and
2-adrenergic modulation of
NE-induced contraction and that both receptor subtypes are located on
smooth muscle and endothelium.
-2-ethanesulfonic acid solution. Under a dissecting microscope, the bronchoesophageal artery was identified at the tracheal carina. The right branch of this
artery arises from the highest right intercostal artery and the left
branch either from the aorta, left common carotid artery, or from the
highest right intercostal artery (4).
60%.
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-2-ethanesulfonic
acid.
When solutions with higher extracellular
K+ concentration
([K+]o)
are used, the addition of extra KCl was subtracted from the concentration of NaCl to maintain the osmolarity and
Cl
concentration.
Before collecting data for each new experimental condition, we verified
in separate tissue preparations that the response to -agonists was
reproducible. For experiments (e.g., Fig.
1B) in
which the effect of one antagonist or inhibitor on -agonist-induced contraction was studied, the reproducibility of tissue response was
confirmed by repeating two consecutive DRCs in the absence of any
inhibitors or antagonist. For experiments in which the effect of
2-antagonists on NE-induced
contraction under the influence of
NG-nitro-L-arginine
methyl ester (L-NAME) or
indomethacin (Indo; see Fig. 5, A-C)
was studied, separate preparations were used to confirm the
reproducibility of the DRCs for NE in the presence of
L-NAME or Indo. If the two DRCs
under control conditions were reproducible, then the actual experiments
were conducted in a different preparation. In this preparation, the
first DRC served as control for the second experimental DRC, which was
performed in the presence of different antagonists and inhibitors. If
the two DRCs under control conditions (like the DRCs induced by NE in
endothelium-denuded arteries) were not reproducible, the values of the
second DRC performed under control conditions
(preparation 1) were compared with
the values of the second DRC under the experimental conditions
(preparation 2). In each
preparation, the developed tension of each cumulative was expressed as
the percentage of the contraction achieved by 5 µM agonist in the
respective, first DRC of the same preparation.
) and endothelium-denuded (
) rabbit
bronchial arteries. Contractions are expressed as %contraction induced
by 72.5 mM KCl. Values are means ± SE of experiments in 3 different
arterial segments in intact and endothelium-denuded arteries.
B and
C: NE-induced contraction of intact
rabbit bronchial arteries in absence (control; ) and presence of 10 µM
NG-nitro-L-arginine
methyl ester (L-NAME; 
;
B) and 1 µM indomethacin (Indo;
; C). Contractions are expressed
as %contraction induced by 5 µM NE under control conditions. Values
are means ± SE of experiments in 5 (B) and 4 (C) different arterial segments.
D: NE-induced contraction of
endothelium-denuded arteries in the absence (control; ) and presence
of 10 µM L-NAME () and 1 µM Indo (). Values are means ± SE of experiments in 4 (), 3 (), and 4 () different arterial segments. Contraction is
expressed as %contraction induced by 5 µM NE under control
conditions. Significantly different vs. intact artery
(A and
D) or control
(B and
C):
* P < 0.05;
** P < 0.01; ***
P < 0.001.
) and presence () of 1 µM yohimbine
(B) and 1 µM idazoxan (A and
C). Values are means ± SE of
experiments in 4 (A), 3 (B), and 4 (C) different arterial segments.
D and
E: NE- and PE-induced contraction in
endothelium-denuded arteries in absence (control; ) and presence
() of 1 µM idaxozan. Values are means ± SE of experiments in 4 different arterial segments. Contractions are expressed as
%contraction induced by 5 µM NE
(D) or 5 µM PE
(E) under control conditions.
Significantly different vs. intact artery (A) or control
(B):
* P < 0.05;
** P < 0.01;
*** P < 0.001.
To compare the corresponding effect in intact and endothelium-denuded arteries, the contractions were expressed as the percentage of the contraction induced by 72.5 mM KCl (maximal contraction). When the effect of inhibitors on a single dose of
2-agonist-induced contraction
was studied (see Fig. 6B), the
control contractions were repeated until three identical consecutive
contractions were seen.
) and endothelium-denuded () bronchial arteries.
Values are means ± SE of experiments in 12 () and 6 ()
different arterial segments. Contractions are expressed as
%contraction induced by 5 µM UK. B:
1 µM UK-induced contraction in absence (control) and presence of 10 µM L-NAME or 1 µM Indo.
Values are means ± SE of experiments in 4 different arterial
segments. Contractions are expressed as %control value. Significantly
different vs. control: * P < 0.05; ** P < 0.01;
*** P < 0.001.
Statistical analysis was performed by either independent or paired Student's t-tests. P < 0.05 was considered as significant. The data were expressed as means ± SE, if not otherwise indicated. Drugs. The following drugs were used: atrenolol (NE) was from Sigma Chemical (St. Louis, MO), and idazoxan, Indo, L-NAME, phenylephrine (PE), prazosin, propranolol, UK-14,304 (UK), and yohimbine were from Research Biochemicals International (Natick, MA).
RESULTS
-AR
antagonist propranolol (1 µM; data not shown).
In endothelium-denuded arteries, the 50% effective concentration
(EC50) value for NE
was shifted to the left compared with intact arteries, indicating the
presence of endothelium-derived relaxing factor(s) (Fig.
1A). The
EC50 values for NE in intact and
endothelium-denuded arteries (made by parallel experiments on different
bronchial arterial segments from same animal) were 1.81 ± 0.34 µM
(n = 3) and 0.65 ± 0.07 µM
(n = 3), respectively (P < 0.001), and the maximal
contraction induced by NE was increased in endothelium-denuded arteries
when contractions were expressed as the percentage of the contraction
induced by 72.5 mM KCl. To test the possibility that nitric oxide (NO)
and/or relaxing prostanoids modulate NE-induced contractions,
the DRCs in intact and endothelium-denuded arteries were obtained in
the absence and presence of 10 µM
L-NAME, a NO synthase inhibitor,
or 1 µM Indo, a cyclooxygenase inhibitor (30-min preincubation). In
intact arteries, the EC50 value
for NE was 1.98 ± 0.14 µM in the absence and 1.28 ± 0.15 µM
in the presence of 10 µM
L-NAME
(n = 5, P < 0.05; Fig.
1B). The corresponding values for 1 µM Indo were 1.70 ± 0.41 and 1.01 ± 0.32 µM, respectively (n = 4, P < 0.05; Fig.
1C). The maximal contraction induced
by NE was increased in the presence of both
L-NAME and Indo. In
endothelium-denuded arteries,
L-NAME and Indo had no
significant effect on NE-induced contractions, indicating that both
relaxing factors originate in the endothelium (Fig.
1D).
Role of 1-ARs in
NE-induced contraction.
In intact arteries, 0.1 µM prazosin, a specific
1-AR antagonist, shifted the
DRC for NE to the right, indicating that
1-AR might be involved in the
contractile effect of NE (Fig.
2A).
This finding was confirmed by the DRCs for the
1-agonist PE, which revealed
EC50 values of 1.49 ± 0.21 and
0.73 ± 19 µM (n = 7) in intact
and endothelium-denuded arteries, respectively (Fig.
2B). In endothelium-denuded
arteries, the EC50 value for PE
was significantly (P < 0.05) shifted
to the left, and the maximal contraction induced by 5 µM PE was
larger than the contraction induced by 5 µM PE in intact arteries
(Fig. 2B). The PE-induced
contractions were repeated in the presence of 1 µM yohimbine, a
specific 2-AR antagonist (Fig.
2C). At PE concentrations >3 µM,
the contractions were sensitive to yohimbine, indicating
2-AR activation.
) and presence () of
0.1 µM prazosin. Contraction is expressed as %contraction induced by
5 µM NE under control conditions. Values are means ± SE of
experiments in 4 different arterial segments.
B: phenylephrine (PE)-induced
contraction in intact () and endothelium-denuded () arteries
expressed as %contraction induced by 72.5 mM KCl. Values are means ± SE of experiments in 7 different arterial segments.
C: PE-induced contraction in absence (control; ) and presence () of 1 µM yohimbine. Values are means ± SE of experiments in 4 different arterial segments. Significantly different vs. control (A and
C) or intact artery
(B):
* P < 0.05; ** P < 0.01;
*** P < 0.001.
To specify which one of the two factors (NO and/or the prostanoid) found in connection with NE activation was involved in the
1-AR activation, DRCs for PE
were performed in the absence (control) and the presence of either 10 µM L-NAME or 1 µM Indo in
intact arteries. PE-induced contraction was sensitive to both but more
to L-NAME than Indo (Fig.
3, A and
B). The effects of L-NAME and Indo on PE- and
NE-induced contractions were compared at 1 µM concentrations to avoid
nonspecific 2-AR activation by PE (Fig. 3C). This comparison showed
that NE-induced contraction was affected by both
L-NAME and Indo, whereas
PE-induced contraction was primarily influenced by
L-NAME, indicating that NO
release is mediated especially by
1-AR.
) and
presence () of 10 µM L-NAME
(A) and 1 µM Indo
(B). Values are means ± SE of
experiments in 7 (A) and 5 (B) different arterial segments.
Contractions are expressed as %contraction induced by 5 µM PE under
control conditions. C: 1 µM NE- and
1 µM PE-induced contractions in absence and in presence of 10 µM
L-NAME and 1 µM Indo. Values
are means ± SE of experiments in different arterial segments. Nos.
above each bar, nos. of arterial segments. Values are expressed as
%contraction produced by 1 µM NE or 1 µM PE alone. In control
experiment, contractions were performed in duplicate, and 2nd value was
expressed as %1st value. Significantly different vs. control:
* P < 0.05;
** P < 0.01;
*** P < 0.001.
Role of
2-ARs in
NE-induced contraction.
In intact arteries, the 2-AR
antagonists idazoxan and yohimbine increased the NE-induced
contractions only at NE concentrations >1 µM (Fig.
4), indicating that NE-induced contraction
might be slightly attenuated through activation of
2-AR.
) and presence () of 0.1 µM idazoxan
(A; n = 8), 1.0 µM idazoxan (B;
n = 8), and 1.0 µM yohimbine
(C; n = 8). Values are means ± SE. Contractions are expressed as
%contraction induced by 5 µM NE under control conditions.
* P < 0.05 vs. control.
To determine whether NO or a prostanoid was involved in the
2-AR antagonist-mediated
attenuation of NE-induced contraction, the effect of idazoxan and
yohimbine in the presence of 10 µM L-NAME or 1 µM Indo was
studied in intact arteries.
L-NAME did not change the
sensitivity of the NE-induced contraction to the 2-adrenergic antagonist
idazoxan (Fig.
5A vs.
Fig. 4B). In contrast, Indo
prevented the yohimbine-induced potentiation of NE-induced contraction
(Fig. 5B vs. Fig.
4C) and converted the
idazoxan-induced potentiation to an attenuation of NE-induced
contraction (Fig. 5C vs. Fig.
4B). These results suggested that
activation of 2-AR might be
involved in NE-induced contraction by releasing a smooth muscle-relaxing prostanoid. These results recorded in intact arteries in the presence of Indo could be repeated in endothelium-denuded arteries in the absence of Indo (Fig.
5D), indicating that the prostanoid
originated from the endothelium. Idazoxan shifted the PE-induced
contraction to the right in endothelium-denuded arteries as well,
suggesting non-2-antagonist
actions (Fig. 5E).
Next, the effect of the
2-adrenergic agonist UK was
studied. In 10 mM KCl solutions, UK induced no or very weak
contractions, but the response to UK was enhanced by increasing the KCl
concentration further to 15 mM. Maximal contractions induced by adding
15 mM KCl solution alone were not >5% of the contraction induced by 72.5 mM KCl. In intact arteries, UK induced a dose-dependent
contraction at concentrations >0.5 µM, and no clear plateau for the
maximal contraction was reached (Fig.
6A).
Endothelium-denuded arteries were more sensitive to UK, suggesting the
presence of 2-ARs on both smooth muscle and
endothelium (Fig. 6A). The effect of 10 µM
L-NAME and 1 µM Indo on the contraction induced by a
single (1 µM) dose of UK was studied in intact arteries. The
UK-activated contraction was substantially increased by Indo, whereas
the effect of L-NAME was small (Fig. 6B),
indicating that the smooth muscle-relaxing prostanoid is released
specially by 2-ARs.
DISCUSSION
We conclude that 1) NE contracts
isolated small bronchial arteries from rabbit by activation of
1- and
2-ARs on smooth muscle, and, in
our experimental conditions,
1-AR-mediated contraction is
more potent than the
2-AR-mediated contraction;
2) activation of
1- and
2-ARs on endothelium modulates
NE-induced contraction; and 3) NO
and a relaxant prostanoid serve as endothelium-relaxing factors, the
former released mainly by 1-AR
activation and the latter mainly by
2-AR activation.
-blocker, to influence
the NE-induced contraction (data not shown), suggests that
-AR-mediated relaxant actions of NE were of minor importance in
rabbit bronchial artery and that NE is mainly acting through -ARs.
1- and
2-ARs on smooth muscle
cells.
In the present study, both 1-
and 2-AR subtypes were involved
in the NE-induced contraction. The NE-induced contraction occurred
largely through activation of
1-ARs, as indicated by the high
sensitivity of the NE-induced contraction to prazosin (1-antagonist). The high
contractile sensitivity of endothelium-denuded arteries to PE
(1-agonist) suggests that NE
caused the contraction through direct activation of smooth muscle
1-ARs. Our results are
consistent with the in vitro findings in bronchial arteries of dogs,
pigs, and cows (23), in which the major part of NE-induced contraction
is due to a direct activation of
1-ARs on smooth muscle cells.
In contrast to the relative ease of demonstrating
1-AR-mediated contractions, the
role of the 2-AR in the
contractile response to NE has been less clear. While postjunctional
2-AR-mediated pressor responses
have been reported in whole animals, it has been much more difficult to
show 1-agonist-resistant,
2-antagonist-sensitive responses in isolated vascular preparations (15, 23). The reason for
this discrepancy is not clear, but one explanation is that
postjunctional 2-ARs are
predominantly located on the resistance vessels (14, 28). Recently, the
presence of 2-ARs has been
shown on rat cremaster arterioles (7) and on human resistance arteries
(20); and with our study we have obtained evidence of functional
2-ARs on isolated rabbit
bronchial resistance arteries.
Because of the simultaneous activation of
2-ARs on endothelial cells, it
was difficult to prove that activation of
2-ARs on smooth muscle was part
of the NE-induced contraction in our study. However, the rather high
contractile response of endothelium-denuded arteries to UK
(2-agonist) activation speaks
for the existence of smooth muscle
2-receptors. We found a wide
variation in UK responsiveness, in both endothelium-denuded and intact
arteries. A possible explanation for this variability is the inconstant presence of 2-AR-sensitizing
factors in vitro (26). Dunn et al. (6) showed in isolated distal
saphenous artery from rabbit that responses mediated through
postjunctional 2-ARs were
influenced by angiotensin II. Recent studies have shown that mediators
such as endothelin-1 and angiotensin II cause sensitization to NE by increasing protein kinase C activity, which, in turn, increases the
sensitivity of contractile proteins to intracellular free Ca2+ (9, 10).
1- and
2-ARs on endothelium.
In our preparations, endothelium regulated the contractile effect of NE
by releasing two endothelial relaxing factors (NO and a prostanoid). In
endothelium-denuded arteries, the sensitivity to PE
(1-agonist) and UK
(2-agonist) was significantly
increased from that in intact arteries, indicating a possible
involvement of both 1- and
2-ARs in the release of
endothelial relaxing factors. In intact arteries,
L-NAME had a greater
potentiating effect than Indo on PE-induced,
1-AR mediated contractions
(Fig. 3), and Indo had a greater potentiating effect than
L-NAME on UK-induced,
2-mediated contractions (Fig.
6B). These findings suggest that, in
rabbit bronchial arteries, the endothelial cells possess both
functional 1- and
2-ARs and that the
1-ARs activate mainly the
release of NO and the 2-ARs the
release of the prostanoid.
The involvement of 2-AR-induced
prostanoid release on NE-induced contractions was demonstrated in
experiments in which the 2-AR-antagonists (yohimbine and
idazoxan) potentiated NE-induced contraction in intact arteries in the
absence and presence of L-NAME
but not in intact arteries when Indo was present or in the
endothelium-denuded arteries (Figs. 4 and 5). The observation that, in
Indo-treated intact arteries, idazoxan created a shift of the
NE-induced DRC to the right but yohimbine did not (Fig. 5,
B and
C) was a reason to suspect that
idazoxan might have actions other than
2-antagonist properties. This
was proven to be true with experiments in endothelium-denuded arteries,
in which idazoxan also shifted the PE-induced contraction to the right.
Many 2-AR agonists and
antagonists, including idazoxan, bind also with high affinity to
nonadrenergic (i.e., imidazole) binding sites (3), and thus the
idazoxan-produced inhibition of the NE- and PE-activated contractions
could be explained by idazoxan-induced activation of imidazole
receptors on the smooth muscle cells.
In other vascular vessels, endothelial cells are also known to release
endothelium-derived relaxing factors by activation of
2- or
1-ARs (11, 12, 29). However,
our study is the first to show that NE simultaneously releases two
different endothelium-derived relaxing factors (NO and a prostanoid)
and that these factors are released by activation of two separate
-AR subtypes (1 for NO and
2 for the prostanoid). For most
preparations studied to date, NO release has been associated with
2-adrenergic activation. In the
rabbit bronchial artery,
2-adrenergic activation appears to release a relaxing prostanoid rather than NO. This suggests that
different relaxant factors and -AR subtypes may be involved in
different vascular beds and animal species.
ACKNOWLEDGEMENTS
This study is supported by National Heart, Lung, and Blood Institute Grant HL-20989.
FOOTNOTES
Address for reprint requests: A. O. A. Zschauer, Dept. of Research, Mount Sinai Medical Center, 4300 Alton Rd., Miami Beach, FL 33140.
Received 4 October 1996; accepted in final form 12 February 1997.
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