Functional Tolerance to α-Adrenergic Receptor Blockade in the Spontaneously Hypertensive Rat Highlights the Multifunctional Role of Vascular Angiotensin II in the Development of Hypertension

1995 ◽  
Vol 32 (4) ◽  
pp. 247-253 ◽  
Author(s):  
Scott D. Smid ◽  
Derek B. Frewin ◽  
Catherine L. Wyartt ◽  
Richard J. Head
Keyword(s):  
Angiotensin Ii ◽  
Adrenergic Receptor ◽  
Spontaneously Hypertensive Rat ◽  
Receptor Blockade ◽  
Spontaneously Hypertensive ◽  
Alpha Adrenergic Receptor ◽  
Hypertensive Rat ◽  
Functional Tolerance ◽  
Adrenergic Receptor Blockade

scholarly journals Distribution and role of angiotensin II receptor in the brain of spontaneously hypertensive rat.

1980 ◽  
Vol 44 (5) ◽  
pp. 403-408 ◽  
Author(s):  
KENJI MIZUNO ◽  
SHUICHI SHIGETOMI ◽  
JUN-ICHIROH MATSUI ◽  
SOITSU FUKUSHI
Keyword(s):  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rat ◽  
Angiotensin Ii Receptor ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
The Brain

scholarly journals Renal alpha-adrenergic receptor abnormality in the spontaneously hypertensive rat.

Hypertension ◽  
1982 ◽  
Vol 4 (6) ◽  
pp. 881-887 ◽  
Author(s):  
R M Graham ◽  
W A Pettinger ◽  
A Sagalowsky ◽  
J Brabson ◽  
T Gandler
Keyword(s):  
Adrenergic Receptor ◽  
Spontaneously Hypertensive Rat ◽  
Spontaneously Hypertensive ◽  
Alpha Adrenergic Receptor ◽  
Hypertensive Rat

Role of beta 2-adrenergic receptors on coronary resistance during exercise

1988 ◽  
Vol 64 (6) ◽  
pp. 2287-2293 ◽  
Author(s):  
S. E. DiCarlo ◽  
R. W. Blair ◽  
V. S. Bishop ◽  
H. L. Stone
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Blockade ◽  
Coronary Resistance ◽  
Alpha Adrenergic Receptor ◽  
Daily Exercise ◽  
Significant Difference ◽  
Beta 2 ◽  
Adrenergic Receptor Blockade

The effects of regional alpha- and specific beta 2-adrenergic receptor blockade on measurements of late diastolic coronary resistance (LDCR) and mean coronary blood flow velocity (CBFV) during exercise were examined in 14 conscious adult mongrel dogs. Specific beta 2-adrenergic receptor blockade (ICI 118.551) significantly decreased CBFV and increased LDCR by blockade of beta 2-vasodilator tone independent of alpha-adrenergic receptor-mediated tone and independent of altering myocardial metabolism. alpha-Adrenergic receptor blockade (phentolamine, 1 mg) significantly increased CBFV and decreased LDCR by blocking sympathetically mediated vasoconstrictor tone. There was no significant difference in the magnitude of response between alpha- and beta 2-adrenergic receptor blockade. These results demonstrate that alpha- and beta 2-adrenergic receptors have a significant and evidently equal influence on CBFV and LDCR during exercise. Four weeks of daily exercise and left stellate ganglionectomy (LSGx) prevented phentolamine-induced vasodilation but not ICI 118.551-induced vasoconstriction. This suggests that daily exercise and LSGx significantly decreased the alpha-adrenergic receptor-mediated vasoconstrictor tone on the coronary circulation, resulting in an apparently greater role for the coronary vascular beta 2-adrenergic receptor on the control of CBFV and LDCR during exercise.

Modulation of neurotransmitter release by NO is altered in mesenteric arterial bed of spontaneously hypertensive rats

2004 ◽  
Vol 287 (4) ◽  
pp. H1842-H1847 ◽  
Author(s):  
Lacy L. Kolo ◽  
Thomas C. Westfall ◽  
Heather Macarthur
Keyword(s):  
Nerve Stimulation ◽  
Neurotransmitter Release ◽  
Adrenergic Receptor ◽  
Spontaneously Hypertensive Rat ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Subsequent Decrease ◽  
Mesenteric Arterial Bed ◽  
Nos Inhibitor ◽  
Neuroeffector Junction

Nitric oxide (NO) reacts with catecholamines resulting in their deactivation. In the present study with the use of the perfused mesenteric arterial bed as a model of the sympathetic neuroeffector junction, the NO synthase (NOS) inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) resulted in the enhancement of the periarterial nerve stimulation-induced increase in perfusion pressure and norepinephrine overflow while decreasing neuropeptide Y (NPY) overflow. These changes were prevented by l-arginine, demonstrating that the effects of l-NAME were specific to the inhibition of NOS. From the fact that norepinephrine acts on prejunctional α2-adrenoceptors to inhibit the evoked release of sympathetic cotransmitters, we carried out experiments in the presence of the α2-adrenergic receptor antagonist yohimbine to investigate the possibility that the decrease in NPY observed in the presence of l-NAME was due to the increase in bioactive norepinephrine acting on its autoreceptor. Periarterial nerve stimulation in the presence of both l-NAME and yohimbine prevented the previously observed decrease in NPY, indicating that the cause of this decrease was, as predicted, due to α2-adrenoceptor activation. The periarterial nerve stimulation-induced increase of norepinephrine overflow was greater in the spontaneously hypertensive rat compared with normotensive rats. In contrast to what was observed in the isolated perfused mesenteric arterial bed obtained from normotensive animals, inhibition of NOS did not result in a further increase in the overflow of norepinephine or in a subsequent decrease in NPY. These results demonstrate that, in addition to being a direct vasodilator, NO, by deactivating norepinephrine, can modulate sympathetic neurotransmission and that this modulation is altered in the spontaneously hypertensive rat.

scholarly journals Alpha-adrenergic receptor blockade and hyperaemic response in patients with intermediate coronary stenoses

2004 ◽  
Vol 25 (22) ◽  
pp. 2034-2039 ◽  
Author(s):  
E BARBATO ◽  
J BARTUNEK ◽  
W AARNOUDSE ◽  
M VANDERHEYDEN ◽  
F STAELENS ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Blockade ◽  
Alpha Adrenergic Receptor ◽  
Hyperaemic Response ◽  
Coronary Stenoses ◽  
Adrenergic Receptor Blockade
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