Interaction of Angiotensin II with Catecholamines in the Circulation of the Dog and Cat

1976 ◽  
Vol 51 (s3) ◽  
pp. 451s-454s
Author(s):  
K. K. F. Ng ◽  
S. Duffy ◽  
W. J. Louis ◽  
A. E. Doyle
Keyword(s):  
Angiotensin Ii ◽  
Cardiovascular System ◽  
Rat Aorta ◽  
Pressor Effect ◽  
Intravenous Injections ◽  
Molar Basis ◽  
Vasoconstrictor Effect ◽  
Organ Technique

1. The blood-bathed organ technique was employed to study the effects of angiotensin II and catecholamines on an isolated everted rat aorta bathed in the extracorporeal circulating blood of adult dogs and cats. 2. When the injections were made into the bathing blood close to the everted rat aorta, angiotensin II was half as potent as adrenaline or noradrenaline on a molar basis. 3. After intravenous injections, the vasoconstrictor potency of angiotensin was twenty times that of adrenaline or noradrenaline on the everted rat aorta. The increase in potency was due to the interaction of angiotensin II with catecholamines on the preparation. 4. Intravenous phenoxybenzamine abolished the potentiated vasoconstrictor effect of angiotensin II on the blood-bathed everted rat aorta, but it did not abolish the pressor effect of angiotensin II on the cardiovascular system of the animals. The results suggest that catecholamines released into the circulating blood by intravenous angiotensin II do not play an important role in the pressor effect of angiotensin II.

Protease-activated receptor 1 and 2 contribute to angiotensin II-induced activation of adventitial fibroblasts from rat aorta

2016 ◽  
Vol 473 (2) ◽  
pp. 517-523 ◽  
Author(s):  
Rui-Qing He ◽  
Xiao-Feng Tang ◽  
Bao-Li Zhang ◽  
Xiao-Dong Li ◽  
Mo-Na Hong ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Rat Aorta ◽  
Adventitial Fibroblasts ◽  
Protease Activated Receptor 1

Comparison of fast and slow pressor effects of angiotensin II in the conscious rat

1981 ◽  
Vol 241 (3) ◽  
pp. H381-H388 ◽  
Author(s):  
A. J. Brown ◽  
J. Casals-Stenzel ◽  
S. Gofford ◽  
A. F. Lever ◽  
J. J. Morton
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Control Period ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Pressor Effect ◽  
Ang Ii ◽  
Conscious Rat ◽  
Female Wistar Rats

Female Wistar rats were infused intravenously with 5% dextrose for 3 days, then with angiotensin II (ANG II) in 5% dextrose at 20 ng . kg-1 . min-1 for 7 days, and finally with dextrose for 2.5 days. ANG II raised mean arterial pressure (MAP) gradually; by the 7th day it was 49.7 mmHg higher than during the dextrose control period in the same rats. Control rats were infused with dextrose for 12.5 days; MAP did not change. Plasma ANG II concentration was measured during infusion. In hypertensive rats on the 7th day of ANG II infusion, it was six times higher than in control rats infused with dextrose. Changes of blood pressure and plasma ANG II concentration were compared in further rats infused with much larger doses of ANG II. Rats receiving 270 ng . kg-1 . min-1 for 1 h had an almost maximal direct pressor response, MAP rising 45.3 mmHg and plasma ANG II rising 32-fold compared with controls. Thus, infusion of ANG II at low dose without direct pressor effect gradually raises blood pressure to a level similar to the maximum direct pressor effect produced by larger doses of ANG II. Sodium balance and food and water intakes were also measured and did not change during prolonged infusion of ANG II at 20 ng . kg-1 . min-1. Thus, the slow pressure effect of ANG II develops at a lower and more nearly physiological plasma concentration of the peptide than do the direct pressor effect and the effects on drinking, eating, and urinary sodium excretion.

scholarly journals PP092—Changes in vascular reactivity caused by angiotensin II in isolated vessels of rat aorta in a model of hypertension

2013 ◽  
Vol 35 (8) ◽  
pp. e46
Author(s):  
E.M. Lopez-Calderon ◽  
L.N. Acevedo-Villavicencio ◽  
G.C. Villanueva-Lopez ◽  
E. Lara-Padilla ◽  
G. Guevara-Balcazar ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Vascular Reactivity ◽  
Rat Aorta

Hypertension in insulin-resistant Zucker obese rats is independent of sympathetic neural support

1992 ◽  
Vol 262 (3) ◽  
pp. E368-E371 ◽  
Author(s):  
M. B. Zemel ◽  
J. D. Peuler ◽  
J. R. Sowers ◽  
L. Simpson
Keyword(s):  
Angiotensin Ii ◽  
Neural Activity ◽  
Vascular Reactivity ◽  
Zucker Rats ◽  
Ganglionic Blockade ◽  
Intravenous Injections ◽  
Insulin Resistant ◽  
Arterial Blood ◽  
Obese Rats ◽  
Blood Pressure Responses

We have previously reported that insulin-resistant Zucker obese rats exhibit hypertension associated with impaired vascular smooth muscle (VSM) Ca2+ transport and proposed that this results from failure of insulin to regulate VSM Ca2+ transport in insulin resistance. However, hypertension in insulin-resistant states is generally attributed to hyperinsulinemia, with a consequent stimulation of sympathetic neural activity. Accordingly, the present study was conducted to determine whether the hypertension observed in Zucker obese rats compared with their lean controls was dependent on either increased sympathetic neural activity or exaggerated vascular reactivity. Intra-arterial blood pressure responses to ganglionic blockade with Ecolid (chlorisondamine chloride) and to graded intravenous injections of angiotensin II and norepinephrine were compared in 6- to 8-wk-old male Zucker rats and their lean controls (n = 10/group). The obese rats exhibited significant hypertension before ganglionic blockade (P less than 0.001), and this difference was largely sustained during ganglionic blockade (P less than 0.005). Furthermore, the obese rats exhibited greater pressor sensitivity to both angiotensin II and to norepinephrine during ganglionic blockade (P less than 0.01). Thus enhanced pressor sensitivity, independent of sympathetic neural activity, appears to support hypertension in Zucker obese rats.

Effects of intracellular alkalinization on resting and agonist-induced vascular tone

1989 ◽  
Vol 256 (3) ◽  
pp. H867-H875 ◽  
Author(s):  
N. R. Danthuluri ◽  
R. C. Deth
Keyword(s):  
Angiotensin Ii ◽  
Vascular Tone ◽  
Rat Aorta ◽  
Slow Phase ◽  
Dependent Manner ◽  
Rapid Phase ◽  
Aortic Smooth Muscle ◽  
Uptake Studies ◽  
Transient Relaxation ◽  
Intracellular Alkalinization

To evaluate the influence of intracellular alkalinization on basal and agonist-induced vascular tone, we studied the effect of NH4Cl on rat aorta. NH4Cl induced a gradually developing contraction in a dose-dependent manner. Although the contractile response to 20 mM NH4Cl was associated with a latent period (LP) of 23.4 +/- 2.8 min, intracellular pH (pHi) measurements in cultured rat aortic smooth muscle cells showed that NH4Cl-induced intracellular alkalinization was immediate and transient, returning to basal pHi levels in about 30-35 min. Agents that elevate Ca2+, such as A23187 and high KCl, significantly reduced the LP associated with 20 mM NH4Cl-induced contraction. NH4Cl-induced contractions were sensitive to extracellular Ca2+ removal and to the addition of forskolin (1 microM); however, NH4Cl by itself did not cause Ca2+-influx as shown by 45Ca-uptake studies. Addition of 20 mM NH4Cl to precontracted tissues resulted in a transient relaxation, which was complete in approximately 10 min, followed by a contraction above the original level of tone. NH4Cl pretreatment caused time-dependent alterations in both the rapid and slow phases of phenylephrine and angiotensin II contractions. Rapid-phase of phenylephrine and angiotensin II contractions. Rapid-phase responses were diminished at shorter NH4Cl incubation times (10 min), whereas slow-phase response was augmented after a longer incubation (20 min). Overall, the vasorelaxant and vasoconstrictor effects induced by NH4Cl suggest a complex relationship between intracellular alkalinization and arterial contractility.

Potentiation of angiotensin II-stimulated vascular contraction by lithium

1995 ◽  
Vol 268 (5) ◽  
pp. H2009-H2016
Author(s):  
M. E. Ullian ◽  
L. G. Walsh ◽  
K. C. Wong ◽  
C. J. Allan
Keyword(s):  
Angiotensin Ii ◽  
Inositol Phosphate ◽  
Cytosolic Calcium ◽  
Rat Aorta ◽  
Dependent Manner ◽  
Ang Ii ◽  
Concentration Dependent Manner ◽  
Adrenergic Agents ◽  
Phosphoinositide Signaling ◽  
Protein Kinase C Inhibitor

Previous studies have suggested that lithium prolongs or enhances vascular contractions stimulated by alpha-adrenergic agents. The present study was performed to determine whether a similar phenomenon occurs with angiotensin II (ANG II)-stimulated contractions and whether this phenomenon results from interactions with the phosphoinositide signaling system. Contractions of rat aortic rings with 100 nM ANG II were 38% greater in the presence of 20 mM LiCl than in its absence (0.47 +/- 0.07 vs. 0.34 +/- 0.05 g tension/mg dry tissue wt, P < 0.01). The effects of lithium on inositol phosphate responses, diacylglycerol responses, and intracellular calcium concentration on single or repeated stimulations with ANG II were then examined in vascular smooth muscle cells cultured from rat aorta. Cells exposed twice to 100 nM ANG II contained 50% lower inositol trisphosphate levels (InsP3) and 10% lower diacylglycerol levels than cells exposed to ANG II only once. LiCl or lithium acetate abolished these desensitizations in a concentration-dependent manner. Similarly, InsP3 and diacylglycerol responses to a single exposure of ANG II were heightened by lithium (by 75 and 25%, respectively), and the duration of the responses was prolonged by lithium (5- and 2-fold, respectively). In contrast, ANG II-stimulated calcium transients were not enhanced or prolonged by lithium, nor was desensitization of ANG II-stimulated cytosolic calcium mobilization upon serial exposures abolished by lithium. When ring contraction studies were repeated in the presence of the protein kinase C inhibitor staurosporine (150 nM), lithium no longer potentiated ANG II contractions [0.38 +/- 0.03 (control) vs. 0.35 +/- 0.06 g tension/mg dry tissue wt (lithium)].(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Angiotensin II Type 1 Receptor Antagonist Downregulates Nonmuscle Myosin Heavy Chains in Spontaneously Hypertensive Rat Aorta

Hypertension ◽  
1999 ◽  
Vol 33 (4) ◽  
pp. 975-980 ◽  
Author(s):  
Kozo Fujii ◽  
Seiji Umemoto ◽  
Akihisa Fujii ◽  
Takahito Yonezawa ◽  
Toshihiro Sakumura ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Spontaneously Hypertensive Rat ◽  
Rat Aorta ◽  
Myosin Heavy Chains ◽  
Nonmuscle Myosin ◽  
Spontaneously Hypertensive ◽  
Heavy Chains ◽  
Hypertensive Rat
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