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

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

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

scholarly journals Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation

Cardiology ◽  
2016 ◽  
Vol 136 (4) ◽  
pp. 258-268 ◽  
Author(s):  
Silvio Antoniak ◽  
Jessica C. Cardenas ◽  
Laura J. Buczek ◽  
Frank C. Church ◽  
Nigel Mackman ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Heart Function ◽  
Coronary Vessels ◽  
Wall Thickening ◽  
Ang Ii ◽  
Cardiovascular Remodeling ◽  
Protease Activated Receptor 1 ◽  
Pressure Independent ◽  
Fractional Shortening

Background: Angiotensin II (Ang II) plays an important role in cardiovascular disease. It also leads to the activation of coagulation. The coagulation protease thrombin induces cellular responses by activating protease-activated receptor 1 (PAR-1). We investigated whether PAR-1 contributes to Ang II-induced cardiovascular remodeling and inflammation. Methods and Results: PAR-1+/+ (wild-type; WT) and PAR-1-/- mice were infused with Ang II (600 ng/kg/min) for up to 4 weeks. In WT mice, this dose of Ang II did not cause a significant increase in blood pressure but it did cause pathological changes in both the aorta and the heart. Ang II infusion resulted in vascular remodeling of the aorta, demonstrated by a significant increase in medial wall thickening and perivascular fibrosis. Importantly, both parameters were significantly attenuated by PAR-1 deficiency. Furthermore, perivascular fibrosis around coronary vessels was reduced in Ang II-treated PAR-1-/- mice compared to WT mice. In addition, PAR-1 deficiency significantly attenuated Ang II induction of inflammatory cytokines and profibrotic genes in the aortas compared to WT mice. Finally, PAR-1 deficiency had no effect on Ang II-induced heart hypertrophy. However, the heart function measured by fractional shortening was less impaired in PAR-1-/- mice than in WT mice. Conclusion: Our data indicate that PAR-1 plays a significant role in cardiovascular remodeling mediated by a blood pressure-independent action of Ang II.

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