Cholesterol Modulates Vascular Reactivity to Endothelin-1 by Stimulating a Pro-inflammatory Pathway

2000 ◽  
Vol 274 (2) ◽  
pp. 553-558 ◽  
Author(s):  
Daniel Paris ◽  
Terrence Town ◽  
James Humphrey ◽  
Kiyoko Yokota ◽  
Michael Mullan
Keyword(s):  
Vascular Reactivity ◽  
Inflammatory Pathway ◽  
Endothelin 1

Endothelin-1 and pancreatic islet vasculature: studies in vivo and on isolated, vascularly perfused pancreatic islets

2007 ◽  
Vol 292 (6) ◽  
pp. E1616-E1623 ◽  
Author(s):  
En Yin Lai ◽  
A. Erik G. Persson ◽  
Birgitta Bodin ◽  
Örjan Källskog ◽  
Arne Andersson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Vascular Reactivity ◽  
Blood Perfusion ◽  
Receptor Subtype ◽  
Endothelin 1 ◽  
Islet Blood Flow ◽  
Endothelin B

Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor, which also stimulates insulin release. The aim of the present study was to evaluate whether exogenously administered ET-1 affected pancreatic islet blood flow in vivo in rats and the islet arteriolar reactivity in vitro in mice. Furthermore, we aimed to determine the ET-receptor subtype that was involved in such responses. When applying a microsphere technique for measurements of islet blood perfusion in vivo, we found that ET-1 (5 nmol/kg) consistently and markedly decreased total pancreatic and especially islet blood flow, despite having only minor effects on blood pressure. Neither endothelin A (ETA) receptor (BQ-123) nor endothelin-B (ETB) receptor (BQ-788) antagonists, alone or in combination, could prevent this reduction in blood flow. To avoid confounding interactions in vivo, we also examined the arteriolar vascular reactivity in isolated, perfused mouse islets. In the latter preparation, we demonstrated a dose-dependent constriction in response to ET-1. Administration of BQ-123 prevented this, whereas BQ-788 induced a right shift in the response. In conclusion, the pancreatic islet vasculature is highly sensitive to exogenous ET-1, which mediates its effect mainly through ETA receptors.

Evidence for NO involvement in regulating vascular reactivity in balloon-injured rat carotid artery

1995 ◽  
Vol 269 (3) ◽  
pp. H988-H996 ◽  
Author(s):  
T. C. Major ◽  
R. W. Overhiser ◽  
R. L. Panek
Keyword(s):  
Carotid Artery ◽  
Factor Viii ◽  
Vascular Reactivity ◽  
Carotid Arteries ◽  
Muscarinic Agonist ◽  
Ang Ii ◽  
Histomorphometric Analysis ◽  
Balloon Injury ◽  
Contractile Responses ◽  
Endothelin 1

The present study evaluated the influence of this newly formed intima on vascular reactivity in balloon-injured carotid arteries and the regulatory role of the vasodilator, nitric oxide (NO). Balloon injury was performed using a 2-F Fogarty catheter. After 2 and 4 wk, carotid artery segments were removed for both histomorphometric analysis and determination of in vitro contractile responses. Histomorphometric analysis showed a marked intimal thickening with an intima-to-media ratio of 126 +/- 19% (n = 5). The lack of factor VIII staining in injured carotid arteries revealed the absence of endothelium, since factor VIII-related antigen is a glycoprotein synthesized by endothelial cells. Functionally, maximal contractile responses to norepinephrine, angiotensin II (ANG II), endothelin-1, and serotonin were all attenuated in the injured vessels compared with the uninjured carotid arteries [0.38 +/- 0.11 vs. 0.73 +/- 0.10 g (n = 5), norepinephrine; 0.15 +/- 0.06 vs. 0.38 +/- 0.05 g (n = 4), ANG II; 0.60 +/- 0.14 vs. 1.05 +/- 0.12 g (n = 4), endothelin-1; 0.23 +/- 0.07 vs. 0.60 +/- 0.06 g (n = 12), serotonin]. Contractile responses induced by KCl were not affected by the balloon injury (0.62 +/- 0.10 vs. 0.64 +/- 0.09 g, n = 4). Interestingly, carbachol, a muscarinic agonist and vasodilator, caused concentration-dependent relaxations in 2- as well as 4-wk postinjured vessels despite the absence of endothelium. The NO synthase inhibitors, N omega-L-arginine methyl ester (L-NAME) and N omega-nitro-L-arginine (L-NNA), blocked the relaxation responses evoked by carbachol. Exogenously administered L-arginine reversed this blockade of the NOS inhibitors on the carbachol-induced relaxations. In addition, L-NAME partially reversed in a concentration-dependent manner the reduced maximal contractile force elicited by serotonin in the injured carotid artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of lysophosphatidic acid in endothelin-1- and hematoma-induced alteration of cerebral microcirculation

1997 ◽  
Vol 273 (2) ◽  
pp. R703-R709 ◽  
Author(s):  
M. A. Yakubu ◽  
K. Liliom ◽  
G. J. Tigyi ◽  
C. W. Leffler
Keyword(s):  
Lysophosphatidic Acid ◽  
Vascular Reactivity ◽  
Intrathecal Injection ◽  
Brain Parenchyma ◽  
Cerebrovascular Reactivity ◽  
Lipid Mediator ◽  
Endothelin 1 ◽  
Potential Contributor ◽  
Cerebral Hematoma ◽  
Left Parietal Cortex

Cerebral hematoma increases cerebrospinal fluid (CSF) endothelin-1 (ET-1). Inhibitors of ET-1 synthesis prevent this increment and hematoma-induced modification of cerebral arteriolar reactivity. We hypothesized that intrathecal ET-1 injection could 1) modify pial arteriolar reactivity similarly to hematoma; 2) increase CSF lysophosphatidic acid (LPA), a potential contributor to altered cerebrovascular reactivity; and 3) reduce the level of adenosine 3',5'-cyclic monophosphate (cAMP) in the CSF. Either ET-1 (10(-7) M) or artificial CSF was injected over the left parietal cortex of newborn pigs. Four days later, cranial windows were implanted. CSF ET was increased from a basal level of 11 fmol/ml to 18 fmol/ml 4 days after ET-1 injection, whereas CSF cAMP was reduced from 2,700 to 950 fmol/ml. The mean diameter of pial arterioles was reduced 31%. In control animals, 10(-12) M ET caused dilation, and higher concentrations induced vasoconstriction. Four days after ET-1 injection topical ET-1 caused constriction instead of dilation at 10(-12) M, and constrictions at higher doses were enhanced. Norepinephrine-induced constrictions were potentiated in the ET-1-injected group. Dilations to cAMP-dependent (but not independent) vasodilators were attenuated after ET-1. The concentration of the vasoconstrictor lipid mediator LPA increased approximately fourfold. Thus intrathecal injection of ET-1 mimics hematoma-induced modification of cerebral vascular reactivity and increase in LPA production. The mechanism(s) of ET-1- and hematoma-induced modifications may involve LPA, which is known to contribute to the loss of dilator responses by inhibition of cAMP product on. The present study further suggests that ET-1 together with LPA could be causing changes in cerebrovascular reactivity following cerebral hemorrhage. ET-1 stimulates the release of LPA from brain parenchyma independent of serum so that LPA could serve as a secondary mediator.

Pulmonary Vascular Reactivity to Endothelin-1 in Normal and Chronically Pulmonary Hypertensive Rats

1991 ◽  
Vol 17 ◽  
pp. S358-361 ◽  
Author(s):  
S. Eddahibi ◽  
B. Raffestin ◽  
P. Braquet ◽  
P. E. Chabrier ◽  
S. Adnot
Keyword(s):  
Vascular Reactivity ◽  
Hypertensive Rats ◽  
Endothelin 1

Coronary vascular reactivity to endothelin-1 is exaggerated in diabetic rats

2001 ◽  
Vol 33 (6) ◽  
pp. A180
Author(s):  
Subodh Verma ◽  
Emi Arikawa ◽  
Sammy Lee ◽  
John H. McNeill
Keyword(s):  
Vascular Reactivity ◽  
Diabetic Rats ◽  
Endothelin 1

scholarly journals Ovarian Hormones Modulate Endothelin-1 Vascular Reactivity and mRNA Expression in DOCA-Salt Hypertensive Rats

Hypertension ◽  
2001 ◽  
Vol 38 (3) ◽  
pp. 692-696 ◽  
Author(s):  
Flavia L. David ◽  
Maria Helena C. Carvalho ◽  
Ana L.N. Cobra ◽  
Dorothy Nigro ◽  
Zuleica B. Fortes ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Vascular Reactivity ◽  
Ovarian Hormones ◽  
Hypertensive Rats ◽  
Endothelin 1

Gender Differences in Vascular Reactivity to Endothelin-1 in Deoxycorticosterone-Salt Hypertensive Rats

2000 ◽  
Vol 36 (Supplement 1) ◽  
pp. S99-S101 ◽  
Author(s):  
Rita C.A. Tostes ◽  
Flavia L. David ◽  
Maria Helena C. Carvalho ◽  
Dorothy Nigro ◽  
Regina Scivoletto ◽  
...  
Keyword(s):  
Gender Differences ◽  
Vascular Reactivity ◽  
Hypertensive Rats ◽  
Endothelin 1
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