Involvement of Hydrogen Sulfide in Endothelium-Derived Relaxing Factor-Mediated Responses in Rat Cerebral Arteries

2016 ◽  
Vol 53 (3-4) ◽  
pp. 172-185 ◽  
Author(s):  
Mei Wang ◽  
Youyang Hu ◽  
Yifei Fan ◽  
Yan Guo ◽  
Fanglin Chen ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Cerebral Arteries ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor

Modulation of cerebral arterial tone by endothelium-derived relaxing factor

1993 ◽  
Vol 264 (4) ◽  
pp. H1245-H1250 ◽  
Author(s):  
J. E. Brian ◽  
R. H. Kennedy
Keyword(s):  
Nitric Oxide ◽  
Muscle Tone ◽  
Cerebral Arteries ◽  
Maximum Tension ◽  
Relaxing Factor ◽  
Middle Cerebral Arteries ◽  
Endothelium Derived Relaxing Factor ◽  
Vascular Smooth Muscle Tone ◽  
Dose Dependent ◽  
Arterial Tone

This study was designed to further elucidate the role of the endothelium in regulation of cerebral vascular smooth muscle tone. Dose-dependent vasoconstrictive effects of serotonin (5-HT) were examined in endothelium-intact and endothelium-denuded ring segments prepared from canine basilar and middle cerebral arteries. Some preparations were pretreated with 10(-5) M N omega-nitro-L-arginine (L-NNA), an agent that inhibits the production of L-arginine-derived nitric oxide, one of the compounds proposed to be endothelium-derived relaxing factor. L-NNA alone elicited marked dose-dependent increases in tension in endothelium-intact preparations; a significantly smaller response was seen in endothelium-denuded preparations. The effects of L-NNA on endothelium-intact preparations were partially reversed by washing and treatment with L-arginine. The maximum tension induced by 5-HT was approximately doubled by removal of the endothelium as well as by L-NNA treatment of endothelium-intact preparations; a slight increase in maximum tension occurred in endothelium-denuded preparations treated with L-NNA. The concentration of 5-HT producing half-maximal contraction (ED50) was not affected by L-NNA. These data suggest that L-arginine-derived nitric oxide modulates canine cerebral arterial tone in both the resting state and during contraction with 5-HT.

scholarly journals Triphasic Response of Rat Intracerebral Arterioles to Increasing Concentrations of Vasopressin in vitro

1993 ◽  
Vol 13 (2) ◽  
pp. 304-309 ◽  
Author(s):  
Masakazu Takayasu ◽  
Yasukazu Kajita ◽  
Yoshio Suzuki ◽  
Masato Shibuya ◽  
Kenichiro Sugita ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Vascular Tone ◽  
Cerebral Arteries ◽  
Specific Inhibitor ◽  
In Vitro Study ◽  
Relaxing Factor ◽  
Pathological Conditions ◽  
Cerebral Arterioles ◽  
Endothelium Derived Relaxing Factor

To determine how vasopressin affects the vascular tone of the smaller cerebral arterioles, we carried out an in vitro study of isolated and cannulated intracerebral arterioles of rats. We found that increasing concentrations of vasopressin induced a triphasic response of vasodilation (10−12–10−11 M), vasoconstriction (10−10–10−8 M), and vasodilation stabilizing to control diameter (10−7–10−6 M) and that the maximum constriction was twice the maximum dilation in these smaller arterioles [21.2 ± 13.1% (mean ± SD) decrease in diameter vs. 11.2 ± 5.7% increase]. Pretreatment of the arterioles with NG-monomethyl-l-arginine (10−4 M), a specific inhibitor of endothelium-derived relaxing factor, abolished the vasopressin-induced vasodilation and significantly increased the vasoconstriction. These results suggest that these arterioles were maintained in a dilated state by an endothelium-derived relaxing factor activated by vasopressin. Both vasodilation and vasoconstriction were found to be mediated through vasopressin V1 receptors in a study of arterioles pretreated with d(CH2)5Tyr(Me)arginine vasopressin (10−6 M), a vasopressin V1 receptor antagonist. These results support the hypothesis that vasopressin may constrict smaller cerebral arterioles while simultaneously dilating larger cerebral arteries. Our results also suggest that vasopressin may aggravate cerebral ischemia in pathological conditions, such as subarachnoid hemorrhage, when the arteriolar response to vasopressin shifts from vasodilation to vasoconstriction due to increased vasopressin levels in plasma and CSF and impaired endothelium-derived relaxation.

Responses of cerebral arteries after ischemia and reperfusion in cats

1988 ◽  
Vol 255 (4) ◽  
pp. H879-H884 ◽  
Author(s):  
W. G. Mayhan ◽  
S. M. Amundsen ◽  
F. M. Faraci ◽  
D. D. Heistad
Keyword(s):  
Cerebral Ischemia ◽  
Topical Application ◽  
Cerebral Arteries ◽  
Base Line ◽  
Ischemia And Reperfusion ◽  
Relaxing Factor ◽  
Cerebral Ischemia And Reperfusion ◽  
Before And After ◽  
Cerebral Vasodilatation ◽  
Endothelium Derived Relaxing Factor

Our goal was to determine whether responses of cerebral arteries are altered after cerebral ischemia and reperfusion. We measured diameter of cerebral arteries (150-180 micron) in cats in response to topical application of acetylcholine (ACh) and serotonin, which release endothelium-derived relaxing factor (EDRF), and adenosine and angiotensin, which do not release EDRF. Diameter of arteries was measured before and after 10 or 30 min of cerebral ischemia, when base-line diameter had returned to control levels. Under control conditions, serotonin and angiotensin constricted cerebral arteries by 16 +/- 2 and 23 +/- 3% (means +/- SE), respectively, and ACh and adenosine dilated cerebral arteries by 22 +/- 2 and 23 +/- 3%, respectively. During reperfusion after 10 min of cerebral ischemia, constrictor responses of cerebral arteries were preserved. Vasodilator responses of arteries to ACh after 10 min of ischemia were heterogeneous. In 6 of 15 cats, vasodilatation in response to ACh was preserved. In contrast, in 9 of 15 cats, vasodilatation in response to ACh was impaired (7 +/- 3%). In both groups, vasodilatation in response to adenosine was not impaired after 10 min of ischemia. During reperfusion after 30 min of cerebral ischemia, constrictor responses of cerebral arteries were preserved. In contrast, dilatation of cerebral arteries in response to ACh and adenosine was impaired. We speculate that impaired cerebral vasodilatation after ischemia, with maintenance of vasoconstriction, may contribute to impaired reperfusion after cerebral ischemia.

Mechanisms of contracting action of oxyhemoglobin in isolated monkey and dog cerebral arteries

1990 ◽  
Vol 258 (1) ◽  
pp. H57-H63 ◽  
Author(s):  
N. Toda
Keyword(s):  
Cerebral Artery ◽  
Inhibitory Concentration ◽  
Contractile Response ◽  
Cerebral Arteries ◽  
Superoxide Anions ◽  
Relaxing Factor ◽  
Thromboxane Synthase Inhibitor ◽  
Endothelium Derived Relaxing Factor ◽  
Synthase Inhibitor ◽  
Median Effective Concentration

Oxyhemoglobin (HbO2) produced a concentration-dependent contraction of monkey and dog cerebral artery strips, which was significantly attenuated by endothelium denudation. The contractile response was suppressed by treatment with indomethacin, aspirin, and diphloretin phosphate, a prostaglandin (PG) receptor antagonist. OKY 046, a thromboxane synthase inhibitor, attenuated both the contractions caused by HbO2 and PGF2 alpha. Contractions by arachidonic acid (AA) of the monkey arteries were markedly inhibited by indomethacin and moderately attenuated by endothelium denudation. Treatment with superoxide dismutase and catalase failed to reduce the response to HbO2 and AA. The median effective concentration of HbO2 in producing dog cerebral artery contraction was approximately 1,000 times as high as the median inhibitory concentration in inhibiting the effect of endothelium-derived relaxing factor (EDRF) released from dog femoral arteries in response to acetylcholine. It is concluded that contractions caused by HbO2 are not associated with suppression of EDRF released spontaneously from monkey and dog cerebral arteries, but with vasoconstrictor PGs released mainly from endothelium. Thromboxane A2, superoxide anions, and hydrogen peroxide do not appear to be involved.

Prostaglandin F2 alpha-induced endothelium-dependent relaxation in isolated monkey cerebral arteries

1991 ◽  
Vol 260 (5) ◽  
pp. H1538-H1543 ◽  
Author(s):  
Y. Kawai ◽  
T. Ohhashi
Keyword(s):  
Endothelial Cells ◽  
Cerebral Arteries ◽  
Relaxing Factor ◽  
Prostaglandin F2 Alpha ◽  
Low Concentrations ◽  
Endothelium Derived Relaxing Factor ◽  
Dose Dependent ◽  
Endothelium Dependent Relaxation

Effects of prostaglandin F2 alpha (PGF2 alpha) on isolated monkey and dog cerebral arteries were investigated to reevaluate PGF2 alpha's possible action on the endothelium. Low concentrations of PGF2 alpha ranging from 10(-11) to 10(-8) M produced a dose-dependent relaxation in the monkey arteries. PGF2 alpha (10(-7) M) produced a transient contraction followed by a small relaxation, whereas higher concentrations (greater than 10(-6) M) of PGF2 alpha induced only contractions. The PGF2 alpha-induced relaxation was not observed in the canine cerebral arteries. The PGF2 alpha-induced relaxation of the monkey cerebral arteries was not affected by treatment with 10(-7) M propranolol, 10(-7) M atropine, or 10(-6) M cimetidine. In monkey cerebral arteries without endothelium, PGF2 alpha in concentrations ranging from 10(-11) to 10(-6) M caused no relaxation. Treatment with 5 X 10(-5) M aspirin, 3 X 10(-5) M NG-monomethyl-L-arginine, and 10(-5) M oxyhemoglobin significantly suppressed the PGF2 alpha-induced relaxation. These results suggest that low concentrations of PGF2 alpha may produce an endothelium-dependent relaxation in monkey cerebral arteries and that the relaxation may be mediated by release of both endogenous vasodilative prostaglandins and endothelium-derived relaxing factor from endothelial cells.

scholarly journals Endothelium-Derived Relaxing Factor Inhibits Constrictor Responses of Large Cerebral Arteries to Serotonin

1992 ◽  
Vol 12 (3) ◽  
pp. 500-506 ◽  
Author(s):  
Frank M. Faraci ◽  
Donald D. Heistad
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Cerebral Arteries ◽  
Large Arteries ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

Endothelium-derived relaxing factor [EDRF, nitric oxide (NO) or a NO-containing compound] influences basal tone of cerebral blood vessels and mediates vasodilation in response to several stimuli. It is not known whether EDRF also modulates responses to cerebral vasoconstrictor stimuli in vivo. Our goal was to determine whether formation of EDRF inhibits constrictor responses of large cerebral arteries to serotonin. We measured cerebral blood flow (microspheres) and pial microvascular pressure (servo null) in anesthetized rabbits and calculated resistance of large cerebral arteries. Responses to an inhibitor of NO formation, NG-nitro-l-arginine (l-NNA, 3 mg/kg i.v.), were examined. l-NNA produced an increase in resistance of large arteries and total cerebral vascular resistance of approximately 15% (p < 0.05 for both variables) and a small decrease in cerebral blood flow (35 ± 9 vs. 32 ± 7 ml min−1 100 g−1, mean ± SD, p < 0.05). Under control conditions, infusion of serotonin (10 μg kg−1 min−1, into the left atrium) produced an increase in resistance of large arteries. Following treatment with l-NNA, the change in resistance of large arteries in response to serotonin was increased more than twofold (0.20 ± 0.17 vs. 0.43 ± 0.21 mm Hg ml−1 min 100 g, p < 0.05). In contrast, l-NNA did not alter the increase in resistance of large arteries during hypocapnia. l-arginine inhibited the effects of l-NNA on baseline cerebral vascular resistance and on responses of large arteries to serotonin. Thus, formation of EDRF (NO) from l-arginine (a) has a modest influence on cerebral blood flow under basal conditions and (b) inhibits constriction of large cerebral arteries to serotonin, but not hypocapnia.

Human basilar and middle cerebral arteries exhibit endothelium-dependent responses to peptides

1994 ◽  
Vol 267 (3) ◽  
pp. H880-H886 ◽  
Author(s):  
H. Onoue ◽  
N. Kaito ◽  
M. Tomii ◽  
S. Tokudome ◽  
M. Nakajima ◽  
...  
Keyword(s):  
Substance P ◽  
Cerebral Arteries ◽  
Isometric Tension ◽  
Relaxing Factor ◽  
Prostaglandin F2 Alpha ◽  
Middle Cerebral Arteries ◽  
Vasopressin Receptors ◽  
Basilar Arteries ◽  
Human Cadavers ◽  
Endothelium Derived Relaxing Factor

We examined the activities of bradykinin, substance P, and vasopressin in isolated human cerebral arteries to better understand humoral control of cerebrovascular tone. Basilar and middle cerebral arteries were isolated from human cadavers during autopsy, and isometric tension was measured in helical strips of the arteries. Both bradykinin and substance P relaxed strips of both arteries precontracted with prostaglandin F2 alpha to similar extents. The relaxations induced by both peptides were abolished by removal of the vascular endothelium and were markedly reduced by pretreatment with NG-nitro-L-arginine, an inhibitor of endothelium-derived relaxing factor. Treatment with indomethacin, a cyclooxygenase inhibitor, did not attenuate the relaxations. These results indicate that the responses of human cerebral arteries to bradykinin and substance P are mediated by endothelium-derived relaxing factor. In contrast, vasopressin primarily produced endothelium-independent contractions in human cerebral arteries. Contractions of basilar arteries induced by vasopressin were much less than those of middle cerebral arteries. Two of eighteen basilar arteries, but none of the middle cerebral arteries, responded to vasopressin with endothelium-dependent relaxation. This suggests that the function of vasopressin receptors differs in basilar and middle cerebral arteries.

Why is a new journal dedicated to vascular biology required?

2018 ◽  
Author(s):  
Paolo Madeddu
Keyword(s):  
Myocardial Ischemia ◽  
Tumor Growth ◽  
Vascular Tone ◽  
50Th Anniversary ◽  
Vascular Biology ◽  
Active Process ◽  
Master Regulators ◽  
Relaxing Factor ◽  
Tissue Healing ◽  
Endothelium Derived Relaxing Factor

The year 2018 marked the 110th anniversary of Goldmann’s discovery that vascularization is an active process in tissues1 and the 50th anniversary of the concomitant reports from Greenblatt and Shubik2 and Ehrmann and Knoth3 that soluble morphogenic factors are required for cancer angiogenesis. Many other radically transformative paradigms have been introduced in the last decades. To name a few, the molecular search for the identity of master regulators of vascular tone led to the discovery of the Endothelium-Derived Relaxing Factor (EDRF; i.e., NO4), while clinically inspired investigations led to the recognition of the pathophysiological relevance of neoangiogenesis in cancer and tissue healing. This brought about the proposal of blocking angiogenesis to halt tumor growth and stimulating angiogenesis to treat myocardial ischemia and heart failure5-7.

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