20 Endothelium-dependent relaxation in human subcutaneous fat resistance vessels in pre-eclampsia

1991 ◽  
Vol 9 (11) ◽  
pp. 1089 ◽  
Author(s):  
A McCarthy ◽  
R G Woolfson ◽  
K S R Raju ◽  
L Poston
Keyword(s):  
Subcutaneous Fat ◽  
Resistance Vessels ◽  
Endothelium Dependent Relaxation

Free-radical scavengers, thiol-containing reagents and endothelium-dependent relaxation in isolated rat and human resistance arteries

1993 ◽  
Vol 84 (3) ◽  
pp. 287-295 ◽  
Author(s):  
W. Sunman ◽  
A.D. Hughes ◽  
P.S. Sever
Keyword(s):  
Superoxide Dismutase ◽  
Free Radical ◽  
Methyl Ester ◽  
Enzyme Inhibitor ◽  
Subcutaneous Fat ◽  
Free Radical Scavengers ◽  
Radical Scavenger ◽  
Resistance Arteries ◽  
Rat Mesentery ◽  
Endothelium Dependent Relaxation

1. Small arteries were isolated from either rat mesentery or human subcutaneous fat, and mounted in a myograph for the measurement of isometric force. 2. Superoxide dismutase, either in the presence or absence of catalase, relaxed noradrenaline-induced tone. This effect was abolished by removal of the endothelium or incubation with an inhibitor of NO synthase, N-ω-nitro-L-arginine methyl ester. Catalase alone had a negligible effect on noradrenaline-induced tone. 3. Captopril, an angiotensin-converting enzyme inhibitor and putative free-radical scavenger, did not relax pre-contracted isolated vessels. N-Acetylcysteine caused an endothelium-independent relaxation of rat vessels. Similar effects were observed in human vessels. 4. Acetylcholine induced a concentration-dependent relaxation of isolated resistance arteries, which was inhibited by removal of the endothelium or N-ω-nitro-L-arginine methyl ester, but unaffected by indomethacin. Preincubation with captopril, N-acetylcysteine or catalase alone did not alter the acetylcholine concentration-response relationship, but superoxide dismutase in combination with catalase enhanced responses to acetylcholine, causing a six-fold increase in potency. 5. Superoxide dismutase causes endothelium-dependent relaxation of resistance arteries and potentiates responses to acetylcholine. This action is probably due to the ability of the enzyme to scavenge superoxide anions which inhibit endothelium-dependent relaxation. 6. N-Acetylcysteine causes an endothelium-independent relaxation of resistance arteries which is probably unrelated to the putative ability of this compound to scavenge superoxide radicals and may reflect a direct action on vascular smooth muscle.

Small Artery Structural Alterations of Patients with Microvascular Angina (Syndrome X)

1996 ◽  
Vol 91 (6) ◽  
pp. 739-743 ◽  
Author(s):  
S. J. Bund ◽  
A. Tweddel ◽  
I. Hutton ◽  
A. M. Heagerty
Keyword(s):  
Subcutaneous Fat ◽  
Lumen Diameter ◽  
Syndrome X ◽  
Microvascular Angina ◽  
Contractile Responses ◽  
Small Arteries ◽  
Control Subjects ◽  
Media Thickness ◽  
Number Of Patients ◽  
Endothelium Dependent Relaxation

1. There is increasing evidence that a substantial number of patients who suffer from angina have normal epicardial arteries (Syndrome X), and it has been suggested that these individuals have a generalized disorder of small vessels not confined to the intramyocardial vasculature. 2. Small arteries were therefore obtained from biopsies of skin and subcutaneous fat from nine normotensive patients with Syndrome X and nine matched control subjects. Vessels were dissected and mounted as ring preparations in a myograph for morphological and functional assessment. 3. Morphological measurements revealed a significant increase in media thickness/lumen diameter ratio in arteries from patients with Syndrome X. Contractile responses to U46619 were similar in arteries from patients and control subjects. Endothelium-dependent relaxation induced with acetylcholine and bradykinin was greater in arteries from patients although differences were not statistically significant. Endothelium-independent relaxation induced by forskolin and sodium nitroprusside was not different. 4. In conclusion, these data demonstrate that subcutaneous small arteries from patients with Syndrome X are characterized by increased media thickness/lumen diameter ratios, although contractile responses were normal. Additionally, endothelium-dependent relaxation was not impaired in arteries from these patients. Thus, no significant functional abnormalities were associated with the observed structural differences.

scholarly journals Endothelium-Dependent Relaxation of Small Resistance Vessels Is Impaired in Patients with Autosomal Dominant Polycystic Kidney Disease

2000 ◽  
Vol 11 (8) ◽  
pp. 1371-1376 ◽  
Author(s):  
DAN WANG ◽  
JENS IVERSEN ◽  
SVEND STRANDGAARD
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Dose Response ◽  
Autosomal Dominant ◽  
No Synthase ◽  
Polycystic Kidney ◽  
Control Subjects ◽  
Resistance Vessels ◽  
Autosomal Dominant Polycystic Kidney ◽  
Endothelium Dependent Relaxation

Abstract. Impaired endothelium-dependent relaxation has been demonstrated previously in resistance vessels of Han:SPRD polycystic kidney disease rats. The aim of the present study was to investigate whether endothelium-dependent relaxation is reduced also in patients with autosomal dominant polycystic kidney disease (ADPKD) and whether this is influenced by the nitric oxide (NO) system. Small subcutaneous resistance vessels from normotensive ADPKD patients with normal or near-normal renal function (n= 9) and from healthy control subjects (n= 10) were mounted in a Mulvany-Halpern myograph. The morphology of the vessels and acetylcholine (ACh)-induced endothelium-dependent relaxation, as well as 3-morpholino-sydnonimine (SIN-1, NO donor)-induced endothelium-independent relaxation were investigated. The results showed that: (1) there were no significant differences in morphologic parameters of resistance vessels between the two groups; (2) the maximal ACh-induced relaxation rate was decreased in ADPKD patients compared with control subjects (71.5 ± 12.1versus85.2 ± 8.7%,P< 0.01); (3) in the presence of L-arginine (a substrate of NO synthase), a left shift of the ACh dose-response curves was found in control subjects, but not in ADPKD patients; (4) in the presence of theNG-nitro-L-arginine methyl ester (an inhibitor of NO synthase), a right shift of the ACh dose-response curve was found in control subjects, but not in ADPKD patients; and (5) endothelium-independent relaxation rate induced with SIN-1 was similar in patients and control subjects. In conclusion, endothelium-dependent relaxation was impaired in resistance vessels from patients with ADPKD. The reduced response of the vessels to both the substrate and inhibitor of NO synthase in ADPKD suggests that an impairment of NO synthase may be involved in the mechanism of endothelial dysfunction in ADPKD.

Contractile actions of C5a on isolated porcine coronary resistance and conductance arteries

1997 ◽  
Vol 272 (1) ◽  
pp. H12-H16 ◽  
Author(s):  
S. V. Rendig ◽  
S. Gray ◽  
E. A. Amsterdam
Keyword(s):  
Coronary Arteries ◽  
Dose Response ◽  
Thromboxane A2 ◽  
Physiological Salt Solution ◽  
Coronary Resistance ◽  
Resistance Arteries ◽  
Response Curves ◽  
Resistance Vessels ◽  
Dose Response Curves ◽  
Endothelium Dependent Relaxation

The comparative effects of the complement component C5a on coronary resistance and conductance arteries have not been evaluated. To clarify the coronary contractile actions of this anaphylatoxin, we studied the effects of C5a on development of isometric tension in isolated porcine coronary conductance and resistance arteries. Internal diameters of conductance and resistance vessels were 367 +/- 21 and 88 +/- 4 microns, respectively. Vessel ring segments were suspended in a microvessel myograph, stretched to the peaks of their length-tension curves, and precontracted with 30 mM K+ physiological salt solution. Dose-response curves to C5a (2, 10, and 50 nM) were obtained. At 50 nM, the C5a-induced increase in tension in resistance arteries (4.1 +/- 0.9 to 5.7 +/- 1.4 mN, 35.8 +/- 3.4%) was significantly greater (P < 0.05) than in conductance arteries (10.7 +/- 2.2 to 12.4 +/- 2.6 mN, 15.6 +/- 3.0%). A specific thromboxane A2 receptor antagonist, SQ-29548, virtually eliminated C5a-induced increases in tension. C5a did not impair endothelium-dependent relaxation in either conductance or resistance vessels, as indicated by the half-maximal effective dose (ED50) calculated from bradykinin dose-response curves before and after exposure of the vessels to 50 nM C5a (resistance: pre-C5a ED50 = 2 nM, post-C5a ED50 +/- 3 nM; conductance: pre-C5a ED50 +/- 13 nM, post-C5a ED50 +/- 14 nM). These results indicate that 1) C5a has a greater vasoconstrictive effect on isolated porcine resistance than conductance coronary arteries; 2) C5a-induced coronary constriction is mediated by thromboxane A2; and 3) C5a does not impair endothelium-dependent relaxation of isolated porcine coronary arteries.

Morphological and functional characteristics of isolated resistance vessels in advanced uraemia

1986 ◽  
Vol 71 (6) ◽  
pp. 657-663 ◽  
Author(s):  
C. Aalkjær ◽  
E. B. Pedersen ◽  
H. Danielsen ◽  
O. Fjeldborg ◽  
B. Jespersen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Vascular Reactivity ◽  
Subcutaneous Fat ◽  
Mean Blood Pressure ◽  
Internal Diameter ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Vascular Morphology ◽  
Resistance Vessels

1. In order to obtain direct information on the properties of the resistance vasculature of patients with advanced uraemia, a technique was developed to dissect out small arteries (internal diameter about 165 μm) from biopsies of subcutaneous fat. 2. Such arteries responded in a concentration-dependent manner to noradrenaline and angiotensin II, and the maximal force developed suggested that the vessels were fully viable. 3. Although the biopsies were normally taken during operations under general anaesthesia, biopsies taken under local anaesthesia also appeared to be fully viable, suggesting that this technique may prove useful as a general method for studying the intrinsic vascular properties of humans. 4. Biopsies were taken from 20 patients with uraemia, all of whom were treated with chronic intermittent dialysis, and 11 control subjects; up to three vessels were examined per biopsy. 5. The uraemic state was not associated with changes in vascular morphology, or in vascular reactivity or sensitivity to noradrenaline, angiotensin II, potassium or calcium. However, for the uraemic patients and for the controls there was a positive correlation between mean blood pressure and the ratio of vessel media thickness to lumen diameter, as well as a negative correlation between mean blood pressure and vessel active media stress. 6. The results suggest that uraemia treated with dialysis may not be associated with altered properties of the resistance vasculature. However, it appears that uraemic hypertension is associated with both morphological and functional abnormalities of the resistance vasculature.

scholarly journals Role of hyperpolarizing mechanism in endothelium-dependent relaxation of resistance vessels

1995 ◽  
Vol 67 ◽  
pp. 39
Author(s):  
Hiroaki Shimokawa ◽  
Hiroshi yasutake ◽  
Kohji Fujii ◽  
Ryuichi Nakaike ◽  
Masatoshi Fujishima ◽  
...  
Keyword(s):  
Resistance Vessels ◽  
Endothelium Dependent Relaxation
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