Endotoxin impairs endothelium-dependent vasodilation more in the coronary and renal arteries than in other arteries of the rat

Piepot, Harro A.; Groeneveld, A. B. Johan; Lambalgen, A.A. van; Sipkema, Pieter

doi:10.1016/s0022-4804(02)00043-4

Cited by 27 publications

(15 citation statements)

References 25 publications

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“…Endothelium-dependent vasorelaxation was tested with acetylcholine in preconstricted isolated vessels. Exposure to endotoxin attenuated the maximum relaxation response to acetylcholine in coronary and in renal arteries in opposition to mesenteric and hepatic arteries (27). Collectively, these results suggest that regional vascular resistance and vascular reactivity of different beds is inversely proportional to local production of NO and ROS.…”

Section: Discussionmentioning

confidence: 73%

“…The general vascular hyporeactivity to vasoconstrictors (Ang II, AVP, and NE) does not seem to explain the renal vasoconstriction (6). However, renal vasoconstriction may result from impaired endothelium-dependent vasodilation, a view supported by results obtained in vitro and in vivo from both humans and animals (25)(26)(27). High plasma levels of catecholamines and Ang II found in clinical and experimental studies during sepsis may contribute to the renal vasoconstriction (12,28).…”

Section: T He Incidence Of Severe Sepsis Is Increasing In the Unitedmentioning

confidence: 99%

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Maintenance of Renal Vascular Reactivity Contributes to Acute Renal Failure during Endotoxemic Shock

Boffa

Arendshorst

2005

Journal of the American Society of Nephrology

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Septic shock is characterized by hypotension and decreased systemic vascular resistance and impaired vascular reactivity. Renal vasoconstriction markedly contrasts with sepsis-induced generalized systemic vasodilation, which is strongly dependent on nitric oxide. Whether maintained renal vascular reactivity to vasoconstrictors contributes to the decrease in renal blood flow (RBF) and GFR observed during LPS-induced sepsis was tested by assessment of the acute effects of pressor agents on mean arterial pressure (MAP) and renal hemodynamics in endotoxemic and control mice. LPS-injected mice displayed lower MAP, RBF, and GFR than controls (P < 0.001). Despite a lower MAP, basal renal vascular resistance (RVR) was higher during endotoxemia (P < 0.02). Angiotensin II infusion produced a weaker MAP response in septic mice (24 versus 37%; P < 0.005), suggesting impaired vasoconstriction and hyporeactivity. A similar MAP increase was observed between groups during norepinephrine (NE) infusion. The MAP increase to nitric oxide synthase inhibition by N G -nitro-L-arginine methyl ester (L-NAME) was much greater in LPS-treated mice (41 versus 15%, P ‫؍‬ 0.01), indicating a strong influence of nitric oxide in sepsis. In contrast, the RBF and RVR responses to angiotensin II, NE, or L-NAME were similar in both groups. Moreover, vasopressin produced greater changes in MAP, RBF, and RVR in septic mice than in controls. Among the vasoconstrictor challenges, only NE ameliorated the decrease in GFR 14 h after LPS injection. The in vivo results demonstrate that the renal microvasculature displays a normal or enhanced reactivity to constrictor agents as compared with nonrenal circulatory beds. Such responsiveness may contribute to reduced RBF and GFR during endotoxemia.

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Section: Discussionmentioning

confidence: 73%

Section: T He Incidence Of Severe Sepsis Is Increasing In the Unitedmentioning

confidence: 99%

Maintenance of Renal Vascular Reactivity Contributes to Acute Renal Failure during Endotoxemic Shock

Boffa

Arendshorst

2005

Journal of the American Society of Nephrology

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“…Impaired vascular relaxation responses to Ach in different tissues can be attributed to blunted endothelium-dependent relaxation to various receptor-dependent agonists, including Ach. 25 As it has been shown, the M 3 subtype muscarinic receptors, which are responsible for relaxation, are located on endothelial cells of the vasculature, 26 and when stimulated, they release NO, which diffuses to adjacent smooth muscle and causes them to relax. 27 Vasoconstriction responses to Ach in endothelium damaged hypercholesterolemic MA is a result of Ach, which stimulates M 2 receptors on vascular smooth muscle cells and cause vasoconstriction.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of vascular smooth muscle and corpus cavernosum on hypercholesterolemia. Is resveratrol promising on erectile dysfunction?

et al. 2010

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The aim of this study is to evaluate the effects of hypercholesterolemia in thoracic aorta (TA), mesenteric artery (MA), renal artery (RA), and corpus cavernosum (CC) isolated from cholesterolfed rabbits. For determination of the maximum detrimental effect, vasorelaxation and vasoconstriction results of arteries and CC have been compared. Animals were fed with a diet that contained 2% w/w cholesterol and 2% w/w high cholesterol plus resveratrol (4 mg kg -1 per day) for 6-week duration. Total cholesterol levels in the plasma were measured. Vascular and endothelial functions in RA, TA, MA, and CC were assessed by isolated tissue bath with cumulative doses of acetylcholine and sodium nitroprusside. The statistical significance of differences of groups was analyzed by means of one-way ANOVA or Student's t-test. P-values o0.05 were considered significant. There have been no significant changes on plasma total cholesterol levels between cholesterol and cholesterol þ resveratrol-treated groups. Vasorelaxation responses to acetylcholine in resveratroltreated group showed significant changes when compared with hypercholesterolemic group. No statistically significant differences were seen between non-receptor-mediated vasorelaxation responses between the three groups. Resveratrol might be an effective treatment in the prevention of atherosclerotic changes in arteries and CC. The initial effects of hypercholesterolemia on erectile dysfunction and endothelial dysfunction may be precluded with resveratrol. This protective effect may also ensure the prevention of coronary arterial diseases and renovascular diseases in hypercholesterolemic patients.

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“…Independent of TP receptor activation, the apparent absence of autoregulatory vasodilation in response to the decrease in MAP may contribute to the persistent decreases in RBF and GFR. In this regard, impaired endothelium-dependent dysfunction and impaired renal vasodilation are well documented during endotoxemia in humans and animals (36,37). Of related interest, NO production attenuates the myogenic contribution to RBF autoregulation (A.J.…”

Section: Discussionmentioning

confidence: 99%

Thromboxane Receptor Mediates Renal Vasoconstriction and Contributes to Acute Renal Failure in Endotoxemic Mice

Boffa

Just²,

Coffman

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Sepsis is a major cause of acute renal failure (ARF) and death. Thromboxane A2 (TxA 2 ) may mediate decreases of renal blood flow (RBF) and/or GFR associated with LPSinduced sepsis. This study tested whether TxA 2 receptor blockade, with the use of TxA 2 receptor knockout (TP-KO) mice or a selective TP receptor antagonist (SQ29,548), would alleviate LPS-induced renal vasoconstriction and ARF. Under basal conditions, anesthetized TP-KO mice displayed a lower mean arterial pressure than wild-type (WT) mice (102 versus 94 mmHg; P Ͻ 0.05). RBF, renal vascular resistance (RVR), GFR, and urine flow did not differ among groups under basal conditions, suggesting little tonic influence of TxA 2 on renal TP receptors in health. In endotoxemic WT mice, 14 h after LPS (Escherichia coli LPS 8.5 mg/kg intraperitoneally), mean arterial pressure was reduced to 85 mmHg (P Ͻ 0.001), as were RBF (5.0 versus 9.3 ml/min per g kidney wt; P Ͻ 0.001) and GFR (0.38 versus 1.03 ml/min per g kidney wt; P Ͻ 0.001). Heart rate and RVR (71 versus 47 mmHg/ml per min; P Ͻ 0.05) increased. The decreases in RBF and GFR after LPS were attenuated in TP-KO mice versus WT mice (both P Ͻ 0.05). In both TP-KO and TP antagonist-treated mice, RVR remained stable in response to LPS versus WT mice that did not receive LPS. Delayed TP-antagonist treatment (12 h after LPS injection) ameliorated RBF and RVR but did not restore GFR. In other WT animals, TP-antagonist treatment for 2 h before intravenous LPS abolished the early renal vasoconstriction and alleviated the decrease in GFR. These results demonstrate that renal vasoconstriction during endotoxemic shock induced by LPS is mediated by TP receptors as indicated by pharmacologic blockade and genetic disruption of TP receptors.

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Endotoxin impairs endothelium-dependent vasodilation more in the coronary and renal arteries than in other arteries of the rat

Cited by 27 publications

References 25 publications

Maintenance of Renal Vascular Reactivity Contributes to Acute Renal Failure during Endotoxemic Shock

Maintenance of Renal Vascular Reactivity Contributes to Acute Renal Failure during Endotoxemic Shock

Evaluation of vascular smooth muscle and corpus cavernosum on hypercholesterolemia. Is resveratrol promising on erectile dysfunction?

Thromboxane Receptor Mediates Renal Vasoconstriction and Contributes to Acute Renal Failure in Endotoxemic Mice

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