Endothelin-1 Reduces Microvascular Fluid Permeability through Secondary Release of Prostacyclin in Cat Skeletal Muscle

Bentzer, Peter; Holbeck, Staffan; Grände, Per‐Olof

doi:10.1006/mvre.2001.2365

Cited by 13 publications

(16 citation statements)

References 30 publications

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“…With this technique the whole microvascular bed was exposed to the same increase in transcapillary pressure. The validity of the CFC technique when used in combination with the present experimental approach, including the fact that the CFC determinations were always made during constant arterial pressure and vascular resistance to eliminate blood volume effects in the volume registration, has been confirmed in several studies [17, 21, 22, 23]. Thus, it has been shown that the CFC technique can also be used for evaluation of hydraulic permeability when the surface area is altered during the experiment, a conclusion based on the results that CFC was not influenced by vasoconstrictors or vasodilators, nor by microocclusion with microspheres [21, 22].…”

Section: Methodsmentioning

confidence: 84%

“…Thus, it has been shown that the CFC technique can also be used for evaluation of hydraulic permeability when the surface area is altered during the experiment, a conclusion based on the results that CFC was not influenced by vasoconstrictors or vasodilators, nor by microocclusion with microspheres [21, 22]. As mentioned, the initial blood volume effects have passed at the time of CFC measurement 3 min after the transmural pressure change, as confirmed both at normal [21]and at a change in vascular tone [23]. More arguments specifically confirming the validity of the technique during muscle exercise are presented in the discussion section.…”

Section: Methodsmentioning

confidence: 99%

“…With this technique, all capillaries in the organ are exposed to an equally large, strictly defined and evenly distributed [33]decrease in interstitial hydrostatic pressure along their whole length, which is not the case with the venous pressure technique [21]. CFC should not be measured until the blood volume component is completed (see Methods), which has occurred 2.5–3 min after the pressure change [21, 23]. This means that, in studies where CFC was measured at an earlier time point, there may have been an overestimation of CFC [1, 31, 34].…”

Section: Discussionmentioning

confidence: 99%

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Endogenous Nitric Oxide Reduces Microvascular Permeability and Tissue Oedema during Exercise in Cat Skeletal Muscle

Persson

Ekelund²,

Grände

2003

J Vasc Res

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Based on a proposed increase in the release of the vasodilators nitric oxide (NO) and prostacyclin during exercise, and the fact that these substances have vascular permeability-reducing properties, this study was designed to evaluate (1) possible effects of exercise on hydraulic permeability, (2) whether permeability and muscle swelling are reduced by an increased release of NO and prostacyclin during exercise and (3) whether NO and prostacyclin are involved in exercise hyperaemia. The study was performed on an autoperfused cat calf muscle preparation with ligated lymph vessels, and exercise was induced by somatomotor nerve stimulation. Change in microvascular hydraulic permeability was estimated by a capillary filtration coefficient (CFC) technique. We found that the marked muscle volume increase after the start of the exercise gradually decreased, reaching an isovolumetric state within 25 min where CFC had decreased by about 25% (p < 0.05). CFC recovered completely after exercise was stopped. The decrease in CFC was abolished during blockade of endogenous NO by the NO synthase inhibitor L-NAME, but was preserved during blockade of endogenous prostacyclin by tranylcypromine. The muscle volume increase during exercise was about 60% greater with L-NAME than during vehicle or tranylcypromine (p < 0.01). Neither L-NAME nor tranylcypromine had any effect on exercise hyperaemia. We conclude that microvascular hydraulic permeability is reduced during exercise, that this effect reduces exercise-induced muscle swelling, and that the effects are mediated via release of NO. NO and prostacyclin are not involved in exercise hyperaemia.

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Section: Methodsmentioning

confidence: 84%

Section: Methodsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Endogenous Nitric Oxide Reduces Microvascular Permeability and Tissue Oedema during Exercise in Cat Skeletal Muscle

Persson

Ekelund²,

Grände

2003

J Vasc Res

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“…Both ET-1 and PGI 2 are endothelial-derived vasoactive mediators. ET-1 is a 21-amino acid peptide synthesized by endothelial cells,(5) and PGI 2 is an eicosanoid synthesized from arachadonic acid by vascular endothelial cells and vascular smooth muscle. (6) The pharmacologically stable prostacyclin analogue, iloprost, has been used clinically as a vasodilator to treat pulmonary hypertension and Raynaud’s phenomenon, as well as to decrease platelet aggregation.…”

Section: Introductionmentioning

confidence: 99%

“…(6, 7) Previous studies have shown that ET-1 and PGI 2 are involved in maintaining endothelial barrier integrity and decreasing microvascular hydraulic permeability. (5, 8–10) In addition, ET-1 may exert its permeability-decreasing effect by stimulating PGI 2 production. (5, 8) Since PGI 2 release appears to be involved in the microvascular permeability-decreasing action of ET-1, (5, 8) PGI 2 may also be able to prevent increases in microvascular permeability due to inflammatory mediators.…”

Section: Introductionmentioning

confidence: 99%

Endothelin 1 and Prostacyclin Attenuate Increases in Hydraulic Permeability Caused by Platelet-Activating Factor in Rats

Cureton

Chong²,

Kwan³

et al. 2010

Shock

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We have previously documented that endothelin-1 (ET-1) and prostacyclin (PGI2) decrease basal state hydraulic permeability (Lp). The aim of this study was to investigate the ability of ET-1 and PGI2 to modulate trans-endothelial fluid flux during situations in which Lp was artificially elevated with platelet activating factor (PAF). We hypothesized that ET-1 and PGI2 administration before PAF exposure would prevent the increase in Lp secondary to PAF. Additionally, in a potentially more clinically relevant situation, we also hypothesized that ET-1 and PGI2 administration after PAF exposure would attenuate the increase in Lp secondary to PAF. Microvascular Lp was measured in rat mesenteric post-capillary venules. Exposure to 10 nM PAF increased Lp 4-fold (p<0.001). If the administration of 80 pM ET-1 or 10 μM PGI2 was completed prior to PAF exposure, no PAF-associated increase in Lp was observed (p<0.001). The administration of ET-1 or PGI2 after PAF exposure attenuated the peak increase in Lp due to PAF alone by 55% and 57%, respectively (p<0.001). We conclude that ET-1 and PGI2 administration prior to PAF exposure prevents PAF-induced elevations in Lp, and in a more clinically relevant situation, ET-1 and PGI2 administered after PAF exposure attenuates the PAF-induced increase in Lp. ET-1 and PGI2 receptors may provide important therapeutic targets for decreasing the microvascular fluid leak-associated morbidity resulting from shock and sepsis.

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Receptor‐Mediated Events in the Microcirculation

Watts¹,

Kanagy²,

Lombard³

2008

Comprehensive Physiology

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Endothelin-1 Reduces Microvascular Fluid Permeability through Secondary Release of Prostacyclin in Cat Skeletal Muscle

Cited by 13 publications

References 30 publications

Endogenous Nitric Oxide Reduces Microvascular Permeability and Tissue Oedema during Exercise in Cat Skeletal Muscle

Endogenous Nitric Oxide Reduces Microvascular Permeability and Tissue Oedema during Exercise in Cat Skeletal Muscle

Endothelin 1 and Prostacyclin Attenuate Increases in Hydraulic Permeability Caused by Platelet-Activating Factor in Rats

Receptor‐Mediated Events in the Microcirculation

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