Involvement of Endogenous Endothelin-1 in Exercise-Induced Redistribution of Tissue Blood Flow

Maeda, Seiji; Miyauchi, Takashi; Iemitsu, Motoyuki; Tanabe, Takumi; Irukayama-Tomobe, Yoko; Goto, Katsutoshi; Yamaguchi, Iwao; Matsuda, Mitsuo

doi:10.1161/01.cir.0000038362.16740.a2

Cited by 42 publications

(58 citation statements)

References 7 publications

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“…In endothelin receptor knockout mice, it was demonstrated that only ET A mediate ET-1-induced contractions of arteries of the gastric fundus [20]. ET A blockade with TA-0201 has been shown to improve the microcirculatory blood flow in the gastric mucosa of rats during treadmill running [21]. Anti-ulcer properties were also found for the ET A and ET B antagonist bosentan in indomethacin and water immersion-restrained stress rats [22].…”

Section: Discussionmentioning

confidence: 99%

Vasopressin Aggravates Cardiopulmonary Bypass-Induced Gastric Mucosal Ischemia

Bomberg

Bierbach²,

Flache³

et al. 2014

Eur Surg Res

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Background/Aim: Upper gastrointestinal bleeding (UGIB) is one of the most frequent gastrointestinal complications after cardiac surgery with cardiopulmonary bypass (CPB). Endothelin expression and microcirculatory dysfunction have been shown to be involved in UGIB. The aim of this study was to analyze the effect of vasopressin during CPB on the gastric mucosal microcirculation and the involvement of the endothelin system. Methods: Eighteen pigs were randomized into three groups (n = 6 each): group I = sham, group II = CPB (1-hour CPB) and group III = CPB + vasopressin (1-hour CPB and vasopressin administration during CPB to maintain baseline arterial pressure). All animals were observed for a further 90 min after termination of CPB. Systemic hemodynamics as well as blood flow and oxygen saturation of the gastric mucosa were measured continuously. At the end of the experiment, the gastric mucosal expressions of endothelin-1 (ET-1) and its receptor subtypes A (ET_A) and B (ET_B) were determined by polymerase chain reaction. Gastric mucosal injury, apoptotic cell death and leukocytic infiltration were determined by histology and immunohistochemical analyses of cleaved caspase-3 and myeloperoxidase. Results: CPB decreased gastric microvascular perfusion, which was associated with an increased expression of ET-1 and ET_A. Vasopressin aggravated the CPB-associated malperfusion, whereas it completely abrogated the upregulation of ET-1 and ET_A. Interestingly, vasopressin did not induce gastric mucosal morphologic injury, leukocytic infiltration or apoptotic cell death. Conclusion: Vasopressin aggravates CPB-associated microvascular malperfusion of the gastric mucosa but does not induce gastric mucosal injury.

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Section: Discussionmentioning

confidence: 99%

Vasopressin Aggravates Cardiopulmonary Bypass-Induced Gastric Mucosal Ischemia

Bomberg

Bierbach²,

Flache³

et al. 2014

Eur Surg Res

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“…In addition, endothelin-1 release may be stimulated by insulin, and may be involved in maintaining vasomotor tone at rest and during insulin stimulation [4,7]. Endothelin-1 is also thought to be involved in the redistribution of flow seen during exercise, causing con-striction in the gut and non-working muscles [8,9]. Although plasma endothelin-1 has a short half-life of approximately 3.6 min [10] and is cleared rapidly from circulation by the pulmonary, splanchnic and renal systems, endothelin-1 has long-lasting and potent vasoconstrictor effects [11].…”

Section: Introductionmentioning

confidence: 99%

Acute blockade by endothelin-1 of haemodynamic insulin action in rats

et al. 2006

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Aims/hypothesis Plasma levels of endothelin-1 are frequently elevated in patients with hypertension, obesity and type 2 diabetes. We hypothesise that this vasoconstrictor may prevent full perfusion of muscle, thereby limiting delivery of insulin and glucose and contributing to insulin resistance. Materials and methods The acute effects of endothelin-1 on insulin-mediated haemodynamic and metabolic effects were examined in rats in vivo. Endothelin-1 (50 pmol min −1 kg −1 for 2.5 h) was infused alone, or 30 min prior to a hyperinsulinaemic-euglycaemic insulin clamp (10 mU min −1 kg −1 for 2 h). Insulin clamps (10 or 15 mU min −1 kg −1 ) were performed after 30 min of saline infusion. Results Endothelin-1 infusion alone increased plasma endothelin-1 11-fold (p<0.05) and blood pressure by 20% (p<0.05). Endothelin-1 alone had no effect on femoral blood flow, capillary recruitment or glucose uptake, but endothelin-1 with 10 mU min −1 kg −1 insulin caused a decrease in insulin clearance from 0.35±0.6 to 0.19± 0.02 ml/min (p=0.02), resulting in significantly higher plasma insulin levels (10 mU min −1 kg −1 insulin: 2,120± 190 pmol/l; endothelin-1+10 mU min −1 kg −1 insulin: 4,740± 910 pmol/l), equivalent to 15 mU min −1 kg −1 insulin alone (4,920±190 pmol/l). The stimulatory effects of equivalent doses of insulin on femoral blood flow, capillary recruitment and glucose uptake were blocked by endothelin-1.Conclusions/interpretation Endothelin-1 blocks insulin's haemodynamic effects, particularly capillary recruitment, and is associated with decreased muscle glucose uptake and glucose infusion rate. These findings suggest that elevated endothelin-1 levels may contribute to insulin resistance of muscle by increasing vascular resistance and limiting insulin and glucose delivery.

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“…KC is considered a precancerous stage of cancer [14][15][16]. Renal blood flow is reported to decrease to 20% during exercise, returning to a resting state after exercise [24]. This is similar to ischemiareperfusion and may increase generation of ROS after exercise [24].…”

Section: Discussionmentioning

confidence: 99%

Effect of habitual exercise on renal carcinogenesis by ferric nitrilotriacetate

Kato

Kawaguchi

Miyoshi

et al. 2010

Environ Health Prev Med

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Objectives We investigated whether habitual exercise (HE) (treadmill running) suppresses development of renal cell carcinoma (RCC) induced by ferric nitrilotriacetate (Fe-NTA). Methods Male Fischer 344 rats were divided into six groups: group I, saline treatment (12 weeks = initiation period) and non-HE; group II, Fe-NTA treatment (12 weeks) and non-HE; group III, saline treatment and short-term (12 weeks) HE; group IV, Fe-NTA treatment and short-term HE; group V, saline treatment and long-term (40 weeks) HE; and group VI, Fe-NTA treatment and long-term HE. Saline treatment groups did not develop RCC, therefore we investigated the effects of HE among Fe-NTA treatment groups.Results Gross nodules (diagnosed as RCC), RCC represented by microcarcinomas (Mcs), karyomegalic cells (KCs), and degenerative tubules (DTs) were seen in rats treated with Fe-NTA. The number of Mcs, KCs, and DTs were increased in the short-term HE group when compared with those in the non-HE group, but were decreased in the long-term HE group when compared with those in the short-term HE group. Conclusions Short-term (initiation period) HE promoted renal carcinogenesis induced by Fe-NTA; however, longterm HE after the initiation period suppressed the promoted carcinogenesis.

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Involvement of Endogenous Endothelin-1 in Exercise-Induced Redistribution of Tissue Blood Flow

Cited by 42 publications

References 7 publications

Vasopressin Aggravates Cardiopulmonary Bypass-Induced Gastric Mucosal Ischemia

Vasopressin Aggravates Cardiopulmonary Bypass-Induced Gastric Mucosal Ischemia

Acute blockade by endothelin-1 of haemodynamic insulin action in rats

Effect of habitual exercise on renal carcinogenesis by ferric nitrilotriacetate

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