Endothelin stimulates angiotensin I to angiotensin II conversion in cultured pulmonary artery endothelial cells

Kawaguchi, Hideaki; Sawa, Hirofumi; Yasuda, H.

doi:10.1016/0022-2828(90)90115-i

Cited by 100 publications

(43 citation statements)

References 18 publications

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“…ET has been suggested as the most potent vasoconstrictor in general and a potential spasmogen for blood vessels [10,11]. It has also been suggested that the sensitivity of smooth muscle to ET is both species and tissue specific [26][27][28] and that ET-1 may play an important role in regulating vascular tone by modulating the conversion of angiotensin I to angiotensin II [29]. At low dosages ET induces vasodilatation and at high dosages, vasoconstriction in resistance vessels of normal humans.…”

Section: Discussionmentioning

confidence: 99%

Interaction between endothelin and vasodilators in the human internal mammary artery.

He¹,

Yang²,

Mack³

et al. 1994

Brit J Clinical Pharma

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1. The internal mammary artery (IMA) is the primary choice as an arterial graft for coronary artery bypass surgery. Endothelin (ET) has been recently measured with an increased release after cardiopulmonary bypass for coronary artery bypass grafting. Threshold concentrations of ET‐1 have been found to amplify specifically contractions induced by noradrenaline and serotonin. This study was designed to investigate the effect of glyceryl trinitrate (GTN) and calcium antagonists on ET‐1 contraction in the human IMA. 2. Human IMA segments taken from 21 patients undergoing IMA‐coronary artery bypass grafting were mounted in an organ bath under the physiological pressure determined from their own length‐tension curves. Four ring segments were allocated into four groups. One served as a control and the others were treated with GTN (10, 100 nM, or 30 microM) for 5 min or nifedipine (20 or 200 nM, or 30 microM) for 25 min before concentration‐contraction curves to ET‐1 were established. In separate experiments, the concentration‐relaxation curves to GTN or nifedipine were established in the IMA rings precontracted with ET‐1 (10 nM). 3. Pretreatment of IMA with GTN for 5 min did not alter the ET‐1‐induced contraction. Pretreatment with 20 or 200 nM of nifedipine slightly but not significantly, altered the maximum contraction induced by ET‐1. Higher concentrations (30 microM) significantly reduced the maximum contraction force (P = 0.008). On the other hand, GTN caused 76.44 +/‐ 6.35% relaxation in ET‐1‐precontracted IMA. In contrast, the nifedipine‐induced relaxation was difficult to establish due to unsustained contraction to ET‐1.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 99%

Interaction between endothelin and vasodilators in the human internal mammary artery.

He¹,

Yang²,

Mack³

et al. 1994

Brit J Clinical Pharma

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“…Angiotensin augments ET-1 secretion and ET-1 stimulates the conversion of angiotensin I to angiotensin II. 42,43 Angiotensin-converting enzyme inhibitors block these effects and attenuate ET-1 production in vivo. 44 Possible mechanisms for the preservation of endothelial function by chronic endothelin receptor antagonists include many of the same mechanisms as those suggested for chronic angiotensin-converting enzyme inhibitors, including augmentation of nitric oxide.…”

Section: Best Et Al April 6 1999mentioning

confidence: 99%

Chronic Endothelin Receptor Antagonism Preserves Coronary Endothelial Function in Experimental Hypercholesterolemia

et al. 1999

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Background-Endothelin-1 (ET-1) is an endothelium-derived peptide that constricts coronary vessels through stimulation of the ET-A and ET-B receptors. Experimental porcine hypercholesterolemia is associated with impaired coronary endothelial function and elevated ET-1 concentrations. This study was designed to test the hypothesis that chronic endothelin receptor antagonism preserves coronary endothelial function in experimental hypercholesterolemia. Methods and Results-Acetylcholine (10 Ϫ6 to 10 Ϫ4 mol/L) was serially infused into the left anterior descending coronary artery in pigs at baseline and after 12 weeks of a high-cholesterol diet. In the interim, the animals were randomized to 3 groups: Group 1 received no therapy, group 2 received 3 mg/kg per day RO 48-5695, a combined ET-A/ET-B receptor antagonist, and group 3 received 4 mg/kg per day ABT-627, a selective ET-A receptor antagonist. Percent change in coronary artery diameter, coronary blood flow, and coronary vascular resistance were calculated on the basis of quantitative coronary angiography and intracoronary Doppler. At 12 weeks, total cholesterol was significantly and similarly increased in all groups. Chronic endothelin receptor antagonism significantly increased coronary blood flow in response to acetylcholine at 12 weeks (group 1: Ϫ41.6%Ϯ10.7%, group 2: Ϫ4.7%Ϯ11.9%, group 3: 11.4%Ϯ7.4%). Conclusions-Chronic

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“…Ang II infusion into rats increases aortic ET-1 content 3-fold, and this response is blocked by the AT 1 receptor antagonists losartan (d'Uscio et al, 1998). Conversely, ET-1 treatment of pulmonary endothelial cells stimulates the conversion of Ang I to Ang II (Kawaguchi et al, 1990). BQ-123 (a peptidic ET A receptor antagonist) shifted the Ang II-mediated contraction response curves of rabbit aortas to the right (Webb et al, 1992), and ET A receptor antagonism inhibits vasoconstriction due to Ang II (Wenzel et al, 2001).…”

mentioning

confidence: 99%

Novel Dual Action AT₁ and ET_A Receptor Antagonists Reduce Blood Pressure in Experimental Hypertension

Kowala¹,

Murugesan²,

Tellew³

et al. 2004

J Pharmacol Exp Ther

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Angiotensin II and endothelin-1 activate their respective AT 1 and ET A receptors on vascular smooth muscle cells, producing vasoconstriction, and both peptides are implicated in the pathogenesis of essential hypertension. Angiotensin II potentiates the production of endothelin, and conversely endothelin augments the synthesis of angiotensin II. Both AT 1 and ET A receptor antagonists lower blood pressure in hypertensive patients; thus, a combination AT 1 /ET A receptor antagonist may have greater efficacy and broader utility compared with each drug alone. By rational drug design a biphenyl ET A receptor blocker was modified to acquire AT 1 receptor antagonism. These compounds (C and D) decreased Sar-Ile-Angiotensin II binding to AT 1 receptors and endothelin-1 binding to ET A receptors, and compound C inhibited angiotensin II-and endothelin-1-mediated Ca 2ϩ transients. In rats compounds C and D reduced blood pressure elevations caused by intravenous infusion of angiotensin II or big endothelin-1. Compound C decreased blood pressure in Na ϩ -depleted spontaneously hypertensive rats and in rats with mineralocorticoid hypertension. Compound D was more efficacious than AT 1 receptor antagonists at reducing blood pressure in spontaneously hypertensive rats, and its superiority was likely due to its partial blockade of ET A receptors. Therefore compounds C and D are novel agents for treating a broad spectrum of patients with essential hypertension and other cardiovascular diseases.

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Endothelin stimulates angiotensin I to angiotensin II conversion in cultured pulmonary artery endothelial cells

Cited by 100 publications

References 18 publications

Interaction between endothelin and vasodilators in the human internal mammary artery.

Interaction between endothelin and vasodilators in the human internal mammary artery.

Chronic Endothelin Receptor Antagonism Preserves Coronary Endothelial Function in Experimental Hypercholesterolemia

Novel Dual Action AT₁ and ET_A Receptor Antagonists Reduce Blood Pressure in Experimental Hypertension

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Endothelin stimulates angiotensin I to angiotensin II conversion in cultured pulmonary artery endothelial cells

Cited by 100 publications

References 18 publications

Interaction between endothelin and vasodilators in the human internal mammary artery.

Interaction between endothelin and vasodilators in the human internal mammary artery.

Chronic Endothelin Receptor Antagonism Preserves Coronary Endothelial Function in Experimental Hypercholesterolemia

Novel Dual Action AT1 and ETA Receptor Antagonists Reduce Blood Pressure in Experimental Hypertension

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Novel Dual Action AT₁ and ET_A Receptor Antagonists Reduce Blood Pressure in Experimental Hypertension