Endothelin stimulated by angiotensin II augments contractility of spontaneously hypertensive rat resistance arteries.

Dohi, Yasuaki; Hahn, Alfred W.A.; Boulanger, Chantal; Bühler, Fritz R.; Lüscher, Thomas F.

doi:10.1161/01.hyp.19.2.131

Cited by 250 publications

(117 citation statements)

References 32 publications

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“…37 In cultured endothelial cells, Ang II may increase the release of ET-1. 38 In the present study, significant increased systemic venous levels of ACE activities were found in psychogenic and organogenic ED subgroups compared to controls. In addition, the cavernosal level of ACE activity was significantly higher in diabetic compared to psychogenic ED patients.…”

Section: Vasoactive Mediators and Erectile Dsyfunction E A Hamed Et Alsupporting

confidence: 57%

Role of some vasoactive mediators in patients with erectile dysfunction: their relationship with angiotensin-converting enzyme and growth hormone

et al. 2003

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The imbalance between vasoconstrictors and vasodilators may play an important role in the pathogenesis of erectile dysfunction (ED). A total of 36 patients with ED, organogenic [diabetic (n ¼ 12) and nondiabetic (n ¼ 12)] and psychogenic (n ¼ 12) etiology, and 12 healthy adult men as controls were included. The levels of endothelin-1 (ET-1), growth hormone (GH), angiotensinconverting enzyme activity (ACE), nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) were determined in the flaccid penis cavernosal blood of patients and in cubital blood of patients and controls. In psychogenic ED, systemic ACE activity was elevated compared to controls (Po0.05). In diabetic and nondiabetic ED patients, systemic levels of ET-1 (Po0.0001 for both) and ACE activity (Po0.01 and o0.05) were higher while GH (Po0.0001 and o0.001), NO (Po0.0001 for both) and cGMP (Po0.01 for both) levels were lower compared to controls. In diabetic patients, systemic and cavernosal ET-1 levels (Po0.0001 for both) and cavernosal ACE activity levels (Po0.05) were significantly elevated while systemic and cavernosal NO (Po0.0001 for both) and GH (o0.001 and o0.05) levels were declined compared to psychogenic. In nondiabetic patients, systemic and cavernosal ET-1 levels (Po0.0001 for both) were significantly elevated while systemic and cavernosal NO (Po0.0001 for both) and systemic GH levels (Po0.05) were declined compared to psychogenic. Systemic NO was positively correlated with GH in psychogenic (r ¼ 0.616, Po0.05), diabetic (r ¼ 0.583, Po0.05) and nondiabetic (r ¼ 0.615, Po0.05) patients and correlated positively with cGMP (r ¼ 0.605, Po0.05) but negatively with ACE activities (r ¼ À0.585, Po0.05) in diabetic patients. In conclusion, plasma levels of ET-1, ACE activities are elevated and associated with reduction of GH, NO and cGMP levels in the systemic and cavernous blood of ED patients. This disturbance may indicate endothelial dysfunction that may hind at their significance in the pathophysiology of ED.

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Section: Vasoactive Mediators and Erectile Dsyfunction E A Hamed Et Alsupporting

confidence: 57%

Role of some vasoactive mediators in patients with erectile dysfunction: their relationship with angiotensin-converting enzyme and growth hormone

et al. 2003

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“…Pastore et al 14 demonstrated increased expression and plasma levels of cell adhesion molecule ICAM-1 with intravenous angiotensin II infusion. Furthermore, angiotensin II have been shown to stimulate production of endothelin-1 16 and plasminogen-activator inhibitor-1 17 in vivo. Increased ICAM-1 levels have recently been reported in patients with coronary artery disease and were regarded as an independent risk factor of myocardial infarction in patients with coronary artery disease 18 and in healthy males.…”

Section: Discussionmentioning

confidence: 99%

Circulating intercellular cell adhesion molecule-1, endothelin-1 and von Willebrand factor-markers of endothelial dysfunction in uncomplicated essential hypertension: the effect of treatment with ACE inhibitors

et al. 2002

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The aim of the study was to examine whether the circulating cell adhesion molecules, von Willebrand factor (vWf) and endothelin-1, are elevated in patients with essential hypertension with no other risk factors for atherosclerosis and thus may serve as a markers of endothelial dysfunction in uncomplicated hypertension. Furthermore, the effect of treatment with the ACE inhibitor, quinapril, on levels of endothelial dysfunction markers were studied. The levels of adhesion molecules (intercellular cell adhesion molecule-1 [ICAM-1], E-selectin, P-selectin), von Wilebrand factor (vWf) and endothelin-1 were measured in patients with hypertension without any other risk factors of atherosclerosis before and after treatment with quinapril (n = 22) and in normotensive controls (n = 22). Compared with normotensive subjects, the hypertensive patients had significantly higher levels of ICAM-1 (238 vs 208 ng/ml, P = 0.02), vWf (119 vs 105 IU/dl, P Ͻ 0.05) and endothelin-1 (5.76 vs 5.14 fmol/ml, P Ͻ 0.05). Three-month treatment of hyper-

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“…Moreover, there is a positive correlation between ET-1 plasma level and systolic blood pressure in humans, 9 and the vascular production of ET-1 under angiotensin II (Ang II) stimulation is higher in hypertensive than in normotensive rats. 10 The amplification is nevertheless blocked by Ca 2+ entry blocker in human arteries 4 and in the rat mesenteric bed. 6 In contrast, the direct effect of ET-1 is relatively insensitive to Ca 2+ entry blockers.…”

Section: Camentioning

confidence: 97%

Potentiation of norepinephrine-induced contractions by endothelin-1 in the rabbit aorta.

Henrion

Laher

1993

Hypertension

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Subthreshold concentrations of endothelin-1 potentiated the norepinephrine-induced contraction in isometrically mounted rings of the rabbit aorta. Pretreatment with endothelin-1 (0.1 nM) for 10 minutes increased the sensitivity of the aortic rings to norepinephrine without affecting the maximal contraction. This amplification was unaffected by removal of the endothelium but was prevented by the protein kinase C inhibitors staurosporine (0.01 (iM) and calphostin C (0.1 fiM). Pretreatment of the aortic rings for 24 hours with phorbol 12-myristate 13-acetate (0.1 fiM) also abolished the potentiation. Norepinephrineinduced contraction was potentiated by pretreating with phorbol 12-myristate 13-acetate (10 nM) and by increasing the concentration of K + in the bath solution from 4.6 to 8.6 mM. The potentiation of the norepinephrine-induced contraction by endothelin-1 (0.1 nM) or by phorbol 12-myristate 13-acetate (10 nM) was not associated with an increase in norepinephrine-induced 45 Ca 2+ uptake or influx, whereas the potentiation due to an increase in the concentration of K + in the bath solution from 4.6 to 8.6 mM was associated with an increase in norepinephrine-induced 45 Ca 2+ uptake. We conclude that endothelin-1 potentiation of the norepinephrine-induced contraction occurs in the absence of changes in stimulated Ca 2+ entry and is endothelium independent. It is probable that endothelin-1 increases the sensitivity of the contractile apparatus to Ca 2+ by activating protein kinase C-dependent mechanisms. produced by endothelial cells. 1 Its direct contractile effect has been widely studied, although it is not yet completely understood.2 On the other hand, subthreshold concentrations of ET-1, compatible with the plasma level, 3 potentiate the contractile effect of different agonists such as norepinephrine in human arteries 4 and rat mesenteric beds 5 -6 and serotonin in rat aortic rings 7 and pulmonary arteries. 8 Such a phenomenon might have a pathological importance since it could be involved in hypertension and vasospastic syndrome.4 Indeed, the potentiation of serotonininduced contractions by ET-1 might increase the vasospasms induced by aggregating platelets. Moreover, there is a positive correlation between ET-1 plasma level and systolic blood pressure in humans, 9 and the vascular production of ET-1 under angiotensin II (Ang II) stimulation is higher in hypertensive than in normotensive rats. 10 The amplification is nevertheless blocked by Ca 2+ entry blocker in human arteries 4 and in the rat mesenteric bed. 6 In contrast, the direct effect of ET-1 is relatively insensitive to Ca 2+ entry blockers.

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Endothelin stimulated by angiotensin II augments contractility of spontaneously hypertensive rat resistance arteries.

Cited by 250 publications

References 32 publications

Role of some vasoactive mediators in patients with erectile dysfunction: their relationship with angiotensin-converting enzyme and growth hormone

Role of some vasoactive mediators in patients with erectile dysfunction: their relationship with angiotensin-converting enzyme and growth hormone

Circulating intercellular cell adhesion molecule-1, endothelin-1 and von Willebrand factor-markers of endothelial dysfunction in uncomplicated essential hypertension: the effect of treatment with ACE inhibitors

Potentiation of norepinephrine-induced contractions by endothelin-1 in the rabbit aorta.

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