A sensitive radioimmunoassay measuring endothelin-like immunoreactivity in human plasma: Comparison of levels in patients with essential hypertension and normotensive control subjects

Davenport, Anthony P.; Ashby, Michael; Easton, Patricia; Ella, Sarah; Bedford, Joy; Dickerson, Claire; Nunez, Derek J.; Capper, S. J.; Brown, Morris J.

doi:10.1042/cs0780261

Cited by 192 publications

(69 citation statements)

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“…In situ hybridization with antisense ET-1 mRNA revealed increased ET-1 mRNA expression in the resistance vessels of subjects with essential hypertension. 28 In keeping with this finding, some investigators, 13,18 but not others, 29,30 have found elevated plasma ET-1 levels in subjects with hypertension. However, the majority of ET-1 is released abluminally, and increased production might not raise plasma levels substantially.…”

Section: Increased Endogenous Et-1 Activity In Hypertensionmentioning

confidence: 73%

Endothelin-1 and Vascular Tone in Subjects With Atherogenic Risk Factors

et al. 2003

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Abstract-Endothelin-1 (ET-1) is a potent vasoconstrictor that increases vascular tone in the resistance vessels of subjects with hypertension. It is unclear whether endogenous ET-1 affects resistance-vessel function equally in patients with other cardiovascular risk factors. Vasoconstriction to ET-1 is mediated principally via the endothelin-A (ET A ) receptor on vascular smooth muscle cells. Accordingly, we used an ET A -specific antagonist, BQ-123, to test the hypothesis that endogenous ET-1 increases vascular resistance selectively in subjects with hypertension compared with other risk factors. BQ-123 was infused at 100 nmol/min for 80 minutes into the brachial artery of 10 subjects with hypertension (meanϮSEM arterial pressure, 106Ϯ5 mm Hg), 12 subjects with hypercholesterolemia (meanϮSEM total cholesterol, 7.1Ϯ0.2 mmol/L), 10 active smokers (meanϮSEM, 42Ϯ11 pack-years), and 11 healthy, age-matched individuals. ET-1 levels are elevated in patients with atherosclerosis, 10 and atherosclerotic coronary lesions exhibit enhanced ET-1-mediated vascular tone. 11,12 Risk factors for atherosclerosis are also associated with elevated plasma ET-1 levels. [13][14][15][16][17][18][19] Several studies have found that endogenous ET-1 causes vasoconstriction in the resistance vessels of subjects with hypertension. 20 -22 One group has reported that ET-1 also contributes to vascular tone in subjects with hypercholesterolemia, 23 and there are conflicting reports regarding the response to ET-1 blockade in diabetic individuals. 24,25 There have been no studies evaluating the role of endogenous ET-1 in cigarette smokers. There has also been a difference of opinion regarding the effect of ET-1 on vascular resistance in healthy individuals. 4,7,20,22,23 The fact that these observations come from several different laboratories makes it difficult to gauge whether ET-1 contributes to vascular tone equally among the various cardiac risk factors.To evaluate the relative contribution of ET-1 to vasomotor dysfunction in patients with atherogenic risk factors, we performed a single, comparative study with an ET A -selective antagonist, , to compare the activity of endogenous ET-1 in the forearm resistance vessels of subjects with hypertension, hypercholesterolemia, and cigarette smokers, relative to healthy volunteers. Methods Subject SelectionThe study population consisted of 10 subjects with hypertension (systolic blood pressure Ͼ140 mm Hg or diastolic blood pressure Ͼ90 mm Hg), 12 subjects with hypercholesterolemia (fasting cholesterol Ͼ75th percentile for age and gender), 10 active cigarette smokers (average of Ն1 pack/d for Ն3 years), and 11 healthy, age-matched controls. Subjects were recruited by advertisement in local newspapers and provided written, informed consent. Subjects were screened by history, physical examination, and routine biochemical analyses. Subjects with risk factors were excluded if they

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Section: Increased Endogenous Et-1 Activity In Hypertensionmentioning

confidence: 73%

Endothelin-1 and Vascular Tone in Subjects With Atherogenic Risk Factors

et al. 2003

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“…ET-1 is mainly released albuminally from the endothelium towards the underlying smooth muscle, and it is rapidly cleared from the circulation. In arterial hypertension high-to-low circulating values of ET-1 have been reported, 15,29,30 probably due to different methods of assay and different normal range, wideness of the population studied as well as different criteria of enrolment employed. Therefore, it is clear that there are a few difficulties in interpreting the significance of plasma ET-1 concentrations.…”

Section: Discussionmentioning

confidence: 99%

Comparison of tumour necrosis factor and endothelin-1 between essential and renal hypertensive patients

et al. 1998

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The present study was performed to compare circulating levels of tumour necrosis factor-␣ (TNF␣) and plasma endothelin 1 (ET-1), of hypertensive patients with or without renal failure and with those of normotensive healthy subjects. The study population consisted of 21 healthy normotensive subjects and 22 hypertensive patients, 11 with essential hypertension, and 11 with hypertension and chronic renal failure (CRF).Plasma ET-1 levels, serum TNF␣ and creatinine, creatinine clearance, 24-h urinary albumin excretion (UAE) were assayed, and 24-h blood pressure monitoring was obtained in all subjects. Office blood pressure was similar between hypertensive patients with and without CRF. However, 24-h blood pressure was greater in patients with CRF than in those with essential hypertension and

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“…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.…”

Section: Camentioning

confidence: 99%

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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A sensitive radioimmunoassay measuring endothelin-like immunoreactivity in human plasma: Comparison of levels in patients with essential hypertension and normotensive control subjects

Cited by 192 publications

References 0 publications

Endothelin-1 and Vascular Tone in Subjects With Atherogenic Risk Factors

Endothelin-1 and Vascular Tone in Subjects With Atherogenic Risk Factors

Comparison of tumour necrosis factor and endothelin-1 between essential and renal hypertensive patients

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

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