Effects of angiotensin converting enzyme inhibition on endothelial vasodilator function in primary human hypertension

Kiowski, Wolfgang; Linder, Lilly; Nüesch, Reto; Martina, Benedict

doi:10.1093/eurheartj/14.suppl_c.5

Cited by 12 publications

(9 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Patients in that study were being treated with a variety of antihypertensive medications, and most were not taking an ACE inhibitor. Our findings are also consistent with a preliminary report by Kiowski et al, 37 who reported that long-term treatment with the ACE inhibitor perindopril did not affect endothelium-dependent vasodilation of forearm resistance vessels of hypertensive patients. The findings, however, appear to conflict with those of Hirooka et al, 21 who reported that administration of a single dose of captopril, but not nifedipine, improved endothelium-dependent vasodilation in forearm resistance vessels of hypertensive patients.…”

Section: Effect Of Antihypertensive Treatmentsupporting

confidence: 94%

Effect of captopril and enalapril on endothelial function in hypertensive patients.

1994

View full text Add to dashboard Cite

Endothelium-dependent vasodilation is impaired in patients with essential hypertension. The objective of this study was to determine whether long-term treatment with angiotensin-converting enzyme inhibitors improves endothelium-dependent vasodilation in forearm resistance vessels of patients with hypertension. Furthermore, since tissue thiols may be relevant to nitric oxide-mediated vasodilation, we queried whether an angiotensin-converting enzyme inhibitor with a sulf hydryl group preferentially augments endotheliumdependent vasodilation in these individuals. The study included 24 patients with essential hypertension (mean age, 45±2 years) and 20 normotensive subjects (mean age, 47±1 years). Methacholine chloride (0.3 to 10 jtg/min) was infused via the brachial artery to assess endothelium-dependent vasodilation in forearm resistance vessels. Nitroglycerin (1 to 30 /ig/min) was administered to evaluate endothelium-independent vasodilation. Forearm blood flow was determined by venous occlusion strain-gauge plethysmography. Forearm vascular function studies were performed in hypertensive patients before and 7 to 8 weeks after randomization to either captopril or enalapril, angiotensin-converting enzyme inhibitors with and without a sulf hydryl moiety, respectively. Normotensive subjects were studied on only one occasion. Before treatment, the forearm vasodilative response to methacholine was atten-T he endothelium synthesizes a variety of vasoactive substances that regulate vascular tone, including the endothelium-derived relaxing factor (EDRF) nitric oxide.

show abstract

Section: Effect Of Antihypertensive Treatmentsupporting

confidence: 94%

Effect of captopril and enalapril on endothelial function in hypertensive patients.

1994

View full text Add to dashboard Cite

show abstract

“…This has been observed in the abdominal aorta, carotid arteries or mesenteric vessels after treatment with hydralazine or reversal of the hypertensive stimulus. However, most of the human studies in which endothelial function has been assessed before and after normalization of hypertension with conventional therapy have not shown an improvement in the endothelial-dependent responses [12,28,29,31]. It seems, therefore, that endothelial dysfunction in human hypertension, once established, is more difficult to reverse than in the rat.…”

Section: Discussionmentioning

confidence: 99%

“…A fundamental question which remains unanswered is whether endothelial dysfunction in hypertension, if indeed present, is a cause or consequence of the condition. Whereas studies in hypercholesterolaemia have shown the reversal of endothelial dysfunction with effective treatment [26,27], this has not been consistently demonstrated in hypertension [11,12,[28][29][30][31]. The study of individuals who, although clinically normal, are at increased genetic risk for hypertension offers an alternative approach which avoids any confounding effects of treatment.…”

Section: Introductionmentioning

confidence: 99%

Basal nitric oxide production is impaired in offspring of patients with essential hypertension

et al. 1999

View full text Add to dashboard Cite

There is considerable evidence that endothelium-dependent nitric oxide (NO)-mediated vasodilatation in response to acetylcholine is impaired in essential hypertension, whereas the endothelium-independent response to sodium nitroprusside is normal. More limited data have suggested that there is also reduced vasoconstriction in response to N(G)-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of basal NO release. As it is not known whether endothelial dysfunction in hypertension, if indeed present, is a cause or consequence of the condition, we have studied the normotensive offspring of parents with essential hypertension. Both basal and stimulated vascular responses were examined in 12 normotensive offspring [mean age (+/-S.E.M.) 26.1+/-1.4 years] of parents with essential hypertension and compared with those in 12 age-matched offspring (mean age 25.6+/-1.1 years) of normotensive subjects. Forearm blood flow was measured simultaneously in both arms by venous occlusion plethysmography, both at baseline and during intra-arterial brachial infusion of increasing doses of acetylcholine, sodium nitroprusside, noradrenaline and L-NMMA. There were no significant differences between the groups in the responses to acetylcholine, sodium nitroprusside or noradrenaline. In contrast, the vasoconstrictor response to L-NMMA was significantly blunted in the offspring of hypertensive parents compared with that in the offspring of normotensive parents (P=0.005). Thus endothelial dysfunction, as demonstrated by impaired basal production of NO, is present in subjects at high risk of essential hypertension, and does not occur simply as a consequence of the condition.

show abstract

“…Evaluation of the forearm blood flow (FBF) response to intra-arterial infusion of vasodilator agents by venous occlusion plethysmography is the most widely used method in the study of EDV in the peripheral circulation in humans [50][51][52][53][54][55][56][57][58][59][60][61][62][63][64].…”

Section: Human Forearm Modelmentioning

confidence: 99%

“…The defect response to L-NMMA observed in essential hypertensive patients has been found to be reversed by antihypertensive treatment [156], but one controlled randomized trial [157], two open treatment studies [158,159] and one observational study [160] failed to show that antihypertensive treatment improves EDV. However, four recently published studies showed that the ACE-inhibitors captopril [64] and lisinopril [161], as well as the Ca-channel blockers nifedipine [96] and lacidipine [162] improved EDV during long-term use, while no beneficial effect was seen with atenolol [96].…”

Section: Human Hypertensionmentioning

confidence: 99%

Endothelium-dependent Vasodilation in Hypertension: A Review

Lind

Granstam²,

Millgård³

2000

Blood Pressure

View full text Add to dashboard Cite

Using both in vitro and in vivo techniques, it has repeatedly been shown that endothelium-dependent vasodilation (EDV) is impaired in different forms of experimental hypertension (SHR, Dahl salt-sensitive rat, DOCA-salt rat and renovascular hypertension). EDV has also been found to be impaired in primary, as well as in secondary forms of human hypertension. Although impaired EDV is a general finding in hypertension, the pathophysiological mechanisms might differ between different forms of hypertension and between different types of vessels and vascular beds. Impaired activity of nitric oxide synthase, increased release of endothelin-1, increased production of a prostanoid-derived contracting factor, decreased generation of endothelium-derived hyperpolarizing factor/s and impairment caused by superoxide ions have all been shown to contribute to the impairment of EDV during different conditions. While most antihypertensive treatments improve EDV in experimental hypertension, no uniform picture has been seen in human hypertension, possibly because different antihypertensive drugs have different direct actions on EDV. This review shows that while impaired EDV has been found to be a general feature of hypertension, the mechanisms involved and the therapeutic opportunities have still to be established.

show abstract

Effects of angiotensin converting enzyme inhibition on endothelial vasodilator function in primary human hypertension

Abstract: KEY WORDS: Angiotensin-converting enzyme inhibition, cilazapril, endothelium, acetylcholine, forearm blood flow, hypertension

Cited by 12 publications

References 11 publications

Effect of captopril and enalapril on endothelial function in hypertensive patients.

Effect of captopril and enalapril on endothelial function in hypertensive patients.

Basal nitric oxide production is impaired in offspring of patients with essential hypertension

Endothelium-dependent Vasodilation in Hypertension: A Review

Contact Info

Product

Resources

About