Cerebral Blood Flow and Antihypertensive Treatment with Enalapril

Frei, Arthur; Müller-Brand, Jan

doi:10.1097/00004872-198606000-00018

Cited by 26 publications

(6 citation statements)

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“…This absence of effect on baseline cerebral blood flow has also been previously observed with cilazapril, 21 captopril, 30 -31 and enalapril. 32 In contrast, during seizures, vasodilation of the cerebral vasculature is maximal. 25 - 26 There is no more active vascular tone.…”

Section: Discussionmentioning

confidence: 99%

Effects of cilazapril on the cerebral circulation in spontaneously hypertensive rats.

1989

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Chronic hypertension is associated with a lower cerebral vascular reserve due to thickening of the media of cerebral vessels. The goal of the present study was to determine if long-term inhibition of angiotensin converting enzyme with cilazapril, a new long-acting angiotensin converting enzyme inhibitor, could improve cerebral vascular reserve. For this purpose, two groups of 12 spontaneously hypertensive rats were compared. One group was treated with 10 mg/kg/day cilazapril from 14 weeks to 33 weeks of age and was compared with a group treated with placebo. A third group of 12 Wistar-Kyoto rats treated with placebo was used as reference. At the end of the treatment period, cerebral vascular reserve was evaluated by measuring cerebral blood flow (radioactive microspheres) at rest and during maximal vasodilatlon induced by seizures provoked by bicuculline. Then, the rats were perfusion-fixed, and morphometry of the cerebral vasculature was performed. Cerebral vascular reserve was severely impaired in the spontaneously hypertensive rats since their maximal cerebral blood flow was decreased by 52% compared with the Wistar-Kyoto rats. Cilazapril normalized cerebral blood flow reserve. This normalization was associated with a decreased thickness of the medial layer in the carotid artery, the middle cerebral artery, and in the pial arteries larger than 100 fim. Further studies are required to determine whether this decreased medial thickness is due to the normalization of blood pressure induced by cilazapril or to the reduction of trophic factors such as angiotensin D. (Hypertension 1989;14:645-651) A rterial hypertension is associated with hyper-/ \ trophy of the medial layer of cerebral arter-.Z \ -ies and arterioles.1 -5 This vascular hypertrophy is responsible for a decrease of the cerebral blood flow reserve 6 -7 and for the fact that cerebral blood flow autoregulation occurs at higher than normal arterial pressures. 2 -3 It was believed that this vascular hypertrophy was secondary to hypertension. However, it has been shown recently that vascular hypertrophy appears in non-cerebral vessels before hypertension in spontaneously hypertensive rats (SHR) 8 -10 and is not influenced by a hypotensive treatment with hydralazine given before or after installation of hypertension. 11 Moreover, normalization of blood pressure in SHR with the combination of hydralazine, reserpine, and chlorothiazide did not completely reverse vascular hypertrophy in large pial

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Section: Discussionmentioning

confidence: 99%

Effects of cilazapril on the cerebral circulation in spontaneously hypertensive rats.

1989

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“…Two separate studies have examined the effect of prolonged treatment schedules on CBF. Enalapril administered daily (10-80 mg) 179S for 8 weeks to patients with chronic hypertension did not change CBF as measured by the intravenous xenon-133 method (Frei & Muller-Brand, 1986). Treatment with captopril for 7 days did not change CBF as measured by xenon-133 inhalation technique (Minematsu et al, 1987).…”

Section: Chronic Arterial Hypertensionmentioning

confidence: 92%

“…The effect of a single oral dose of captopril (25-50 mg) on CBF autoregulation was recently investigated in patients with chronic arterial hypertension as well as in normotensive volunteers (Waldemar et al, 1989c (Frei & Muller-Brand, 1986). Treatment with captopril for 7 days did not change CBF as measured by xenon-133 inhalation technique (Minematsu et al, 1987).…”

Section: Clinical Studies Chronic Arterial Hypertensionmentioning

confidence: 99%

Angiotensin converting enzyme inhibition and cerebral circulation‐a review.

Waldemar

Paulson

1989

Brit J Clinical Pharma

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1. The identification of a vascular wall renin angiotensin system and of angiotensin converting enzyme on the luminal surface of the endothelium in many tissues, including the brain, has stimulated research on the influence of the renin angiotensin system on regional blood flows. 2. In experimental studies inhibition of the angiotensin converting enzyme shifts the limits of cerebral blood flow autoregulation towards lower blood pressure values. 3. In patients with chronic arterial hypertension and in patients with chronic heart failure cerebral blood flow is not changed by acute or chronic angiotensin converting enzyme inhibition, despite in some cases pronounced reductions in the mean arterial blood pressure. Angiotensin converting enzyme inhibition does not change ischaemic regional cerebral blood flow in acute stroke. 4. It is concluded that following angiotensin converting inhibition cerebral blood flow is maintained at an unchanged level. The mechanism may include inhibition of locally produced angiotensin II leading to a selective dilation of larger cerebral arteries with a compensatory constriction of the smaller cerebral arteries.

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“…From a theoretical point of view, cerebral blood flow autoregulation makes the cerebral circulation independent from the underlying hemodynamic conditions. From a clinical point of view, it has been established in healthy volunteers (Waldemar et al, 1989;Schmidt et al, 1990) and in hypertensive patients (Frei and Muller-Brand, 1986;Minematsu et al, 1987;Waldemar et al, 1989) that ACEIs do not change cerebral blood flow. However, these data have been obtained by invasive (oxygen arterio-venous difference) or radioactive ('33Xe dynamic single-photon-emission-computerized-tomography) techniques which did not easily allow repeated measurements and hence the kinetic assessment of drugs' effects on cerebral blood flow.…”

Section: Discussionmentioning

confidence: 99%

“…It has been established, from experimental (Richer er al, 1986) as well as from clinical studies (Richer et ul, 1987;Bellissant et al, 1992) that the ACEIs-induced vasodilatation is inhomogeneous, preferentially affecting some vascular beds. For example, ACEIs increase the blood flows of the brachial artery Bellissant et al, 1992), and of the common carotid artery in healthy volunteers (Richer er al, 1987;DCmolis et al, 1992DCmolis et al, , 1993b and in hypertensive patients (Safar et al, 1986) but in contrast, they appear not to affect the baseline cerebral blood flow (Frei and Muller-Brand, 1986;Waldemar er al, 1989; al, 1990), as expected because of its autoregulation. However, the methods classically used for determination of cerebral hemodynamics are invasive (oxygen arteriovenous difference) or require the use of radioactive compounds ( '"'Xe clearance measurements) and thus they d o not easily allow repeated measurements.…”

Section: Introductionmentioning

confidence: 93%

Systemic, regional and cerebral hemodynamic effects of a new angiotensin converting enzyme inhibitor, imidapril, in healthy volunteers

Démolis

Annane

Duhaze

et al. 1994

Fundamemntal Clinical Pharma

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The effects of two single oral doses (5 mg and 20 mg) of a new angiotensin I-converting enzyme inhibitor, imidapril, on a) systemic hemodynamics (arterial pressure, heart rate, cardiac output), b) brachial and common carotid arteries' hemodynamics (diameter and blood flow, pulsed Doppler technique), c) cerebral hemodynamics (middle cerebral artery mean blood flow velocity, transcranial Doppler technique), and d) biological parameters (plasma converting enzyme activity, active plasma renin, plasma aldosterone, catecholamines, and atrial natriuretic factor) were investigated and compared with those of a placebo during the 24 h period following administration in a randomized, double-blind, cross-over study performed in six healthy volunteers. Imidapril induced a strong, dose-dependent and sustained inhibition of plasma converting enzyme activity and at the 20 mg an increase in active plasma renin. Other investigated biological parameters were not drug-affected. Imidapril, whatever the dose, did not significantly affect systemic hemodynamic parameters. Imidapril, 20 mg, significantly increased common carotid artery blood flow and diameter and brachial artery diameter. Brachial blood flow also tended to increase but this was not significant. The middle cerebral artery mean blood flow velocity investigated in only five volunteers, underwent spontaneous variations after placebo, and these variations were not affected by imidapril, suggesting that imidapril, whatever the dose, does not influence cerebral blood flow. Thus, imidapril's vasodilating properties apparently affect only the muscular (brachial artery) and cutaneous (external carotid artery) territories, but do not influence the cerebral vascular bed.

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Cerebral Blood Flow and Antihypertensive Treatment with Enalapril

Cited by 26 publications

References 0 publications

Effects of cilazapril on the cerebral circulation in spontaneously hypertensive rats.

Effects of cilazapril on the cerebral circulation in spontaneously hypertensive rats.

Angiotensin converting enzyme inhibition and cerebral circulation‐a review.

Systemic, regional and cerebral hemodynamic effects of a new angiotensin converting enzyme inhibitor, imidapril, in healthy volunteers

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