Effect of the Ace Inhibitor Ceronapril on Cerebral Blood flow in Hypertensive Patients

Cutler, Neal R.; Sramek, John J.; Luna, A; Mena, Ismaël; Brass, Eric P.; Kurtz, Neil M.; Brennan, John J.; Dalmady-Israel, Christina; Vanier, Marie-Claude

doi:10.1177/106002809603000601

Cited by 7 publications

(9 citation statements)

References 16 publications

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“…two opposing effects will occur. This may be why oral ACE inhibition did not alter cerebral blood flow in one study [41], but lowered cerebral blood flow in another [42]. In an evaluation of regional blood flow in heart failure, calf blood flow showed a slight but non-significant increase with ACE inhibition.…”

Section: Discussionmentioning

confidence: 85%

Lisinopril improves endothelial function in chronic cigarette smokers

2001

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Cigarette smoking is a pernicious risk factor for the pathogenesis of coronary artery disease, and endothelial dysfunction is an important antecedent event in this process. This is important, as cigarette smoke is directly toxic to endothelial cells. Inhibitors of angiotensin-converting enzyme (ACE) have been shown to improve endothelial function in diabetes and hypercholesterolaemia, and are a promising option in smokers. We treated 23 subjects (age 38+/-12 years; mean+/-S.D.) for 8 weeks with 20 mg of lisinopril in a randomized controlled trial. Endothelial function was assessed by measurement of forearm blood flow responses to intra-arterial infusions of endothelial-dependent and -independent vasodilators and an endothelial-dependent vasoconstrictor [acetylcholine, sodium nitroprusside and monomethyl-L-arginine (L-NMMA) respectively] using venous occlusion plethysmography. Lisinopril significantly increased the forearm blood flow response to acetylcholine by 20% [lisinopril, 3.12+/-0.37 (mean+/-S.E.M.); placebo, 2.58+/-0.25; P=0.02, 95% confidence intervals (CI) 0.09, 1.06] (values given are ratios of flow in the infused arm to that in the control arm); there was no effect on the response to sodium nitroprusside (lisinopril, 3.97+/-0.40; placebo, 3.92+/-0.39; P=0.84; 95% CI -0.50, 0.61). The vasoconstrictor response to L-NMMA demonstrated a significant improvement (lisinopril, 0.77+/-0.06; placebo, 0.95+/-0.05; P<0.001; 95% CI -0.09, -0.27). In conclusion, these results indicate that ACE inhibition can improve endothelial function in cigarette smokers. We show that lisinopril improves both receptor-mediated and tonic NO release. The mechanism could be either that lisinopril limits the angiotensin II-induced production of superoxide radicals which would normally inactivate NO, or that lisinopril may increase bradykinin-mediated NO release.

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Section: Discussionmentioning

confidence: 85%

Lisinopril improves endothelial function in chronic cigarette smokers

2001

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“…Only one study showed a significant decrease in global CBF after treatment with ceronapril for 9 weeks. 41 In contrast, 5 studies showed a significant increase in global CBF with chronic AHT. 34 , 35 , 42 , 45 , 49 Of these, 3 studies investigated the effect of AHT over time in one intervention group.…”

Section: Resultsmentioning

confidence: 92%

“…Thirty studies included participants with hypertension. 27–54,56,57 Six studies included participants with dementia or MCI. 26,27,29,31,54,55 Fifteen studies used a calcium channel blocker, 26,29,31,32,34,36,38,39,43,44,47,48,52,55,57 but our data also included angiotensin receptor blockers, 27,31,36,49,50 diuretics, 27,28,36,38–40,42,51,52 angiotensin-converting enzyme inhibitors, 27,30,36,37,41,42,44,53,54,56 β blockers, 28,30,37,45,46,48 and α blockers.…”

Section: Resultsmentioning

confidence: 99%

“…27–54,56,57 Six studies included participants with dementia or MCI. 26,27,29,31,54,55 Fifteen studies used a calcium channel blocker, 26,29,31,32,34,36,38,39,43,44,47,48,52,55,57 but our data also included angiotensin receptor blockers, 27,31,36,49,50 diuretics, 27,28,36,38–40,42,51,52 angiotensin-converting enzyme inhibitors, 27,30,36,37,41,42,44,53,54,56 β blockers, 28,30,37,45,46,48 and α blockers. 36,44,48 Measurement techniques for CBF were 133-Xenon inhalation technique, 28,33,37–39,44–46,53,56 arterial spin labeling, 26,35,36 single photon emission computed tomography, 29,31,32,40,42,49,51,52,54 transcranial Doppler, 26,27,48,57 and PET.…”

Section: Resultsmentioning

confidence: 99%

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Effect of Antihypertensive Treatment on Cerebral Blood Flow in Older Adults: a Systematic Review and Meta-Analysis

et al. 2022

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Background: In older age, the benefits of antihypertensive treatment (AHT) become less evident, with greater associated risk. Of particular concern is compromising cerebral blood flow (CBF), especially in those with cognitive impairment. Methods: We created a synthesis of the published evidence by searching multiple electronic databases from 1970 to May 2021. Included studies had participants with mean age ≥50 years, hypertension and cognitive impairment, and assessed CBF before and after initiating AHT. Two authors independently determined eligibility and extracted data. Study quality was assessed using The Risk of Bias in Nonrandomized Studies of Interventions tool. We summarized study characteristics (qualitative synthesis) and performed random-effects meta-analyses (quantitative synthesis). Results: Thirty-two studies (total n=1306) were included, of which 23 were eligible for meta-analysis. In line with the qualitative synthesis, the meta-analysis indicated no effect of AHT initiation on CBF (standardized mean difference, 0.08 [95% CI, −0.07 to 0.22]; P =0.31, I 2 =42%). This was consistent across subgroups of acute versus chronic AHT, drug class, study design, and CBF measurement. Subgroups by age demonstrated an increase in CBF after AHT in those aged >70 years (standardized mean difference, 4.15 [95% CI, 0.16–8.15]; P =0.04, I 2 =42%), but not in those aged 50 to 65 and 65 to 70 years (standardized mean difference, 0.18 [95% CI,−2.02 to 2.38]; P =0.87, I 2 =49%; standardized mean difference, 1.22 [95% CI, −0.45 to 2.88]; P =0.15, I 2 =68%). Overall, risk of bias was moderate-to-high and quality of evidence (Grading of Recommendations Assessment, Development and Evaluation) was very low, reflecting the observational nature of the data. Conclusions: Accepting the observed limitations, current evidence does not suggest a harmful effect of AHT on CBF. Concerns over CBF should not preclude treatment of hypertension.

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“…However, only a few studies have directly investigated the cerebral perfusion status in patients with AH (6)(7)(8)(9)(10). Moreover, the efficacy of antihypertensive therapy to prevent vascular dementia in AH patients merits study in its own right.…”

Section: Introductionmentioning

confidence: 99%