Effects of Aspirin on Endothelial Function and Hypertension

Dzeshka, Mikhail S.; Shantsila, Alena; Lip, Gregory Y.H.

doi:10.1007/s11906-016-0688-8

Cited by 40 publications

(35 citation statements)

References 125 publications

(137 reference statements)

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“…We speculate that the observed effect could be mediated by an increase in NO production. Aspirin has been shown to prevent NO degradation and acetylate and activate the endothelial NO synthase (eNOS), leading to an increase in NO availability . We cannot conclude that this is the case in our study, but we consider it to be possible.…”

Section: Discussioncontrasting

confidence: 88%

Differential vascular effects of aspirin in people with Type 2 diabetes without cardiovascular disease and matched controls without diabetes

Vernstrøm¹,

Laugesen²,

Grove

et al. 2019

Diabet. Med.

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Aim We investigated whether the effect of low‐dose aspirin on endothelium‐dependent vasodilation and arterial stiffness in people with Type 2 diabetes is different from a matched control group. We examined acute and chronic effects, and effects over the 24h dosing interval. Methods In an open‐label parallel group intervention study, we included 21 participants with Type 2 diabetes and 21 age‐ and sex‐matched controls. Endothelium‐dependent vasodilation was assessed as the reactive hyperaemia index (lnRHI) measured by peripheral arterial tonometry (EndoPAT®). Arterial stiffness was assessed as pulse wave velocity (PWV) measured by applanation tonometry (SphygmoCor®). Measurements were performed prior to aspirin intake and 1h after aspirin administration (75 mg). Participants were then treated for 6 days, and measurements were repeated at 24 h and 1 h after aspirin intake. Results Baseline lnRHI did not differ between groups. The controls had an immediate increase in lnRHI after the first aspirin tablet. This was not observed in participants with diabetes (difference between groups; P < 0.05). After 1 week, both groups demonstrated increased lnRHI compared with baseline (P < 0.01). In participants with diabetes, lnRHI was significantly lower 24 h after aspirin administration compared with 1 h after administration (P < 0.05). This difference was not observed in controls (P = 0.84, difference between groups; P = 0.12). The effect on PWV did not differ between groups. Conclusion Aspirin had a reduced immediate effect on endothelium‐dependent vasodilation in participants with diabetes. Both groups had improved endothelial function after 1 week of treatment. Further, the effect of aspirin on endothelial function may be declining during a 24 h dosing interval in people with Type 2 diabetes. (Clinical Trial Registry No: 2016‐000515‐32)

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Section: Discussioncontrasting

confidence: 88%

Differential vascular effects of aspirin in people with Type 2 diabetes without cardiovascular disease and matched controls without diabetes

Vernstrøm¹,

Laugesen²,

Grove

et al. 2019

Diabet. Med.

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show abstract

“…Indeed, we found an association between endothelial dysfunction and diabetes mellitus. However, we found no association between dysfunctional endothelium and other cardiovascular comorbidities or aspirin, a medication considered to influence endothelial function [34]. This is surprising and could point to a technical fault, yet, the RHI measured for patients with arterial hypertension (RHI = 1.8 ± 0.7) was similar to that reported by Weisrock et al (RHI = 1.7 ± 0.4 to 1.8 ± 0.4) [35].…”

Section: Discussionsupporting

confidence: 54%

Endothelial dysfunction is not a predictor of outcome in chronic obstructive pulmonary disease

et al. 2020

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Background: Local airway inflammation may cause systemic changes which result in endothelial dysfunction. Only a few studies have used reactive hyperemia peripheral arterial tonometry (RH-PAT) in patients with chronic obstructive pulmonary disease (COPD) in order to measure their endothelial dysfunction. Objective: To determine the efficacy of endothelial dysfunction, measured by RH-PAT, in assessing disease severity and systemic burden in a cohort of COPD patients. Methods: In this prospective, monocentric study, 157 patients with moderate to very severe COPD (GOLD class II-IV) were examined for endothelial dysfunction using RH-PAT (Itamar medical Ltd., Caesarea, Israel). In a nestedcohort, examination was repeated at exacerbation. The association between reactive hyperemia index (RHI), augmentation index (AI) and disease severity and outcome parameters was analysed. Results: 57% of the COPD patients had a dysfunctional endothelium and the median (IQR) RHI was 1.42 (1.27-1.53). Exacerbation of COPD was not associated with a significant change in RHI (p = 0.625) or ΑΙ (p = 0.530). None of the diagnostic or clinical outcomes of COPD was associated with RHI or arterial stiffness. Conclusion: Endothelial dysfunction is common in COPD. However, it does not seem to be a predictor neither of disease severity, nor of outcome and does not change during exacerbations of the disease.

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“…43,44 Therefore, the above adverse effects of EP3 and TP associated with IP-mediated activity need to be taken into consideration when PGI 2 and its analogues or some COX inhibitors, for example, aspirin, are clinically used in cardiovascular diseases based on the traditional effect of endothelial PGI 2 production. [45][46][47][48] We noted that in TP −/− /EP3 −/− mice the increase of MAP after L-NAME was higher than in WT counterparts. This could result from undefined compensatory mechanisms due to loss of two vasoconstrictor receptors; however, the exact underling mecahnism(s) still remains to be investigated.…”

Section: Discussionmentioning

confidence: 76%

Differential properties of E prostanoid receptor‐3 and thromboxane prostanoid receptor in activation by prostacyclin to evoke vasoconstrictor response in the mouse renal vasculature

et al. 2020

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Vasomotor reactions of prostacyclin (prostaglandin I 2 ; PGI 2) can be collectively modulated by thromboxane prostanoid receptor (TP), E-prostanoid receptor-3 (EP3), and the vasodilator I prostanoid receptor (IP). This study aimed to determine the direct effect of PGI 2 on renal arteries and/or the whole renal vasculature and how each of these receptors is involved. Experiments were performed on vessels or perfused kidneys of wild-type mice and/or mice with deficiency in TP (TP −/−) and/ or EP3. Here we show that PGI 2 did not evoke relaxation, but instead resulted in contraction of main renal arteries (from ~0.001-0.01 µM) or reduction of flow in perfused kidneys (from ~1 µM); either of them was reversed into a dilator response in TP −/− /EP3 −/− counterparts. Also, we found that in renal arteries although it has a lesser effect than TP −/− on the maximal contraction to PGI 2 (10 µM), EP3 −/− but not TP −/− resulted in relaxation to the prostanoid at 0.01-1 µM. Meanwhile, TP −/− only significantly reduced the contractile activity evoked by PGI 2 at ≥0.1 µM. These results demonstrate that PGI 2 may evoke an overall vasoconstrictor response in the mouse renal vasculature, reflecting activities of TP and EP3 outweighing that of the vasodilator IP. Also, our results suggest that EP3, on which PGI 2 can have a potency similar to that on IP, plays a major role in the vasoconstrictor effect of the prostanoid of low concentrations (≤1 µM), while TP, on which PGI 2 has a lower potency but higher efficacy, accounts for a larger part of its maximal contractile activity.

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Effects of Aspirin on Endothelial Function and Hypertension

Cited by 40 publications

References 125 publications

Differential vascular effects of aspirin in people with Type 2 diabetes without cardiovascular disease and matched controls without diabetes

Differential vascular effects of aspirin in people with Type 2 diabetes without cardiovascular disease and matched controls without diabetes

Endothelial dysfunction is not a predictor of outcome in chronic obstructive pulmonary disease

Differential properties of E prostanoid receptor‐3 and thromboxane prostanoid receptor in activation by prostacyclin to evoke vasoconstrictor response in the mouse renal vasculature

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