Impact of serum alkaline phosphatase level on coronary collateral circulation

Karabulut, Ahmet; Şahin, İrfan; Avcı, İlhan İlker; Okuyan, Ertuğrul; Doğan, Zeki; Uzunlar, Bülent; Satılmış, Seçkin

doi:10.5603/kp.a2014.0114

Cited by 5 publications

(7 citation statements)

References 21 publications

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“…A more recent report by Perticone and colleagues described a significant inverse relationship between TNAP and endothelium-dependent vasodilation, 15 and Karabulut and coworkers reported that TNAP levels are associated with an inadequate coronary collateral circulation. 16 Although the studies cited above suggest a role for TNAP in the vasculature, whether TNAP actually regulates vascular responses to vasoconstrictors is an open, and important, question.…”

Section: Introductionmentioning

confidence: 99%

Alkaline Phosphatase Activity Is a Key Determinant of Vascular Responsiveness to Norepinephrine

et al. 2020

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Here, we tested the hypothesis that TNAP (tissue nonspecific alkaline phosphatase) modulates vascular responsiveness to norepinephrine. In the isolated, Tyrode’s-perfused rat mesentery, 50 µmol/L of L-p-bromotetramisole (L-p-BT; selective TNAP inhibitor, Ki=56 µmol/L) significantly reduced TNAP activity and caused a significant 9.0-fold rightward-shift in the norepinephrine concentration versus vasoconstriction relationship. At 100 µmol/L, L-p- BT further reduced mesenteric TNAP activity and caused an additional significant right-shift of the norepinephrine concentration versus vasoconstriction relationship. A higher concentration (200 µmol/L) of L-p-BT had no further effect on either mesenteric TNAP activity or norepinephrine-induced vasoconstriction. L-p-BT did not alter vascular responses to vasopressin, thus ruling-out nonspecific suppression of vascular reactivity. Since in the rat mesenteric vasculature α 1 -adrenoceptors mediate norepinephrine-induced vasoconstriction, these finding indicate that TNAP inhibition selectively interferes with α 1 -adrenoceptor signaling. Additional experiments showed that the effects of TNAP inhibition on norepinephrine-induced vasoconstriction were not mediated by accumulation of pyrophosphate or ATP (TNAP substrates) nor by reduced adenosine levels (TNAP product). TNAP inhibition significantly reduced the Hillslope of the norepinephrine concentration versus vasoconstriction relationship from 1.8±0.2 (consistent with positive cooperativity of α 1 -adrenoceptor signaling) to 1.0±0.1 (no cooperativity). Selective activation of A1-adenosine receptors, which are known to participate in coincident signaling with α 1 -adrenoceptors, reversed the suppressive effects of L-p-BT on norepinephrine-induced vasoconstriction. In vivo, L-p-BT administration achieved plasma levels of .60 µmol/L and inhibited mesenteric vascular responses to exogenous norepinephrine and sympathetic nerve stimulation. TNAP modulates vascular responses to norepinephrine likely by affecting positive cooperativity of α 1 -adrenoceptor signaling via a mechanism involving A1 receptor signaling.

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Section: Introductionmentioning

confidence: 99%

Alkaline Phosphatase Activity Is a Key Determinant of Vascular Responsiveness to Norepinephrine

et al. 2020

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“…58 High ALP concentrations predicted lack of coronary collateral circulation, isolating a population particularly vulnerable to complications of MI. 56 Apart from the general population of patients with MI, ALP and OPN can be used for stratification of critical, high-risk subgroups. Alkaline phosphatase, in synergy with the GFR, could predict survival in male patients with diabetes after MI.…”

Section: Alkaline Phosphatasementioning

confidence: 99%

“…58 High ALP concentrations predicted lack of coronary collateral circulation, isolating a population particularly vulnerable to complications of MI. 56…”

Section: Introductionmentioning

confidence: 99%

The Emerging Role of Bone Markers in Diagnosis and Risk Stratification of Patients With Coronary Artery Disease

et al. 2019

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Molecules that govern bone metabolism, such as osteoprotegerin (OPG) and osteopontin (OPN), have been isolated from other tissues, including blood vessels. Atherosclerosis and coronary artery disease (CAD) are leading causes of mortality worldwide. Despite novel biochemical and imaging techniques, early detection of CAD is still unsatisfactory. Experimental data indicate that bone turnover markers (BTMs) contribute to the development of atherosclerosis. This finding has sparked interest in their clinical use. This narrative review analyzed information from >50 human studies, which strongly suggest that OPG, OPN, and alkaline phosphatase (ALP) serum concentrations are altered in patients with CAD. Osteoprotegerin seems to be more useful for the detection of early disease, while OPN and ALP are recruited in vessels after the establishment of disease. Osteocalcin may be used as a flow cytometry marker for endothelial progenitor cells and can constitute a marker to monitor response to interventional treatments and risk of restenosis. However, most data derive from observational studies. Incorporation of BTMs in multifactorial computational algorithms could further determine their role in CAD diagnosis and prognosis together with other imaging techniques and biochemical markers.

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“…Abnormal AP has been associated with many of the risk factors leading to stroke, including heavy drinking (Ebuehi and Asonye 2007;Shimizu et al 2013a), obesity (Menahan et al 1985;Golik et al 1991), and hypertension (Shimizu et al 2013b). Elevated AP has been shown to correlate with poor functional outcome and mortality in cardiovascular disease (Park et al 2013;Wannamethee et al 2013;Karabulut et al 2014;Kunutsor et al 2014) and in stroke patients (Ryu et al 2010;Kim et al 2013;Tan et al 2016). Investigators theorize that the negative association between AP levels and stroke outcome may be linked to the fact that increased AP levels are associated with increased inflammation and enhanced vascular calcification leading to atherosclerosis (Tonelli et al 2009;Kim et al 2013;Ryu et al 2014).…”

Section: Alkaline Phosphatase As a Diagnostic And Prognostic Stroke Biomarkermentioning

confidence: 99%

Alkaline phosphatase: a potential biomarker for stroke and implications for treatment

Brichacek

Brown

2018

Metab Brain Dis

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Stroke is the fifth leading cause of death in the U.S., with more than 100,000 deaths annually. There are a multitude of risks associated with stroke, including aging, cardiovascular disease, hypertension, Alzheimer's disease (AD), and immune suppression. One of the many challenges, which has so far proven to be unsuccessful, is the identification of a cost-effective diagnostic or prognostic biomarker for stroke. Alkaline phosphatase (AP), an enzyme first discovered in the 1920s, has been evaluated as a potential biomarker in many disorders, including many of the comorbidities associated with stroke. This review will examine the basic biology of AP, and its most common isoenzyme, tissue nonspecific alkaline phosphatase (TNAP), with a specific focus on the central nervous system. It examines the preclinical and clinical evidence which supports a potential role for AP in stroke and suggest potential mechanism(s) of action for AP isoenzymes in stroke. Lastly, the review speculates on the clinical utility of AP isoenzymes as potential blood biomarkers for stroke or as AP-targeted treatments for stroke patients.

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Impact of serum alkaline phosphatase level on coronary collateral circulation

Abstract: Serum ALP is a widely avaliable unfavourable prognostic parameter in coronary heart disease. Elevated ALP levels were associated with inadequate CCC, which supports the previously reported literature concerning the negative prognostic value of ALP levels in cardiovascular settings.

Cited by 5 publications

References 21 publications

Alkaline Phosphatase Activity Is a Key Determinant of Vascular Responsiveness to Norepinephrine

Alkaline Phosphatase Activity Is a Key Determinant of Vascular Responsiveness to Norepinephrine

The Emerging Role of Bone Markers in Diagnosis and Risk Stratification of Patients With Coronary Artery Disease

Alkaline phosphatase: a potential biomarker for stroke and implications for treatment

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