A Pilot Study on the Effect of Angiotensin  Receptor Blockers on Platelet  Aggregation in Hypertensive Patients- A  Prospective Observational Study

Suresh, Arun; Sanji, Narendranath; Kamath, Pallavi Mahadeva; Devendrappa, Srinivas Lokikere; Hanumanthareddy, Shashikala Gowdara; Maniyar, Imran; Rudrappa, Suresh Surappla

doi:10.7860/jcdr/2016/21743.8881

Cited by 5 publications

(5 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Importantly, treatment with losartan significantly reduced the aggregation indicating that the AT1R antagonist provided anti-inflammatory protection in the model. Losartan has also been reported to prevent platelet aggregation in rats [54,58] and humans [59][60][61] and therefore our study gives further support to the antithrombotic influence of this agent and therapeutic potential beyond its classical blood pressure lowering action.…”

Section: Discussionsupporting

confidence: 73%

Endothelium-derived contraction in a model of rheumatoid arthritis is mediated via angiotensin II type 1 receptors

Hamilton

Dunning

Ferrell

et al. 2018

Vascular Pharmacology

View full text Add to dashboard Cite

A role for endothelium-derived constricting factors (EDCF), and the angiotensin II type 1 receptor (AT1R) pathway, in the vascular impairment found in the rat Freund's complete adjuvant (FCA)-model of rheumatoid arthritis (RA) was examined. FCA arthritis was induced in rats±losartan. Vehicle-treated rats served as controls. Knee-joint swelling and red blood cell (RBC) aggregation were measured as indicators of inflammation and endothelium reactivity assessed by response to acetylcholine (ACh) on aortic rings. Results show that knee-joint swelling and RBC aggregation were elevated in the FCA+vehicle group and restored to control levels in the FCA+losartan-treated animals. ACh-induced relaxation of aortic rings taken from FCA+vehicle animals was significantly impaired compared to vehicle-controls and this vasoreactivity was restored to control levels in the FCA+losartan-treated group. Further examination of aorta from the FCA+vehicle animals revealed an EDCF that was reliant on cyclooxygenase-2 (but not cyclooxygenase-1), generation of superoxide anion generation (but not hydrogen peroxide) and activation of thromboxane-prostanoid receptor. Losartan administration in vivo or ex vivo (to aortic rings) prevented the generation of the EDCF. In summary, this is the first evidence of an EDCF in a model of RA and identifies this mechanism as potentially significant in the cardiovascular disorder associated with the disease.

show abstract

Section: Discussionsupporting

confidence: 73%

Endothelium-derived contraction in a model of rheumatoid arthritis is mediated via angiotensin II type 1 receptors

Hamilton

Dunning

Ferrell

et al. 2018

Vascular Pharmacology

View full text Add to dashboard Cite

show abstract

“…This effect was associated with reduced levels of inflammatory biomarkers supporting the link between inflammation and blood pressure elevation. While we suspect this effect is attributed to the leukocytes, we cannot rule out a contribution of platelets as Psgl-1 has been shown to be expressed by platelets 34 and angiotensin receptor blockers have been shown to reduce platelet aggregation in hypertensive patients 35 . A neutralizing anti-Psgl-1 antibody was similarly effective in reducing the blood pressure response to Ang II highlighting a potential therapeutic application.…”

Section: Discussionmentioning

confidence: 92%

Angiotensin II-induced Hypertension is Reduced by Deficiency of P-selectin Glycoprotein Ligand-1

Wang

et al. 2018

Sci Rep

View full text Add to dashboard Cite

Identification of inflammatory mediators that regulate the vascular response to vasopressor molecules may aid in the development of novel therapeutic agents to treat or prevent hypertensive vascular diseases. Leukocytes have recently been shown to be capable of modifying blood pressure responses to vasopressor molecules. The purpose of this study was to test the hypothesis that deficiency of the leukocyte ligand, Psgl-1, would reduce the pressor response to angiotensin II (Ang II). Mice deficient in Psgl-1 (Psgl-1−/−) along with wild-type (WT) controls were treated for 2 weeks with a continuous infusion of Ang II. No differences in blood pressure between the groups were noted at baseline, however after 5 days of Ang II infusion, systolic blood pressures were higher in WT compared to Psgl-1−/− mice. The pressor response to acute administration of high dose Ang II was also attenuated in Psgl-1−/− compared to WT mice. Chimeric mice with hematopoietic deficiency of Psgl-1 similarly showed a reduced pressor response to Ang II. This effect was associated with reduced plasma interleukin-17 (IL-17) levels in Psgl-1−/− mice and the reduced pressor response was restored by administration of recombinant IL-17. In conclusion, hematopoietic deficiency of Psgl-1 attenuates Ang II-induced hypertension, an effect that may be mediated by reduced IL-17.

show abstract

“…Aldosterone antagonists, in addition to hyperkalemia can affect steroid hormone levels and lead to fertility problems ( 41 ). Angiotensin receptor blockers interact with platelet thromboxane A2/prostaglandin H2 (TXA2/PGH2) receptors prolonging bleeding time and decreasing platelet activity ( 42 ). Calcium channels blockers cause serum hypocalcemia and hypoglycemia ( 43 ).…”

Section: Effect Of Antihypertensive Therapy On Laboratory Resultsmentioning

confidence: 99%

Laboratory medicine in arterial hypertension

Aralica¹,

Smolčić

Honović³

et al. 2023

Biochemia Medica

View full text Add to dashboard Cite

In the initial diagnostics of arterial hypertension (AH) laboratory medicine is a cornerstone, along with a blood pressure (BP) measurement and an electrocardiogram. It mainly refers to routine blood and urine tests for diagnosis and monitoring primary hypertension and its associated conditions such as asymptomatic hypertension-mediated organ damage, chronic kidney disease and hypertensive disorders of pregnancy. In addition, long term non-fatal and fatal risks for cardiovascular (CV) events in hypertension are assessed based on clinical and laboratory data. Furthermore, laboratory medicine is involved in the management of hypertension, especially in monitoring the disease progression. However, antihypertensive drugs may interfere with laboratory test results. Diuretics, especially thiazides, can affect blood and urine sodium concentrations, or angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can affect the blood biomarkers of the renin-angiotensin-aldosterone system (RAAS). It’s dysfunction plays a critical role in primary aldosteronism (PA), the most common endocrine disorder in secondary hypertension, which accounts for only small proportion of AH in relative terms but substantial proportion of hypertensives in absolute terms, affecting younger population and carrying a higher risk of CV mortality and morbidity. When screening for PA, aldosterone-to-renin ratio still contributes massively to the increased incidence of the disease, despite certain limits. In conclusion, laboratory medicine is involved in the screening, diagnosis, monitoring and prognosis of hypertension. It is of great importance to understand the preanalytical and analytical factors influencing final laboratory result.

show abstract

A Pilot Study on the Effect of Angiotensin Receptor Blockers on Platelet Aggregation in Hypertensive Patients- A Prospective Observational Study

Cited by 5 publications

References 13 publications

Endothelium-derived contraction in a model of rheumatoid arthritis is mediated via angiotensin II type 1 receptors

Endothelium-derived contraction in a model of rheumatoid arthritis is mediated via angiotensin II type 1 receptors

Angiotensin II-induced Hypertension is Reduced by Deficiency of P-selectin Glycoprotein Ligand-1

Laboratory medicine in arterial hypertension

Contact Info

Product

Resources

About