Essential hypertension is associated with impaired endothelium-dependent vasodilation caused by oxygen free radical-induced nitric oxide (NO) breakdown. Because calcium antagonists can improve endothelial function in patients with essential hypertension, in this study we tested the hypothesis that this beneficial effect could be related to restoration of NO availability by antioxidant properties. In 15 healthy subjects and 15 hypertensive patients, we studied forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (ACh; 0.15, 0.45, 1.5, 4.5, and 15 microg/100 mL per minute), an endothelium-dependent vasodilator in basal conditions, during infusion of N:(G)-monomethyl-L-arginine (L-NMMA, 100 microg/100 mL forearm tissue per minute), an NO-synthase inhibitor, vitamin C (8 mg/100 mL forearm tissue per minute), and finally, simultaneous infusion of L-NMMA and vitamin C. The response to sodium nitroprusside (SNP; 1, 2, and 4 microg/100 mL forearm tissue per minute) was also evaluated. In control subjects, vasodilation to ACh was inhibited by L-NMMA and not changed by vitamin C. In hypertensive patients, vasodilation to ACh was blunted as compared with control subjects and resistant to L-NMMA. Vitamin C, which decreased plasma isoprostanes and increased plasma antioxidant capacity, increased the response to ACh and restored the inhibiting effect of L-NMMA. In hypertensive patients, the study was repeated after 3-month treatment with nifedipine gastrointestinal therapeutic system (30 to 60 mg/daily). Nifedipine treatment decreased circulating plasma lipoperoxides and isoprostanes and increased plasma antioxidant capacity. Moreover, nifedipine increased the vasodilation to ACh but not to SNP and restored the inhibiting effect of L-NMMA on ACh-induced vasodilation, whereas vitamin C no longer exerted its facilitating activity. These results indicate that nifedipine increases endothelium-dependent vasodilation by restoring NO availability, an effect probably determined by antioxidant activity.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1161/01.hyp.37.3.943 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The Kidney Health Score: A Practical Guide to Early Detection of Kidney Disease Risk for Optimal Kidney Health.
Nephrol Nurs J
January 2025
Professor of Medicine, Department of Internal Medicine, Division of Nephrology, School of Medicine, Virginia Commonwealth University.
Chronic kidney disease (CKD) affects 10% of the global population, with increasing prevalence driven by diabetes, hypertension, and aging populations. CKD often progresses asymptomatically, frequently undetected until advanced stages, and may require costly treatments, such as dialysis or transplantation. CKD imposes a substantial financial burden on health care systems, with management costs rising sharply as the disease progresses, underscoring the need for early, cost-effective interventions.
View Article and Find Full Text PDFBackground: Prostaglandin E (PGE) in the rostral ventrolateral medulla (RVLM) has been recognized as a pivotal pressor substance in hypertension, yet understanding of its effects and origins in the RVLM remains largely elusive. This study aimed to elucidate the pivotal enzymes and molecular mechanisms underlying PGE synthesis induced by central Ang II (angiotensin II) and its implications in the heightened oxidative stress and sympathetic outflow in hypertension.
Methods And Results: RVLM microinjections of PGE and Tempol were administered in Wistar-Kyoto rats.
Deciphering the Role of Calcium Signaling Pathway-Associated Single Nucleotide Variants in Susceptibility to Hypertension.
J Clin Lab Anal
January 2025
Department of Clinical Biochemistry, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Background: As a complex disease, hypertension (HTN) is influenced by both genetic and environmental factors and their interaction. The calcium signaling pathway is known to be involved in the regulation of blood pressure, and dysfunction in this pathway may contribute to the development of hypertension. Genome-wide association studies (GWAS) have identified several genes in the calcium signaling pathway associated with susceptibility to HTN, including PLCB1, ATP2B1, and ADRB1.
View Article and Find Full Text PDFAn atrial septal defect (ASD) is a common congenital heart anomaly that results in irregular blood flow between the systemic and pulmonary circulations due to an opening in the atrial septum. Ostium secondum ASD accounts for a large proportion of these defects and often goes unnoticed during childhood and adolescence. Pulmonary hypertension (PH), affecting a significant number of patients with ostium secondum ASD, is associated with functional limitations, heart failure, and tachyarrhythmias.
View Article and Find Full Text PDFThe Role of Intravenous Selexipag in Managing PAH and Bridging Gaps in Oral Treatment: A Narrative Review.
Ther Clin Risk Manag
January 2025
Departments of Medicine and Cardiology, Westchester Medical Center and New York Medical College, Valhalla, NY, USA.
Pulmonary arterial hypertension (PAH) is a rare and potentially fatal condition characterized by progressive increases in blood pressure in the arteries of the lungs. Oral selexipag, approved by the Food and Drug Administration (FDA) in 2015 for the treatment of PAH, targets prostacyclin receptors on pulmonary arterial vascular smooth muscle and endothelial cells to improve blood flow through the lungs and reduce pulmonary vascular resistance. Oral selexipag is effective, but may be discontinued due to factors like side effects, emergency conditions, or inability to take oral medication, potentially leading to severe adverse events, such as rebound pulmonary hypertension and right heart failure.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!