Various mechanisms have been postulated to be involved in angiotensin-(1-7)-induced endothelium-dependent vasodilation. Here, we characterized the vasodilator action of angiotensin-(1-7) in the isolated guinea pig heart. Angiotensin-(1-7) (1-10 nmol, bolus) induced dose-dependent increase in the coronary flow. The coronary vasodilation induced by angiotensin-(1-7) was significantly reduced by the nitric oxide synthase inhibitor, L-N(G)-nitroarginine methyl ester (L-NAME) (100 microM) and abolished by a B(2) receptor antagonist, icatibant (100 nM). Coronary vasodilation induced by bradykinin (3 pmol, bolus) was inhibited by L-NAME and icatibant to similar extent as that induced by angiotensin-(1-7). Neither the selective AT(2) angiotensin receptor antagonist, PD123319 (1 microM), nor the antagonist of a putative angiotensin-(1-7) receptors, [D-alanine-7]-angiotensin-(1-7) (A-779, 1 microM), influenced the response to angiotensin-(1-7). In conclusion, in the isolated guinea pig heart angiotensin-(1-7) induces coronary vasodilation that is mediated by endogenous bradykinin and subsequent stimulation of nitric oxide release through endothelial B(2) receptors. In contrast to other vascular beds, AT(2) angiotensin receptors and specific angiotensin-(1-7) receptors do not appear involved in angiotensin-(1-7)-induced coronary vasodilation in the isolated guinea pig heart.
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http://dx.doi.org/10.1111/j.1742-7843.2007.00057.x | DOI Listing |
J Cardiothorac Surg
January 2025
Department of Anesthesiology, Zibo Central Hospital, No.10 Shanghai Road, Zhangdian District, Zibo City, 255000, Shandong Province, China.
Objective: To investigate the therapeutic effect of levosimendan on hemodynamics in patients undergoing major cardiac surgery and presenting with acute postoperative heart failure.
Methods: The subjects of the study were 160 patients with severe cardiac conditions who underwent surgery and had acute heart failure. Eighty cases each were assigned to the research and control groups using a random number table.
Am J Physiol Heart Circ Physiol
January 2025
Department of Kinesiology & Applied Physiology, University of Delaware, Newark DE.
The endothelin-B receptor (ETR) mediates vasodilation in young women, an effect that is absent in postmenopausal women. We have previously demonstrated that ETR-mediated vasodilation is regulated by estradiol (E) in young women; however, the impact of E on ETR function in postmenopausal women remains unknown. Accordingly, the objective of this study was to test the hypothesis that E exposure restores ETR-mediated dilation in postmenopausal women.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Dipartimento di Biotecnologie e Scienze della Vita, ASST Sette Laghi, Università degli Studi dell'Insubria, 21100 Varese, Italy.
Hypertension exerts a profound impact on the microcirculation, causing both structural and functional alterations that contribute to systemic and organ-specific vascular damage. The microcirculation, comprising arterioles, capillaries, and venules with diameters smaller than 20 μm, plays a fundamental role in oxygen delivery, nutrient exchange, and maintaining tissue homeostasis. In the context of hypertension, microvascular remodeling and rarefaction result in reduced vessel density and elasticity, increasing vascular resistance and driving end-organ damage.
View Article and Find Full Text PDFMedicina (Kaunas)
November 2024
Department of Cardiothoracic Surgery, Weill Cornell Medicine, 1300 York Ave., New York, NY 10065, USA.
The saphenous vein graft (SVG) has been a cornerstone of coronary bypass surgery, but its long-term patency is limited by accelerated atherosclerosis. Recent advancements, including the no-touch technique and the use of SVG as a limb of the left internal thoracic artery (LITA), have shown promise in improving outcomes. Both approaches enhance nitric oxide (NO) availability, a key factor in promoting endothelial stability and arterial-like behavior in the SVG.
View Article and Find Full Text PDFHealthcare (Basel)
December 2024
Stichting Cardio Zorg, Kraayveld 5, 1171 JE Badhoevedorp, The Netherlands.
Introduction: Orthostatic intolerance is highly prevalent in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and is caused by an abnormal reduction in cerebral blood flow (CBF). In healthy controls (HCs), the regulation of CBF is complex and cardiac output (CO) is an important determinant of CBF: a review showed that a 30% reduction in CO results in a 10% reduction in CBF. In previous and separate ME/CFS studies, we showed that CO and CBF decreased to a similar extent during tilt testing.
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