High dietary salt enhances acute depressor responses to metformin

Muntzel, Martin S.; Nyeduala, Benjamin; Barrett, Shean

doi:10.1016/s0895-7061(99)00119-3

Cited by 6 publications

(5 citation statements)

References 19 publications

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“…Clinical studies on the effects of metformin on blood pressure (BP) have shown various findings from decreased to unaltered BP [2, 3]. Metformin has also been reported to lower BP in spontaneously hypertensive rats (SHR) [4]. The protective effect on BP in nondiabetic hypertensives is unclear.…”

Section: Introductionmentioning

confidence: 99%

Metformin prevents vascular damage in hypertension through the AMPK/ER stress pathway

et al. 2019

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Metformin is an antidiabetic drug. However, the pleiotropic beneficial effects of metformin in nondiabetic models still need to be defined. The objective of this study is to investigate the effect of metformin on angiotensin II (Ang II)-induced hypertension and cardiovascular diseases. Mice were infused with Ang II (400 ng/kg per min) with or without metformin for 2 weeks. Mice infused with angiotensin II displayed an increase in blood pressure associated with enhanced vascular endoplasmic reticulum (ER) stress markers, which were blunted after metformin treatment. Moreover, hypertension-induced reduction in phosphorylated AMPK, endothelial nitric oxide synthase (eNOs) phosphorylation, and endothelium-dependent relaxation (EDR) in mesenteric resistance arteries (MRA) were rescued after metformin treatment. Infusion of ER stress inducer (tunicamycin, Tun) in control mice induced ER stress in MRA and reduced phosphorylation of AMPK, eNOS synthase phosphorylation, and EDR in MRA without affecting systolic blood pressure (SBP). All these factors were reversed subsequently with metformin treatment. ER stress inhibition by metformin improves vascular function in hypertension. Therefore, metformin could be a potential therapy for cardiovascular diseases in hypertension independent of its effects on diabetes.

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Section: Introductionmentioning

confidence: 99%

Metformin prevents vascular damage in hypertension through the AMPK/ER stress pathway

et al. 2019

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“…Insulin sensitizers were described to lead to NO enhancement, reduce oxidative stress and alterations in vascular smooth muscle cells, and inhibit the α-adrenergic tone in patients with diabetes mellitus [ 22 , 30 – 33 ]. In type-2 diabetes patients, metformin was shown to have an impact on the mesenteric artery by suppressing prostanoids and improving vascular resistance in animal studies [ 31 ].…”

Section: Introductionmentioning

confidence: 99%

Statins, metformin, and RAS inhibitors did not reduce variceal bleeding risk and mortality in a large, real-life cohort of patients with cirrhosis

Pfisterer,

Schwarz,

Schwarz

et al. 2024

PLoS ONE

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Background Previous experimental and clinical studies suggested a beneficial effect of statins, metformin, angiotensin-converting-enzyme inhibitors and angiotensin II receptor blockers (RASi) on portal hypertension. Still, their effects on hard cirrhosis-related clinical endpoints, such as variceal bleeding and bleeding-related mortality, remain to be investigated. Methods Thus, we recorded the use of statins, metformin and RASi in a large cohort of cirrhotic patients undergoing endoscopic band ligation (EBL) for primary (PP, n = 440) and secondary bleeding prophylaxis (SP, n = 480) between 01/2000 and 05/2020. Variceal (re-) bleeding and survival rates were compared between patients with vs. without these co-medications. Results A total of 920 cirrhotic patients with varices were included. At first EBL, median MELD was 13 and 515 (56%) patients showed ascites. Statins, metformin and RASi were used by 49 (5.3%), 74 (8%), and 91 (9.9%) patients, respectively. MELD and platelet counts were similar in patients with and without the co-medications of interest. Rates of first variceal bleeding and variceal rebleeding at 2 years were 5.2% and 11.7%, respectively. Neither of the co-medications were associated with decreased first bleeding rates (log-rank tests in PP: statins p = 0.813, metformin p = 0.862, RASi p = 0.919) nor rebleeding rates (log-rank tests in SP: statin p = 0.113, metformin p = 0.348, RASi p = 0.273). Similar mortality rates were documented in patients with and without co-medications for PP (log-rank tests: statins p = 0.630, metformin p = 0.591, RASi p = 0.064) and for SP (statins p = 0.720, metformin p = 0.584, RASi p = 0.118). Conclusion In clinical practice, variceal bleeding and mortality rates of cirrhotic patients were not reduced by co-medication with statins, metformin or RASi. Nevertheless, we recommend the use of these co-medications by indication, as they may still exert beneficial effects on non-bleeding complications in patients with liver cirrhosis.

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“…Insulin sensitizers were described to lead to NO enhancement, reduce oxidative stress and alterations in vascular smooth muscle cells, and inhibit the α-adrenergic tone in patients with diabetes mellitus [22,[30][31][32][33]. In type-2 diabetes patients, metformin was shown to have an impact on the mesenteric artery by suppressing prostanoids and improving vascular resistance in animal studies [31].…”

Section: Introductionmentioning

confidence: 99%

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High dietary salt enhances acute depressor responses to metformin

Cited by 6 publications

References 19 publications

Metformin prevents vascular damage in hypertension through the AMPK/ER stress pathway

Metformin prevents vascular damage in hypertension through the AMPK/ER stress pathway

Statins, metformin, and RAS inhibitors did not reduce variceal bleeding risk and mortality in a large, real-life cohort of patients with cirrhosis

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