Chloroquine reduces blood pressure and forearm vascular resistance and increases forearm blood flow in healthy young adults

Anigbogu, C.N.; Adigun, S. A.; Inyang, Imeobong Joseph; Adegunloye, B. J.

doi:10.1111/j.1475-097x.1993.tb00381.x

Cited by 17 publications

(15 citation statements)

References 6 publications

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“…In accordance with our lowered blood pressure in adult SHR, toxicity studies with chloroquine have observed a reduction in blood pressure in humans and rats [34, 35], as well as the magnitude of pressor responses to cold immersion in humans [34]. However, the mechanisms underlying these reductions were not elucidated from these studies.…”

Section: Discussionsupporting

confidence: 73%

Autoimmune therapeutic chloroquine lowers blood pressure and improves endothelial function in spontaneously hypertensive rats

McCarthy

Wenceslau

Goulopoulou

et al. 2016

Pharmacological Research

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It has been suggested that hypertension results from a loss of immunological tolerance and the resulting autoimmunity may be an important underlying factor of its pathogenesis. This stems from the observations that many of the features involved in autoimmunity are also implicated in hypertension. Furthermore, the underlying presence of hypertension and cardiovascular disease are frequently observed in patients with autoimmune diseases. Antimalarial agents such as chloroquine are generally among the first line treatment options for patients with autoimmune diseases; however, whether they can improve a hypertensive phenotype in a genetic model of essential hypertension remains to be clarified. Therefore, we hypothesized that chloroquine treatment would improve endothelial function and lower blood pressure in spontaneously hypertensive rats (SHR). We treated adult SHR and Wistar-Kyoto rats (12 weeks old), as well as a group of young SHR (5 weeks old), with chloroquine (40 mg/kg/day via intraperitoneal injection) for 21 days. Chloroquine lowered blood pressure in adult SHR, but did not impede the development of high blood pressure in young SHR. In isolated mesenteric resistance arteries from SHR of both ages, chloroquine treatment inhibited cyclooxygenase-dependent contraction to acetylcholine, lowered vascular and systemic generation of reactive oxygen species, and improved nitric oxide bioavailability. Overall, these data reveal the anti-hypertensive mechanisms of chloroquine in the vasculature, which may be important for lowering risk of cardiovascular disease in patients with autoimmune diseases. Furthermore, it adds to the growing body of evidence suggesting that autoimmunity underlies hypertension.

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Section: Discussionsupporting

confidence: 73%

Autoimmune therapeutic chloroquine lowers blood pressure and improves endothelial function in spontaneously hypertensive rats

McCarthy

Wenceslau

Goulopoulou

et al. 2016

Pharmacological Research

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“…They were also associated with lower blood pressure. While the hypotensive effects of antimalarials are well known [24,25], these findings were mainly with chloroquine used to treat malaria and not with hydroxychloroquine in a rheumatological setting. Thus, our findings suggesting that hydroxychloroquine is associated with lower blood pressure in a rheumatological setting, is a novel finding.…”

Section: Discussionmentioning

confidence: 99%

Drugs Used in the Treatment of Rheumatoid Arthritis: Relationship between Current Use and Cardiovascular Risk Factors

Rho

Oeser

Chung

et al. 2009

Archives of Drug Info

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ObjectivesDrugs used for the treatment of rheumatoid arthritis (RA) have the potential to affect cardiovascular risk factors. There is concern that corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs) and COX-2 inhibitors could affect cardiovascular risk adversely, while drugs such as the antimalarial, hydroxychloroquine, may have beneficial effects. However, there is limited information about cardiovascular risk factors in patients with RA receiving different drugs.MethodsWe measured cardiovascular risk factors including systolic and diastolic blood pressure, serum HDL and LDL cholesterol, glucose and homocysteine concentrations and urinary F2-isoprostane excretion in 169 patients with RA. Risk factors were compared according to current use of corticosteroids, methotrexate, antimalarials, NSAIDs, COX-2 inhibitors, leflunomide and TNF-α blockers. Comparisons were adjusted for age, sex, race, disease activity (DAS28 score), current hypertension, diabetes, smoking status and statin use.ResultsNo cardiovascular risk factor differed significantly among current users and non-users of NSAIDs, COX-2 inhibitors, methotrexate and TNF-α blockers. Serum HDL cholesterol concentrations were significantly higher in patients currently receiving corticosteroids (42.2 ± 10.5 vs. 50.2 ± 15.3 mg/dL, adjusted P < 0.001). Diastolic blood pressure (75.9 ± 11.2 vs. 72.0 ± 9.1 mm Hg, adjusted P = 0.02), serum LDL cholesterol (115.6 ± 34.7 vs. 103.7 ± 27.8 mg/dL, adjusted P = 0.03) and triglyceride concentrations (157.7 ± 202.6 vs. 105.5 ± 50.5 mg/dL, adjusted P = 0.03) were significantly lower in patients taking antimalarial drugs. Plasma glucose was significantly lower in current lefunomide users (93.0 ± 19.2 vs. 83.6 ± 13.4 mg/dL, adjusted P = 0.006).ConclusionsIn a cross-sectional setting drugs used to treat RA did not have major adverse effects on cardiovascular risk factors and use of antimalarials was associated with beneficial lipid profiles.

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“…The efficacy of chloroquine in the therapy of porphyria cutanea tarda (69) could be mediated by NO, which has been reported to inhibit heme synthesis (2). On the other hand, an increased NO production may account for some side effects of chloroquine, mainly observed after treatment with high doses of drug or during parenteral administration: inhibition of platelet aggregation (70), transient hypotension (71), reduced forearm vascular resistance (72), in vivo vasodilation (73), mutagenic effects (74), and neuropathies (75). If so, NOS inhibitors could be associated to high dosage chloroquine treatment to prevent the onset of several toxic effects of the drug.…”

Section: Discussionmentioning

confidence: 99%

Chloroquine stimulates nitric oxide synthesis in murine, porcine, and human endothelial cells.

Ghigo

Aldieri²,

Todde³

et al. 1998

J. Clin. Invest.

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Nitric oxide (NO) is a free radical involved in the regulation of many cell functions and in the expression of several diseases. We have found that the antimalarial and antiinflammatory drug, chloroquine, is able to stimulate NO synthase (NOS) activity in murine, porcine, and human endothelial cells in vitro: the increase of enzyme activity is dependent on a de novo synthesis of some regulatory protein, as it is inhibited by cycloheximide but is not accompanied by an increased expression of inducible or constitutive NOS isoforms. Increased NO synthesis is, at least partly, responsible for chloroquine-induced inhibition of cell proliferation: indeed, NOS inhibitors revert the drug-evoked blockage of mitogenesis and ornithine decarboxylase activity in murine and porcine endothelial cells. The NOS-activating effect of chloroquine is dependent on its weak base properties, as it is exerted also by ammonium chloride, another lysosomotropic agent.

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Chloroquine reduces blood pressure and forearm vascular resistance and increases forearm blood flow in healthy young adults

Cited by 17 publications

References 6 publications

Autoimmune therapeutic chloroquine lowers blood pressure and improves endothelial function in spontaneously hypertensive rats

Autoimmune therapeutic chloroquine lowers blood pressure and improves endothelial function in spontaneously hypertensive rats

Drugs Used in the Treatment of Rheumatoid Arthritis: Relationship between Current Use and Cardiovascular Risk Factors

Chloroquine stimulates nitric oxide synthesis in murine, porcine, and human endothelial cells.

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