Evaluation of cardiovascular responses to silver nanoparticles (AgNPs) in spontaneously hypertensive rats.

Silver nanoparticles (AgNPs) are used in the medical, pharmaceutical and food industry. Adverse effects and toxicity induced by AgNPs upon cardiac function related to nitric oxide (NO) and oxidative stress (OS) are described. AgNPs-toxicity may be influenced by cardiovascular pathologies such as hypertension. However, the molecules involved under pathophysiological conditions are not well studied. The aim of this work was to evaluate perfusion pressure (PP) and left ventricle pressure (LVP) as physiological parameters of cardiovascular function in response to AgNPs, using isolated perfused hearts from spontaneously hypertensive rats (SHR), and identify the role of NO and OS. The results suggest that AgNPs reduced NO derived from endothelial/inducible NO-synthase and increased OS, leading to increased and sustained vasoconstriction and myocardial contractility. Additionally, the hypertension condition alters phenylephrine (Phe) and acetylcholine (ACh) classic effects. These data suggest that hypertension intensified AgNPs-cardiotoxicity. Nevertheless, the precise mechanism of action is still under elucidation.

Effect of silver nanoparticles upon the myocardial and coronary vascular function in isolated and perfused diabetic rat hearts.

Silver nanoparticles (AgNPs) are promising antibacterial nanomaterials for diagnostic and treatment of diabetes. However, toxicity and adverse cardiac responses induced by AgNPs related to nitric oxide (NO) and oxidative stress (OS) are described. Moreover, little is known about the diabetes influence upon AgNPs-toxicity. The aim of this work was to evaluate cardiovascular function in response to AgNPs through measuring perfusion pressure (PP) and left ventricle pressure (LVP), using perfused hearts from streptozotocin (STZ)-induced diabetic rats and identify the role of NO and OS. High concentrations but not the lower concentrations of AgNPs, promotes increases in PP and LVP, as well as increased OS. Additionally, diabetes alters the classic effects of phenylephrine (Phe) and acetylcholine (ACh). These data suggest that diabetes may intensify AgNPs-cardiotoxicity. Nevertheless, the precise mechanism of action is still under elucidation.

Evaluation of vascular tone and cardiac contractility in response to silver nanoparticles, using Langendorff rat heart preparation.

Silver nanoparticles (AgNPs) have been widely used because of their antimicrobial properties. However, several reports suggest that AgNPs exposure promote cardiac effects that involve nitric oxide (NO) and oxidative stress (OS). Nevertheless, there are no studies related to AgNPs-induced effects in cardiac physiology. The aim of this study was to evaluate the AgNPs direct actions on coronary vascular tone and cardiac contractility using Langendorff rat heart preparation. Low concentrations of AgNPs (0.1 and 1 µg/mL) increased NO derived from inducible NO-synthase (iNOS), without modifying cardiac parameters. Meanwhile, high concentrations (10 and 100 µg/mL) promoted a sustained vasoconstriction and increased cardiac contractility related to OS, leading to rhabdomyolysis. Furthermore, AgNPs were internalized in the cardiac muscle, hindering classic actions induced by phenylephrine (Phe) and acetylcholine (ACh). These data suggest that AgNPs affect cardiac physiology in function of the concentration and in part of the NO generation, NOS expression and OS.

Role of silver nanoparticles (AgNPs) on the cardiovascular system.

With the advent of nanotechnology, the use and applications of silver nanoparticles (AgNPs) have increased, both in consumer products as well as in medical devices. However, little is known about the effects of these nanoparticles on human health, more specific in the cardiovascular system, since this system represents an important route of action in terms of distribution, bioaccumulation and bioavailability of the different circulating substances in the bloodstream. A collection of studies have addressed the effects and applications of different kinds of AgNPs (shaped, sized, coated and functionalized) in several components of the cardiovascular system, such as endothelial cells, isolated vessels and organs as well as integrative animal models, trying to identify the underlying mechanisms involved in their actions, to understand their implication in the field of biomedicine. The purpose of the present review is to summarize the most relevant studies to date of AgNPs effects in the cardiovascular system and provide a broader picture of the potential toxic effects and exposure risks, which in turn will allow pointing out the directions of further research as well as new applications of these versatile nanomaterials.

The prolactin family hormones regulate vascular tone through NO and prostacyclin production in isolated rat aortic rings.

AIM: Prolactin family hormones include growth hormone, placental lactogen and prolactin, which are able to regulate angiogenesis via NO and prostaglandins. However, their effects on vascular tone are not fully understood. The aim of this study was to evaluate the effects of prolactin family hormones on rat vascular tone in vitro. METHODS: Aortic rings were prepared from adult male rats and precontracted with phenylephrine, then treated with the hormones and drugs. The tension was measured with isometric force displacement transducer connected to a polygraph. NO production and prostacyclin release in physiological solution was determined. Cultured rat aortic endothelial cells (RAECs) were treated with the hormones and drugs, and the phosphorylation of eNOS at serine 1177 was assessed using Western bolt analysis. RESULTS: Administration of growth hormone or placental lactogen (0.01-100 nmol/L) induced endothelium-dependent vasodilation. Both the hormones significantly increased the phosphorylation of eNOS in RAECs and NO level in physiological solution. Preincubation with L-NAME blocked growth hormone- or placental lactogen-induced vasodilation and NO production. Preincubation with an antibody against growth hormone receptors blocked growth hormone- and placental lactogen-induced vasodilation. Addition of a single dose of prolactin (0.01 nmol/L) induced sustained vessel relaxation, whereas multiple doses of prolactin induced a biphasic contraction-relaxation effect. The vascular effects of prolactin depended on endothelium. Prolactin significantly increased the level of prostacyclin I2 in physiological solution. Preincubation with indomethacin or an antibody against prolactin receptors blocked prolactin-induced vasodilation. CONCLUSION: The prolactin family hormones regulate rat vascular tone, selectively promoting either relaxation or contraction of vascular smooth muscle via activation of either growth hormone receptors or prolactin receptors within the endothelium.