Chronic Caffeine Administration Exacerbates Renovascular, but not Genetic, Hypertension in Rats

Ohnishi, Akihiro; Branch, Robert A.; Jackson, Kianna; Hamilton, Robert L.; Biaggioni, Italo; Deray, Gilbert; Jackson, Edwin K.

doi:10.1016/s0022-5347(17)44129-2

Cited by 12 publications

(25 citation statements)

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“…[18] Caffeine has no pathological effects on renal structure and function in normotensive and hypertensive rats that have normal renal function and structure [7,8] yet exacerbates renal disease in nephropathic rats. [7][8][9]12,13] Thus, it seems that pre-existing nephropathy and/or presence of several risk factors for renal disease are required for caffeine to induce adverse renal effects. It is possible that caffeine interacts with some of the risk factors for renal disease and induces renal injury.…”

Section: Discussionmentioning

confidence: 99%

“…[7,8] In contrast, in animals with pre-existing renal injury, including puromycin aminonucleoside nephropathy, 2-kidney 1-clip hypertension, and polycystic kidney disease, chronic caffeine consumption exacerbates renal disease. [7][8][9] Because of the widespread use of caffeine and taking into account the alarmingly high prevalence of obesity and the metabolic syndrome in U.S. adult population, [10,11] we thought it important to investigate the renal and metabolic effects of caffeine in experimental settings of obesity and the metabolic syndrome. Our initial studies indicate that long-term (20-30 weeks) caffeine consumption has adverse renal effects in rodent models of nephropathy associated with the metabolic syndrome.…”

Section: Introductionmentioning

confidence: 99%

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Early Renal Injury Induced by Caffeine Consumption in Obese, Diabetic ZSF₁Rats

et al. 2007

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Our previous studies indicate that prolonged caffeine consumption exacerbates renal failure in nephropathy associated with the metabolic syndrome. Reduced activity of the antioxidant defense system and beneficial effects of antioxidant therapy have been reported in diabetic rats and humans. The purpose of this study was to examine the early renal effects of caffeine consumption and the effects of concomitant antioxidant therapy in young obese, diabetic ZSF1 rats. Eleven-week-old male ZSF1 rats were randomized to drink tap water, caffeine (0.1%), tempol (1 mmol/ L), or a solution containing caffeine and tempol for nine weeks. Caffeine significantly reduced body weight and glycosuria (weeks 2-9), improved glucose tolerance (week 9), had no effect on elevated plasma triglycerides, plasma cholesterol (week 9) and blood pressure (week 9), and significantly increased plasma cholesterol level (weeks 5 and 9). Yet, as early as after two weeks, caffeine greatly augmented proteinuria and increased renal vascular resistance (RVR) and heart rate (HR: week 9). Tempol had no effects on metabolic status and development of proteinuria, did not alter caffeine-induced metabolic changes and early proteinuria, and attenuated caffeine-induced increase in HR and RVR. Immunohistochemical analysis revealed significant glomerular and interstitial inflammation, proliferation, and fibrosis in control animals. Caffeine augmented the influx of glomerular and interstitial macrophages (ED1+ cells) influx, glomerular and tubular proliferative response, and glomerular collagen IV content. Tempol abolished the exacerbation of renal inflammation, proliferation, and fibrosis induced by caffeine. In conclusion, in nephropathy associated with the metabolic syndrome, caffeine-most likely through the interaction with adenosine receptors and interference with anti-inflammatory and/or glomerular hemodynamic effects of adenosine-augments proteinuria and stimulates some of the key proliferative mechanisms involved in glomerular remodeling and sclerosis. Tempol does not prevent early renal injury (i.e., proteinuria) induced by caffeine, yet abolishes late renal inflammatory, proliferative, and fibrotic change induced by chronic caffeine consumption in obese ZSF1 rats.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Early Renal Injury Induced by Caffeine Consumption in Obese, Diabetic ZSF₁Rats

et al. 2007

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“…It appears that caffeine must potentiate 2-kidney, 1-clip hypertension by somehow interacting with the renin-angiotensin system. This conclusion is supported by the facts that caffeine does not exacerbate hypertension in animal models in which plasma renin levels remain low or normal, and that converting enzyme inhibition prevents caffeine from potentiating hypertension in rats with unilateral renal artery stenosis (1). Further, caffeine increases plasma renin activity by sevenfold in 2-kidney, 1-clip rats (1), which suggests that caffeine exacerbates 2-kidney, 1-clip hypertension, at least in part, by enhancing the reninrelease response to renal ischemia.…”

Section: Introductionmentioning

confidence: 83%

“…Recently, we discovered that chronic administration of caffeine to rats with 2-kidney, 1-clip Goldblatt hypertension accelerates the development of hypertension and increases the maximal level of blood pressure achieved (1). We are currently investigating the mechanism by which caffeine exerts this remarkable effect.…”

Section: Introductionmentioning

confidence: 99%

Caffeine enhances the slow-pressor response to angiotensin II in rats. Evidence for a caffeine-angiotensin II interaction with the sympathetic nervous system.

Ohnishi¹,

Li²,

Branch³

et al. 1987

J. Clin. Invest.

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The purpose of this study was to determine if caffeine augments the slow-pressor response to chronic low-dose infusions of angiotensin II (All) or the rapid-pressor response to acute infusions of All. All was infused (125 ng/min i.p.) for 12 d via miniosmotic pumps in four groups of rats: group I, intact rats not treated with caffeine (n = 9); group II, intact rats treated with caffeine (0.1% in dinking water, n = 9, group

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“…In the experiments, twelve rats older than 21 days, weighing between 30-40g were divided into a control group (cg) and treated group (tg) which received a solution of 0.1% of caffeine, a dose method quoted in the literature by Ohnishi et al (1986), managed orally by water fountains. The administration of caffeine started on the 21 st day of life, when weaning occurs, and continued until weaning of the offspring; the solution of caffeine and the commercial food were offered ad libitum.…”

Section: Introductionmentioning

confidence: 99%

Study of sensory-motor and somatic development of the offspring of rats (Wistar) treated with caffeine

Silva

Alexandre

Nascimento

et al. 2009

Braz. J. Pharm. Sci.

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The influence of caffeine, administered to rats, on the somatic and sensory-motor development of the offspring was investigated. Female Wistar rats were divided into a control group and a treated group and received drinking water and a 0.1% solution of caffeine orally, respectively. The offspring, also divided into a control group and a treated group, received daily monitoring until the 20 th day of life to verify alterations in somatic neural development. The offspring of the treated group had reduced weight on the day of birth and on the 1 st , 5 th , 15 th and 20 th days of life; shorter snout-anus length (evaluation done daily); shorter snout-tail length on the day of birth and on the 1 st , 5 th and 10 th days of life, and signs of retardation of somatic and sensory-motor maturation. These results allowed the conclusion that administration of caffeine to rats affects somatic and sensory-motor development of offspring.Uniterms: Caffeine/effects. Postnatal development. Central nervous system/stimulants. Estudou-se a influência da cafeína, administrada a ratos, no desenvolvimento somático e sensorial-motor da prole. Ratos Wistar fêmeas foram divididos em grupo controle e grupo tratado e receberam água e solução de cafeína a 0,1%, respectivamente. A prole, também dividida em grupo controle e grupo tratado, foi monitorada diariamente até o 20º. dia de vida para se observar as alterações no desenvolvimento somático neural. O grupo tratado apresentou peso reduzido no dia do nascimento e nos 1º, 5º., 15º e 20º. dias de vida; comprimento focinho-ânus mais curto (avaliação efetuada diariamente); comprimento focinho-cauda mais curto no dia do nascimento e nos 1º, 5º., 15º e 20º. dias de vida e sinais de retardamento da maturação somática e sensorial-motora. Esses resultados permitem que se conclua que a administração da cafeína a ratos afeta o desenvolvimento somático e sensorial-motor da prole.Unitermos: Cafeína/efeitos. Desenvolvimento pós-natal. Sistema Nervoso Central/estimulantes.

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Chronic Caffeine Administration Exacerbates Renovascular, but not Genetic, Hypertension in Rats

Cited by 12 publications

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Early Renal Injury Induced by Caffeine Consumption in Obese, Diabetic ZSF₁Rats

Early Renal Injury Induced by Caffeine Consumption in Obese, Diabetic ZSF₁Rats

Caffeine enhances the slow-pressor response to angiotensin II in rats. Evidence for a caffeine-angiotensin II interaction with the sympathetic nervous system.

Study of sensory-motor and somatic development of the offspring of rats (Wistar) treated with caffeine

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Chronic Caffeine Administration Exacerbates Renovascular, but not Genetic, Hypertension in Rats

Cited by 12 publications

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Early Renal Injury Induced by Caffeine Consumption in Obese, Diabetic ZSF1Rats

Early Renal Injury Induced by Caffeine Consumption in Obese, Diabetic ZSF1Rats

Caffeine enhances the slow-pressor response to angiotensin II in rats. Evidence for a caffeine-angiotensin II interaction with the sympathetic nervous system.

Study of sensory-motor and somatic development of the offspring of rats (Wistar) treated with caffeine

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Early Renal Injury Induced by Caffeine Consumption in Obese, Diabetic ZSF₁Rats

Early Renal Injury Induced by Caffeine Consumption in Obese, Diabetic ZSF₁Rats