High potassium diets protect against dysfunction of endothelial cells in stroke-prone spontaneously hypertensive rats.

Sugimoto, Tsuneaki; Tobian, Louis; Ganguli, M

doi:10.1161/01.hyp.11.6.579

Cited by 78 publications

(39 citation statements)

References 30 publications

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“…39,40 Moreover, K ϩ prevents nephron loss by exerting a protective action on renal tubules, arteries, and glomeruli. 41 Hence, hypokalemic nephropathy has been contended to be responsible for the increased UAE rate in PA patients, 15 but this hypothesis has never been formally tested.…”

Section: Uae Rate By Serum Kmentioning

confidence: 99%

Renal Damage in Primary Aldosteronism

et al. 2006

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Abstract-Primary aldosteronism (PA) has been associated with cardiovascular hypertrophy and fibrosis, in part independent of the blood pressure level, but deleterious effects on the kidneys are less clear. Likewise, it remains unknown if the kidney can be diversely involved in PA caused by aldosterone-producing adenoma (APA) and idiopathic hyperaldosteronism (IHA). Hence, in the Primary Aldosteronism Prevalence in Italy (PAPY) Study, a prospective survey of newly diagnosed consecutive patients referred to hypertension centers nationwide, we sought signs of renal damage in patients with PA and in comparable patients with primary hypertension (PH). Patients (nϭ1180) underwent a predefined screening protocol followed by tests for confirming PA and identifying the underlying adrenocortical pathology. Renal damage was assessed by 24-hour urine albumin excretion (UAE) rate and glomerular filtration rate (GFR). UAE rate was measured in 490 patients; all had a normal GFR. Of them, 31 (6.4%) had APA, 33 (6.7%) had IHA, and the rest (86.9%) had PH. UAE rate was predicted (PϽ0.001) by body mass index, age, urinary Na ϩ excretion, serum K ϩ , and mean blood pressure. Covariate-adjusted UAE rate was significantly higher in APA and IHA than in PH patients; there were more patients with microalbuminuria in the APA and IHA than in the PH group (Pϭ0.007). Among the hypertensive patients with a preserved GFR, those with APA or IHA have a higher UAE rate than comparable PH patients. Thus, hypertension because of excess autonomous aldosterone secretion features an early and more prominent renal damage than PH. Key Words: hypertension, endocrine Ⅲ aldosterone Ⅲ mineralocorticoids Ⅲ kidney Ⅲ hypertrophy Ⅲ adrenal gland T he results of large intervention trials 1,2 and cross-sectional studies (reviewed by Rossi et al 3 ) have recently refueled the interest on the deleterious cardiovascular effects of excess aldosterone. Moreover, growing evidence 4 indicates that primary aldosteronism (PA) is a common cause of secondary hypertension: in the Primary Aldosteronism Prevalence in Italy (PAPY) study, a prospective survey of 1180 consecutive newly diagnosed hypertensive patients referred to specialized hypertension centers, aldosterone-producing adenoma (APA) and idiopathic hyperaldosteronism (IHA) were found in 4.8% and 6.4% of all patients, respectively, thus leading to an overall prevalence of PA of Ϸ11%. 5 It has been contended that this form of secondary hypertension is relatively "benign," that is, devoid of cardiovascular complications, because of the suppression of the renin-angiotensin system, which plays a substantial role in cardiovascular remodeling and damage. 6,7 This view has, however, been challenged by recent data. 3,8 PA has in fact been associated with widespread tissue fibrosis, 9 vascular remodeling, 10 and excess prevalence of left ventricular hypertrophy and diastolic dysfunction 11 that were corrected by adrenalectomy. 12 A higher incidence of cardiovascular complications, including atrial fibrillation, has also been...

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Section: Uae Rate By Serum Kmentioning

confidence: 99%

Renal Damage in Primary Aldosteronism

et al. 2006

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“…In experimental hypertension, the endothelium-dependent relaxation of vascular smooth muscle is impaired (Konishi & Su, 1983;LUischer et al, 1987;Tesfamariam & Halperin, 1988). Moreover, high sodium chloride diet and severe hypertension in the stroke-prone SHR induce injury to endothelial cells (Tobian, 1988), and a high potassium diet protects against the salt-induced endothelial dysfunction (Sugimoto et al, 1988). ACEI treatment improves the endothelium-dependent vascular relaxation in SHR by increasing the production of endothelium-derived relaxing factor(s) and by preventing the de-gradation of bradykinin liberated from the endothelial cells (Clozel et al, 1990;Wiemer et al, 1991;Arvola et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Replacement of salt by a novel potassium‐ and magnesium‐enriched salt alternative improves the cardiovascular effects of ramipril

Mervaala

Paakkari

Laakso³

et al. 1994

British J Pharmacology

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1The influence of salt (sodium chloride; NaCl) (an additional 6% in the diet) and that of a novel sodium-reduced, potassium-, magnesium-, and L-lysine-enriched salt alternative on the cardiovascular effects of ramipril was studied in stroke-prone spontaneously hypertensive rats in a 6-week study. The intake of sodium chloride was adjusted to the same level by adding the salt alternative at a 1.75 times higher amount than regular salt. 2 Salt produced a marked rise in blood pressure and induced cardiac hypertrophy and significant mortality, while the salt alternative neither increased blood pressure nor caused any mortality and produced less cardiac hypertrophy than salt. 3 Ramipril treatment at a daily dose of 3 mg kg' normalized blood pressure and prevented the development of cardiac hypertrophy of rats on control diet. These effects of ramipril were blocked by the addition of salt but were only slightly attenuated by the addition of the salt alternative. The mortality in -the salt group was prevented by ramipril. 4 Responses of mesenteric arterial rings in vitro were examined at the end of the study. Salt, but not the salt alternative, increased vascular contractile responses to noradrenaline. Ramipril treatment improved the arterial relaxation responses to acetylcholine and to sodium nitroprusside. The vascular relaxation enhancing effect of ramipril was blocked by salt but only slightly attenuated by the salt alternative. 5 Ramipril treatment did not significantly increase plasma renin activity in the presence or in the absence of salt supplementation. The salt alternative did not cause hyperkalaemia, either alone or in combination with ramipril treatment. 6 Both salt supplementations, irrespective of ramipril treatment, induced a six to eight fold increase in the urinary excretion of calcium. There was an expected 90 to 140% rise in the urinary excretion of magnesium and 200% rise in the urinary excretion of potassium in the salt alternative group. Salt also produced an approximately 50% increase in magnesuria. 7 Our findings suggest that replacement of salt by the potassium-, magnesium-and L-lysine-enriched salt alternative improves the cardiovascular effects of ramipril. In the present study the beneficial effect was related to the increased intakes of potassium and/or magnesium and L-lysine from the salt alternative because the amount of sodium chloride was the same.

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“…Tobian and colleagues have shown that stroke-prone SHR and Dahl salt sensitive hypertensive rats fed a high potassium diet had a significant reduction in death rate even though blood pressure was similar in the low and high potassium diet groups (Sugimoto et al, 1988;Tobian et al, 1985). The precise mechanism by which dietary potassium reduces death has yet to be demonstrated.…”

Section: Discussionmentioning

confidence: 99%

“…In this cardiovascular protector context, a pivotal role has been assigned to the anti-hypertensive effects of potassium, as well as to other vasoprotective mechanisms, such as the reduced production of reactive oxygen species (Matsui et al, 2006) and the direct inhibition of intimal hyperplasia (Kido et al, 2008). Several authors have described a beneficial effect of potassium on the generation and release of nitric oxide (NO; see Zhou et al, 1999;Zhou et al, 2000) and a restoration of endothelium-dependent vasorelaxation has been shown in diverse hypertensive rat models (Sudhir et al, 1993;Sugimoto et al, 1988;Zhou et al, 1999). Yet, in these studies, the capacity of potassium supplementation to preserve endothelium-dependent vasorelaxation was always accompanied by a reduction of blood pressure in treated animals, making it impossible to know whether the salutary effect of potassium on vascular function was direct or whether it was indirect, secondary to its antihypertensive action.…”

Section: Introductionmentioning

confidence: 99%

Potassium restores vasorelaxation of resistance arterioles in non-hypertensive DOCA/salt fed mice

Wyss

Wang

Golshayan

et al. 2012

Microvascular Research

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Background: Potassium-enriched diets exert renal and cardiovascular protective effects, but the underlying mechanisms are largely unknown. Methods: Using the dorsal skinfold chamber model for intravital microscopy, we examined endotheliumdependent vasorelaxation of precapillary resistance arterioles in response to acetylcholine or the NO donor SNAP in awake mice. Experiments were performed in uni-nephrectomized one renin gene (Ren-1c) C57BL/6 mice (control group) and in mice having received a continuous administration of deoxycorticosterone acetate and a dietary supplementation of 1% sodium chloride for 8 weeks (DOCA/salt group). An additional group of DOCA/salt treated animals received a dietary supplement of 0.4% KCl for 3 weeks prior to the experiments (DOCA/salt + potassium group). Results: DOCA/salt treatment for 8 weeks resulted in hypokalemia, but blood pressure remained unchanged. In DOCA/salt mice, relaxation of resistance arterioles was blunted in response to acetylcholine, and to a lesser extent to SNAP, suggesting endothelial dysfunction. Endothelium-dependent vasorelaxation was restored by the potassium-enriched diet. Conclusion: This study is the first to demonstrate a protective effect of potassium on endothelium-dependent vasorelaxation in the absence of confounding anti-hypertensive effects, as observed in most animal models and the clinical situation. We propose that the known cardio-and nephro-protective effects of potassium might -at least in part -be mediated by the salutary effects on endothelium-dependent arteriolar relaxation.

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High potassium diets protect against dysfunction of endothelial cells in stroke-prone spontaneously hypertensive rats.

Cited by 78 publications

References 30 publications

Renal Damage in Primary Aldosteronism

Renal Damage in Primary Aldosteronism

Replacement of salt by a novel potassium‐ and magnesium‐enriched salt alternative improves the cardiovascular effects of ramipril

Potassium restores vasorelaxation of resistance arterioles in non-hypertensive DOCA/salt fed mice

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