Usefulness of wide pulse pressure as a predictor of poor outcome after renal artery angioplasty and stenting.

Renal artery stenosis is a common cause of secondary hypertension and ischemic nephropathy. Percutaneous angioplasty and stent placement has allowed select patients with renal artery stenosis to use fewer antihypertensive agents and improve or stabilize renal function. The associations of baseline systolic, diastolic, and pulse pressures (PPs) with outcomes of blood pressure (BP) and renal function were examined in 243 patients who underwent renal angioplasty and stent placement.

Responses in extracellular and intracellular calcium and magnesium in aldosteronism.

We hypothesized the hypercalciuria and hypermagnesuria that accompany aldosteronism could be pharmacologically attenuated to prevent shifts in extracellular and intracellular levels of these divalent cations and the adverse outcomes associated with them. Accordingly, rats administered aldosterone/salt treatment (ALDOST) were cotreated with either hydrochlorothiazide (Hctz), to selectively reabsorb urinary Ca2+, or with Hctz plus spironolactone (Hctz+Spi), where Spi retards the excretion of these cations in both urine and feces. We monitored urinary excretion and responses in extracellular and intracellular Ca2+ and Mg2+, together with indices of oxi/nitrosative stress in plasma and ventricular tissue.

Bone loss in rats with aldosteronism.

Objective: We hypothesized that aldosteronism is accompanied by hypercalciuria and hypermagnesuria that lead to bone loss, which could be rescued by hydrochlorothiazide and spironolactone.

Methods: We monitored 24-hour urinary Ca and Mg excretion; plasma ionized [Ca]o and [Mg]o and plasma K; and bone mineral density of the femur. The following groups (n=5 in each group) were studied: age- and gender-matched, untreated controls; controls + 4 weeks hydrochlorothiazide; 4 weeks aldosterone/salt treatment (ALDOST, 0.

Diuretics and bone loss in rats with aldosteronism.

Objectives: We hypothesized that the increased urinary Ca2+ and Mg2+ excretion and bone loss that accompanies aldosteronism is aggravated with furosemide and is attenuated by spironolactone.

Background: Furosemide, a loop diuretic, is commonly used in patients with congestive heart failure (CHF), in which chronic, inappropriate (dietary Na+) elevations in plasma aldosterone (ALDO) and a catabolic state that includes bone wasting are expected.

Methods: In age- and gender-matched, untreated controls, four weeks of aldosterone/salt treatment (ALDO/salt, 0.

Hyperparathyroidism and the calcium paradox of aldosteronism.

Background: Aldosteronism may account for oxi/nitrosative stress, a proinflammatory phenotype, and wasting in congestive heart failure. We hypothesized that aldosterone/1% NaCl treatment (ALDOST) in rats enhances Ca2+ and Mg2+ excretion and leads to systemic effects, including bone loss.

Methods And Results: At 1, 2, 4, and 6 weeks of ALDOST, we monitored Ca2+ and Mg2+ excretion, ionized [Ca2+]o and [Mg2+]o, parathyroid hormone and 1-antiproteinase activity in plasma, bone mineral density, bone strength, Ca2+ and Mg2+ content in peripheral blood mononuclear cells (PBMCs) and ventricular tissue, and lymphocyte H2O2 production.

Loss of bone minerals and strength in rats with aldosteronism.

Congestive heart failure (CHF) is a clinical syndrome with origins rooted in a salt-avid state largely mediated by effector hormones of the circulating renin-angiotensin-aldosterone system. Other participating neurohormones include catecholamines, endothelin-1, and arginine vasopressin. CHF is accompanied by a systemic illness of uncertain causality.