Hypertension in an experimental model of systemic lupus erythematosus occurs independently of the renal nerves.

Systemic lupus erythematosus (SLE) is a chronic inflammatory disorder with prevalent hypertension and renal injury. In this study, we tested whether the renal nerves contribute to the development of hypertension in an established mouse model of SLE (NZBWF1). Female SLE and control (NZW/LacJ) mice were subjected to either bilateral renal denervation or a sham procedure at 32 wk of age.

Pulmonary emboli from therapeutic sodium hyaluronate.

A patient presented with shortness of breath and pleuritic pain shortly after bilateral knee synovial injections with sodium hyaluronate (HA). He was discharged after a brief hospitalization without a diagnosis when no Doppler or radiologic evidence of deep vein thrombosis or pulmonary emboli was found. Radiologic studies found patchy ground glass opacities that were predominantly peripheral in disposition, with prominent septal lines in the lungs; a subsequent pulmonary function test showed a reduced diffusing capacity of the lung for carbon monoxide (D(LCO)).

Sustained suppression of sympathetic activity and arterial pressure during chronic activation of the carotid baroreflex.

Following sinoaortic denervation, which eliminates arterial baroreceptor input into the brain, there are slowly developing adaptations that abolish initial sympathetic activation and hypertension. In comparison, electrical stimulation of the carotid sinus for 1 wk produces sustained reductions in sympathetic activity and arterial pressure. However, whether compensations occur subsequently to diminish these responses is unclear.

Prolonged activation of the baroreflex decreases arterial pressure even during chronic adrenergic blockade.

Previous studies suggest that prolonged electric activation of the baroreflex may reduce arterial pressure more than chronic blockade of alpha(1)- and beta(1,2)-adrenergic receptors. To determine whether central inhibition of sympathetic outflow has appreciable effects to chronically reduce arterial pressure by actions distinct from well-established mechanisms, we hypothesized that chronic baroreflex activation would lower arterial pressure substantially even during complete alpha(1)- and beta(1,2)-adrenergic receptor blockade. This hypothesis was tested in 6 dogs during adrenergic blockade (AB; 18 days) with and without electric activation of the carotid baroreflex (7 days).

Early renal denervation prevents development of hypertension in growth-restricted offspring.

1. Low birth weight is associated with an increased risk for the development of hypertension. Our laboratory uses a model of reduced uterine perfusion in the pregnant rat that results in intrauterine growth-restricted (IUGR) offspring that develop hypertension at a prepubertal age.

Prolonged activation of the baroreflex abolishes obesity-induced hypertension.

Prolonged electrical activation of the carotid baroreflex produces sustained reductions in sympathetic activity and arterial pressure in normotensive dogs. The main goal of this study was to assess the influence of prolonged baroreflex activation on arterial pressure and neurohormonal responses in 6 dogs with obesity-induced hypertension. After control measurements, the diet was supplemented with cooked beef fat for 6 weeks, whereas sodium intake was held constant.

Renal denervation does not abolish sustained baroreflex-mediated reductions in arterial pressure.

Recent studies indicate that suppression of renal sympathetic nerve activity and attendant increments in renal excretory function are sustained baroreflex-mediated responses in hypertensive animals. Given the central role of the kidneys in long-term regulation of arterial pressure, we hypothesized that the chronic blood pressure-lowering effects of the baroreflex are critically dependent on intact renal innervation. This hypothesis was tested in 6 dogs by bilaterally activating the carotid baroreflex electrically for 7 days before and after bilateral renal denervation.

N-Acetylcysteine improves renal dysfunction, ameliorates kidney damage and decreases blood pressure in salt-sensitive hypertension.

Background: Salt-sensitive hypertension in humans and experimental animals causes progressive increases in renal damage and dysfunction. The Dahl salt-sensitive (S) rat closely mimics human salt-sensitive hypertension.

Aim: Our goal was to test the hypothesis that enhancing the glutathione system with dietary N-acetylcysteine administration in Dahl S rats on a high sodium intake for 5 weeks will attenuate the increases in arterial pressure, the decreases in renal hemodynamics and the increases in renal damage that normally occur in S rats on high sodium.

Influence of prolonged baroreflex activation on arterial pressure in angiotensin hypertension.

Despite recent evidence indicating sustained activation of the baroreflex during chronic infusion of angiotensin II (Ang II), sinoaortic denervation does not exacerbate the severity of the hypertension. Therefore, to determine whether Ang II hypertension is relatively resistant to the blood pressure-lowering effects of the baroreflex, the carotid baroreflex was electrically activated bilaterally for 7 days in 5 dogs both in the presence and absence of a continuous infusion of Ang II (5 ng/kg per minute) producing high physiological plasma levels of the peptide. Under control conditions, basal values for mean arterial pressure (MAP) and plasma norepinephrine concentration (NE) were 93+/-1 mm Hg and 99+/-25 pg/mL, respectively.

Renal denervation abolishes hypertension in low-birth-weight offspring from pregnant rats with reduced uterine perfusion.

Low birth weight is a risk factor for the subsequent development of hypertension in humans. We previously reported that reduced uterine perfusion in the pregnant rat results in growth-restricted offspring predisposed to the development of hypertension. The purpose of this study was to determine whether the sympathetic nervous system plays a role in mediating hypertension in this model of low birth weight.

Sampling airway surface liquid: non-volatiles in the exhaled breath condensate.

Exhaled breath condensate (EBC) samples contain molecules that have no appreciable vapor pressure; such molecules likely derive from droplets of airway fluid. We analyzed EBC gathered from a total of 62 healthy volunteers in order to quantify the volume of airway liquid that was the source of the non-volatiles; saliva was analyzed as a reference secretion. EBC urea averaged 0.

Is obesity a major cause of chronic kidney disease?

Excess weight gain is a major risk factor for essential hypertension and for end-stage renal disease (ESRD). Obesity raises blood pressure by increasing renal tubular sodium reabsorption, impairing pressure natriuresis, and causing volume expansion because of activation of the sympathetic nervous system and renin-angiotensin system and by physical compression of the kidneys, especially when visceral obesity is present. Obesity also causes renal vasodilation and glomerular hyperfiltration that initially serve as compensatory mechanisms to maintain sodium balance in the face of increased tubular reabsorption.

Cigarette smoke-induced airway inflammation as sampled by the expired breath condensate.

Airways exposed to smoke respond with inflammatory processes. The airway inflammation generally present in smokers causes persistent cough and phlegm production, reactive airway disease, and tissue infiltration by inflammatory cells. Although the short-term response may be protective, long-term pathological consequences include swelling of the airway epithelium, mucus hypersecretion, and increased airway reactivity characteristic of chronic bronchitis and chronic obstructive lung disease and the tissue destruction characteristic of emphysema.

The renal pelvis: machinery that concentrates urine in the papilla.

Two decades ago, Bodil Schmidt-Nielsen and Bruce Graves documented the rhythmic contractions of the renal pelvis in a remarkable video, visually demonstrating how peristaltic waves empty the papilla and how the subsequent elastic recoil draws water from the collecting duct and into the tethered-open ascending vasa recta. Thus a periodic hydrostatic gradient generates an axial osmotic gradient. This review recapitulates the video and offers a link to figures and scenes digitized from the original tape.