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At least 613 records · Page 34Linked to original sources
PubMed2003

Hypoxanthine plus xanthine oxidase causes profound natriuresis without affecting renal blood flow autoregulation.

BACKGROUND: Enhanced superoxide (O2-.) production by xanthine oxidase in ischemia/reperfusion has been implicated in structural damage. The reperfusion phase is accompanied by decreased tubular sodium reabsorption, which has been partly attributed to enhanced action of O2-. In the present study we assessed whether intrarenal increases of O2-. accomplished by concomitant intrarenal hypoxanthine and intravenous xanthine oxidase (HX/XO) infusion would decrease or increase sodium excretion, and whether HX/XO infusion could be responsible for the diminished efficacy of renal blood flow (RBF) autoregulation in ischemia/reperfusion. METHODS: In the first group of Sprague-Dawley rats, renal sodium handling was measured before and during O2-. infusion. In the second group, renal hemodynamics and RBF autoregulation were assessed. RESULTS: Intrarenal O2-. infusion dramatically increased urine flow from 14.5 +/- 2.0 microL/min to 46.3 +/- 4.4 microL/min, urinary excretion of sodium (UNaV) from 1.7 +/- 0.4 micromol/min to 8.6 +/- 0.9 micromol/min, and fractional excretion of sodium FENa from 1.2 +/- 0.4% to 7.6 +/- 1.2%. Urinary excretion of thiobarbituric acid reactive substances (TBARS), a measure of lipid peroxidation, increased during HX/XO infusion. These changes were completely reversible. Glomerular filtration rate (GFR) decreased from 1.12 +/- 0.08 during baseline to 0.79 +/- 0.06 during HX/XO (P < 0.05) and tended to increase toward baseline during recovery (0.84 +/- 0.06 mL/min/g kidney weight). HX/XO did not significantly affect mean arterial pressure (MAP). HX/XO decreased RBF in the second group from 8.4 +/- 0.6 mL/min/g kidney weight to 7.4 +/- 0.5 mL/min/g kidney weight (P < 0.05) and renal vascular resistance (RVR) slightly increased from 13.8 +/- 0.9 units under baseline conditions to 15.1 +/- 1.1 units during HX/XO infusion (P < 0.05). HX/XO did not significantly affect RBF autoregulation. Proteinuria and glucosuria were absent and light microscopy revealed no renal morphologic changes. CONCLUSION: Intrarenal O2-. infusion (1) dramatically increased sodium and volume excretion and (2) did not affect autoregulation of RBF. Thus, superoxide can markedly affect glomerulotubular balance by diverging actions on renal hemodynamics and reabsorptive function and could mediate the functional tubular consequences of ischemia/reperfusion.

Animals↗
PubMed2000

Reduced natriuresis after oral sodium load in cholestatic rats: role of compartment volumes and ANP.

The purpose of this study was to assess the participation of the atrial natriuretic peptide (ANP)-cGMP system in electrolyte and volume handling of cholestatic rats submitted to an acute oral sodium load. Cholestasis was induced by ligation and section of the common bile duct (n = 51). Control rats were sham operated (n = 56). Three weeks after surgery, 24-hr urinary volume, sodium, potassium, cGMP and creatinine excretion were measured. Three days later, animals received 10 mmol/kg NaCl (1 M) by gavage, and urinary excretion was measured for 6 hr. In parallel groups of rats, plasma volume, electrolytes and ANP concentration, extracellular fluid volume (ECFV), and renal medullary ANP-induced cGMP production were determined in basal conditions or 1 hr after oral sodium overload. As compared with controls, cholestatic rats had a larger ECFV and higher plasma ANP (67.2 +/- 5.2 vs 39.7 +/- 3.5 pg/ml), but lower hematocrit and blood volume, and were hyponatremic. Cholestatic rats showed higher basal excretion of sodium, potassium, and volume than controls, but equal urinary cGMP. After the NaCl overload, cholestatic rats showed a reduced sodium excretion but equal urinary cGMP. One hr after sodium overload, both groups showed hypernatremia, but whereas in control rats ECFV and ANP increased (50.7 +/- 4.1 pg/ml), in cholestatic rats ECFV was unchanged, and plasma volume and ANP were reduced (37.5 +/- 5.8 pg/ml). ANP-induced cGMP production in renal medulla was similar in cholestatic and control nonloaded rats (14.2 +/- 5.2 vs 13.4 +/- 2.6 fmol/min/mg). One hr after the load, medullary cGMP production rose significantly in both groups, without difference between them (20.6 +/- 3.1 vs 22.7 +/- 1. 7 fmol/min/mg). We conclude that the blunted excretion of an acute oral sodium load in cholestatic rats is associated with lower plasma ANP due to differences in body fluid distribution and cannot be explained by renal refractoriness to ANP.

Animals↗
PubMed1996

Resistance to natriuresis in patients with peritonitis carcinomatosa.

The natriuretic effect of atrial natriuretic peptide (ANP) is blunted in certain clinical disorders such as congestive heart failure and liver cirrhosis, despite the elevated plasma ANP levels. These sodium-retaining states are characterized by increased activity of the renal sympathetic nerves. Recent studies have shown higher levels of circulating and urinary catecholamines in cancer patients. We hypothesized that the increased adrenergic activity may be responsible for ascites formation in patients with peritonitis carcinomatosa (PC). The objective of this study was to determine the renal responses to endogenous ANP in patients with PC. Patients, hospitalized at our institute for PC, were examined using renal clearance studies for 2 h. Non-cancer patients were also examined as control subjects. Statistical analysis was performed using Wilcoxon's rank sum test. The results showed that absolute and fractional sodium excretions were markedly lower in patients with PC (54 +/- 16 microEq/min, means +/- SE, p < 0.0005; 0.55 +/- 0.15%, p < 0.005) than in control patients (166 +/- 14 microEql/min; 1.14 +/- 0.09%, respectively). Plasma ANP concentration was increased in patients with PC (34.7 +/- 8.4 pg/ml, p < 0.001) in comparison with control patients (13.3 +/- 2.0 pg/ml). Plasma and urinary levels of norepinephrine were significantly higher in cancer patients (0.36 +/- 0.10 ng/ml, p < 0.05; 125 +/- 20 ng/dl GF, p < 0.05) than in the controls (0.17 +/- 0.02 ng/ml; 73 +/- 13 ng/dl GF). These results suggest that increased renal sympathetic nerve activity may contribute to the attenuation of the natriuretic effect of ANP in patients with PC.

Adult↗
PubMed1999

Relation between natriuresis and urinary excretion of hydrogen peroxide.

Changes in the urinary hydrogen peroxide by exercise or salt load were studied in six healthy male volunteers. Exercise was performed by bicycle ergometer for 30 min at the intensity of 80% of the maximum heart rate predicted by age. Urinary excretion rate of hydrogen peroxide showed a tendency to increase in the salt load experiment, and to decrease by exercise. Correlation coefficient between urinary excretion rate of sodium and hydrogen peroxide one hour after the load was 0.797 (0.1 > p > 0.05) in the exercise experiment, 0.892 (p <0.05) in the salt load experiment and 0.877 (p < 0.001) in both experiments. Correlation coefficient between area under the curve for sodium excretion and hydrogen peroxide excretion was also as high as 0.822 (p < 0.05) in the exercise experiment, 0.909 (p < 0.05) in the salt load experiment and 0.853 (p < 0.001) in both experiments. These results may suggest that urinary excretion rate of hydrogen peroxide is closely related to metabolism of electrolytes and fluid in the renal tubules.

Adult↗
PubMed2001

Exaggerated natriuresis after selective AT1 receptor blockade in Dahl salt-sensitive rats.

Salt-sensitive individuals are susceptible to develop hypertension when exposed to high salt-diet. Such a phenomenon is considered to be due to a genetic impairment in the renal excretion of sodium. In the present studies extent of endogenous angiotensin-II (Ang-II) mediated antinatriuresis was comparatively evaluated in Dahl salt-sensitive (SS) and salt-resistant (SR) rats, using a selective AT1 receptor antagonist, candesartan. In addition, differences in plasma renin activity and characteristics of Ang-II receptors in the renal cortical tubular membranes were also examined. Under INACTIN anesthesia AT1 receptor blockade resulted in significant increases in renal sodium excretion, which was several-fold greater in SS rats than that observed in SR rats. These observations suggest that antinatriuretic function of endogenous angiotensin-II is exaggerated in SS rats. This functional overexpression appears to be related to an increase in the affinity of Ang-II receptors in renal cortical tubular membranes but not to receptor density or plasma renin activity. It is proposed that salt-dependent hypertension in Dahl salt-sensitive rats may be due to enhanced Ang-II mediated sodium retention.

Angiotensin Receptor Antagonists↗
PubMed1993

Chronic pressure-natriuresis relationship in dogs with inherited essential hypertension.

A genetic model of essential hypertension in the dog was studied to describe the phenotypic expression of the arterial pressure, as well as to determine the relationship between mean arterial blood pressure (MAP), hormone, and renal excretory responses to four different levels of sodium intake (5, 40, 120, 240 mEq/day) delivered intravenously and isotonically. This model was developed at the University of Pennsylvania (U/Penn) and termed Pennsylvania hypertensive dogs (PHD). The MAP was recorded beat-by-beat, 24 h/day, in 16 dogs. Water and sodium balances were determined daily for 4 days at each level of intake and blood samples were collected on the last day of each salt step for analysis of plasma renin activity (PRA), atrial natriuretic peptide (ANP), aldosterone (ALDO), and vasopressin (AVP). After the study, the dogs were designated as hypertensive (PHD-HT) when the 24-h average MAP was greater than 110 mm Hg and systolic pressure was greater than 160 mm Hg. Dogs that failed to meet both criteria were designated as normotensive genetic controls (PHD-NT). Although sodium was retained during the first day of each increase of salt intake in both groups, a return to balance was observed within the 4 days. There was no apparent change in the slope of the chronic renal function curve in either group of PHD studied, although the PHD-HT exhibit a curve shifted to a higher level of MAP. Plasma hormone levels in both groups of PHD studied responded in a manner similar to normal mongrel dogs with reductions of PRA, ALDO, elevations of ANP, and no change in AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1994

Activation/deactivation of renal Na+,K(+)-ATPase: a final common pathway for regulation of natriuresis.

Renal sodium metabolism, a major determinant of blood pressure, is regulated with great precision by a variety of endocrine, autocrine, and neuronal factors. Although these factors are known to regulate sodium metabolism by affecting the rate of tubular sodium reabsorption, the molecular mechanisms by which they act are poorly understood. Na+,K(+)-ATPase plays a pivotal role for sodium reabsorption in all tubular segments. The activity of this enzyme can be dynamically regulated by phosphorylation and dephosphorylation. Here we summarize both old and new evidence that several major substances believed to be involved in the regulation of sodium metabolism and blood pressure, i.e., the antidiuretic agents angiotensin II and norepinephrine, and the diuretic agents dopamine and atrial natriuretic peptide (ANP), may achieve their effects through a common pathway that involves reversible activation/deactivation of renal tubular Na+,K(+)-ATPase. Regulation of Na+,K(+)-ATPase activity was studied using a preparation of single proximal tubule (PT) segments, dissected from rat kidneys. Na+,K(+)-ATPase activity was stimulated by angiotensin II and the alpha-adrenergic agonist, oxymetazoline, at physiological, nonsaturating Na+ concentrations. These stimulatory effects were blocked by dopamine and ANP as well as by their respective second messengers, cAMP and cGMP. They were also blocked by the specific protein phosphatase 2B inhibitor FK506. These results indicate that regulation of sodium excretion by norepinephrine, angiotensin II, dopamine, and ANP can be accounted for by a bidirectionally regulated intracellular protein phosphorylation cascade that modulates the activity of renal tubular Na+,K(+)-ATPase.

Angiotensin II↗
PubMed1989

Cardiorenal effects of atrial natriuretic factor administration in congestive heart failure: natriuresis and diuresis without hemodynamic alterations.

The effects of low bolus dose (70 +/- 6 micrograms [mean +/- SEM]) atrial natriuretic factor (ANF) administration was assessed in 16 patients with chronic congestive heart failure. Measurements were made for at least 60 minutes before and after the dose of ANF. There was a significant increase in urine flow rate (0.81 +/- 0.06 to 1.81 +/- 0.23 ml/min, p less than 0.01), sodium excretion rate (56 +/- 14 to 80 +/- 23 microEq/min, p less than 0.01), fractional excretion of sodium (1.23 +/- 0.49 to 1.63 +/- 0.60 percent, p less than 0.01) and potassium excretion rate (35 +/- 7 to 42 +/- 6 microEq/min, p less than 0.02). However, no significant alterations in renal plasma flow or glomerular filtration rate were observed. Furthermore, there was no significant correlation between the change in urine flow rate or sodium excretion rate and the change in renal plasma flow or glomerular filtration rate, respectively. In addition, there was no significant effect on cardiac index, mean aortic or left ventricular filling pressures, or systemic vascular resistance. There also was no discernible relationship between the response to ANF and the baseline concentrations of plasma ANF, aldosterone, or plasma renin activity. Thus, in patients with congestive heart failure, low dose ANF boluses may produce an increase in urine flow rate and sodium excretion rate that is independent of renal plasma flow or glomerular filtration rate. This suggests a meaningful direct renal tubular effect of exogenous ANF in this setting.

Adult↗
PubMed1989

Effects of intracerebroventricular atrial natriuretic factor on angiotensin II- or sodium-induced blood pressure elevation and natriuresis.

We examined the effects of intracerebroventricular (i.c.v.) administration of atrial natriuretic factor (ANF) on pressor and natriuretic responses induced by i.c.v. angiotensin II (Ang II) or hypertonic NaCl. Conscious male Wistar rats were given one of the following solutions into the lateral ventricle: artificial cerebrospinal fluid (CSF); rat ANF (99-126) 1.0 microgram/kg per min; Ang II 100 ng/kg per min; 0.6 mol/l NaCl; Ang II plus ANF, and 0.6 mol/l NaCl plus ANF. The i.c.v. infusion of artificial CSF or ANF alone did not cause significant changes in mean blood pressure, urinary volume or sodium excretion (UNaV). The i.c.v. infusion of Ang II or 0.6 mol/l NaCl raised mean blood pressure, decreased urinary volume and increased UNaV. When ANF was administered with Ang II, the Ang II-induced responses were diminished significantly (delta mean blood pressure, +10 +/- 3 versus +20 +/- 4 mmHg; delta urinary volume, -38 +/- 9 versus -78 +/- 5 microliters/min; delta UNaV, +0.49 +/- 0.51 versus +2.28 +/- 0.58 mumol/min). The centrally administered ANF opposed the effects of 0.6 mol/l NaCl, though the effect was significant only in respect of blood pressure. Our results indicate that the brain ANF may have an antinatriuretic role in some conditions.

Angiotensin II↗
PubMed1990

Positive inotropic action, natriuresis and atrial natriuretic factor release induced by endothelin in the conscious rat.

Endothelin is a novel endothelium-derived vasoconstrictor peptide. We investigated its effect on atrial natriuretic factor (ANF) release and on several cardiovascular and renal parameter, since ANF release is induced via hemodynamic changes in response to angiotensin II, another vasoconstrictor peptide. Male Sprague-Dawley rats were infused intravenously for 60 min with either saline or endothelin at 10, 50 or 100 ng/kg per min and then allowed to recover for 20 min. A third group was splenectomized 24 h before infusion with 100 ng/kg per min endothelin. Mean arterial, left ventricular end-diastolic and central venous pressures (dP/dtmax), heart rate, plasma ANF-(1-98) concentration, urinary volume, urinary sodium excretion and hematocrit were evaluated. Mean arterial pressure was elevated by both medium and high endothelin doses, and with the high dose this elevation was sustained beyond the infusion period. No increases in either left ventricular end-diastolic or central venous pressures were observed at any dose level. In fact, in rats infused with 100 ng endothelin there was a progressive decline in central venous pressure and a raised hematocrit, even in the splenectomized group, suggesting a loss of plasma volume. All three dose levels elevated the dP/dtmax at different infusion times. The heart rate was not modified by any endothelin dose. Despite the decreased central venous pressure and unaltered left ventricular end-diastolic pressure, the 100 ng/kg per min endothelin infusion induced a threefold increase in plasma ANF levels; these were correlated with changes in the dP/dtmax (r = 0.49, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗