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PubMed1986

The importance of sodium and chloride ions for the development of DOCA-NaCl hypertension: a haemodynamic study.

The role of sodium and its accompanying anion for the development of DOCA-salt hypertension was studied in uninephrectomized DOCA-treated weanling Wistar rats which were fed a diet containing either sodium chloride or sodium bicarbonate (170 mmol/kg). The blood pressure was increased in both groups of rats with sodium overload as compared to rats fed a low-salt diet only. A decreased cardiac output and substantially elevated systemic resistance were demonstrated in both groups of rats with high sodium intake in comparison with rats kept on a low-salt diet. However, these haemodynamic changes were more pronounced in rats with sodium chloride overload than in animals with a high sodium bicarbonate intake. On the other hand, the rigidity of major arteries which was estimated as the pulse pressure/stroke volume ratio, was increased only in rats fed a diet with sodium chloride but not in rats with sodium bicarbonate overload. Thus high sodium intake was responsible for the changes of systemic resistance in DOCA-treated animals and its action was only slightly augmented by a high chloride intake. In contrast to this, the chloride overload seemed to be essential for the induction of increased arterial rigidity.

Animals↗
PubMed1979

[Physiopathology of arterial hypertension in chronic hemodialysis patients].

The increase in total body sodium and hyperactivity of the renin-angiotensin system plays a major part in hypertension in patients underdoing chronic dialysis. After sodium depletion most patients become normotensive. Their hypertension seems to be due to sodium overload but it is favoured by insufficient inhibition of renin secretion. Some renin hypertensive, hypersecretion of renin is the main factor in these cases but its effect is aggravated by the sodium overload. Other factors may play a role as suggested by the studies of hypertensive patients after bilateral nephrectomy. However, their roles and mechanisms are unknown at present.

Humans↗
PubMed1982

Recurrence of hypertension in primary aldosteronism after discontinuation of spironolactone. Time course of changes in cardiac output and body fluid volumes.

Hemodynamic mechanisms underlying the hypertensive action of long-standing sodium overload were studied in ten subjects with aldosterone-producing adenoma. Arterial pressure was 129+/-4/91+/-4 mm Hg (mean+/-SEM) during spironolactone treatment, 177+/-5/114+/-3 mm Hg six weeks after the drug had been stopped, and 136+/-4/94+/-3 mm Hg two months after operation. In the six weeks following cessation of spironolactone, cardiac output, stroke volume, blood volume and sodium space were determined at weekly intervals. In each subject the biochemical syndrome of aldosterone-excess had been fully developed in two weeks. The hemodynamic changes in that period were also uniform. Mean arterial pressure in week 2 was increased by 20+/-3% with parallel increments of cardiac output and stroke volume of 22+/-5 and 30+/-6%. Blood volume and sodium space were increased by 11+/-2 and 29+/-4%. The patterns in weeks 2-6 were not uniform. In five subjects (age 33-49 yr) the hypertension was maintained through increased cardiac output; in week 6 it was 34+/-7% above its initial value, and stroke volume and blood volume were 37+/-4 and 16+/-4% above control. In the remaining five subjects (age 50-60 yr) cardiac output, stroke volume and blood volume returned to their initial values, and total peripheral resistance in week 6 was 36+/-13% above control. Sodium space remained expanded in both groups. The measurements after surgery confirmed the existence of the high-flow and high-resistance patterns; there was a decrease in cardiac output in the former group of subjects and a decrease in resistance in the latter. Apparently, increased resistance is not a direct consequence of increased flow. The observed age-related differences in hemodynamic patterns of sodium overload bear some resemblance to essential hypertension where a high-flow state of long duration may precede the ultimate phase of low vascular capacitance and high resistance.

Aldosterone↗
PubMed2002

Protective effect of propranolol on mitochondrial function in the ischaemic heart.

1. The present study was aimed to determine whether propranolol improves contractile function of the ischaemic/reperfused heart through protection of the mitochondrial function during ischaemia. 2. Isolated perfused rat hearts were subjected to 35-min ischaemia followed by 60-min reperfusion. Pre-treatment with propranolol at the concentrations of 10 to 100 microM for the final 3 min of pre-ischaemia resulted in the improvement of ischaemia/reperfusion-induced contractile dysfunction, release of creatine kinase (CK) into perfusate, and decrease in myocardial high-energy phosphates. Propranolol also attenuated ischaemia-induced accumulation in Na+, suggesting that cytosolic sodium overload during ischaemia was prevented by propranolol. 3. The mitochondrial oxygen consumption rate of skinned bundles from the perfused heart decreased at the end of ischaemia and it further decreased at the end of reperfusion. These decreases were cancelled by treatment with propranolol. A release of cytochrome c from the perfused heart was observed during ischaemia, and this release was suppressed by treatment with propranolol. 4. To elucidate the direct effect of propranolol on mitochondria, the mitochondria were isolated from normal hearts and their activities were determined in the presence of various concentrations of Na+ and propranolol. The addition of sodium lactate, which mimicked sodium overload in the ischaemic heart, reduced the state 3 respiration, whereas this reduction was not attenuated by the presence of propranolol. 5. These results suggest that cardioprotection of propranolol may be exerted via attenuating Na+ influx into cardiac cells followed by prevention of the mitochondrial dysfunction in the ischaemic heart, leading to improvement of energy production of the heart during reperfusion.

Adenosine Triphosphate↗
PubMed2000

Action potential and contractility changes in [Na(+)](i) overloaded cardiac myocytes: a simulation study.

Sodium overload of cardiac cells can accompany various pathologies and induce fatal cardiac arrhythmias. We investigate effects of elevated intracellular sodium on the cardiac action potential (AP) and on intracellular calcium using the Luo-Rudy model of a mammalian ventricular myocyte. The results are: 1) During rapid pacing, AP duration (APD) shortens in two phases, a rapid phase without Na(+) accumulation and a slower phase that depends on [Na(+)](i). 2) The rapid APD shortening is due to incomplete deactivation (accumulation) of I(Ks). 3) The slow phase is due to increased repolarizing currents I(NaK) and reverse-mode I(NaCa), secondary to elevated [Na(+)](i). 4) Na(+)-overload slows the rate of AP depolarization, allowing time for greater I(Ca(L)) activation; it also enhances reverse-mode I(NaCa). The resulting increased Ca(2+) influx triggers a greater [Ca(2+)](i) transient. 5) Reverse-mode I(NaCa) alone can trigger Ca(2+) release in a voltage and [Na(+)](i)-dependent manner. 6) During I(NaK) block, Na(+) and Ca(2+) accumulate and APD shortens due to enhanced reverse-mode I(NaCa); contribution of I(K(Na)) to APD shortening is negligible. By slowing AP depolarization (hence velocity) and shortening APD, Na(+)-overload acts to enhance inducibility of reentrant arrhythmias. Shortened APD with elevated [Ca(2+)](i) (secondary to Na(+)-overload) also predisposes the myocardium to arrhythmogenic delayed afterdepolarizations.

Action Potentials↗
PubMed1991

Investigation of electrophysiologic mechanisms for the antiarrhythmic actions of R 56865 in cardiac glycoside toxicity.

R 56865 is an experimental compound that has been shown to ameliorate the effects of cardiac glycoside toxicity and myocardial ischemia. We evaluated the direct electrophysiological effects of R 56865 and its effects on the electrophysiological sequelae of ouabain toxicity in vivo and in vitro. In normal anesthetized dogs, R 56865 alone at doses of 0.04 to 0.16 mg/kg i.v. had no effect on atrial, AV nodal, or ventricular conduction times and refractoriness, but at doses of 0.64 to 2.5 mg/kg it tended to increase these parameters. In ouabain-pretreated dogs, R 56865 (0.08 to 0.32 mg/kg i.v.) dose-relatedly reduced ouabain-induced ventricular arrhythmias. In normal isolated canine Purkinje fibers, R 56865 (1-10 microM) reduced Vmax at short pacing cycle lengths and decreased the action potential duration at concentrations of 0.1 to 10 microM. R 56865 at concentrations through 10 microM had no significant effect on normal action potentials of canine ventricular muscle and slow response action potentials in guinea pig papillary muscles. In Purkinje fibers exposed to toxic concentrations of ouabain, R 56865 (1 microM) reduced the delayed after depolarization (DAD) amplitude and inhibited triggered activity. R 56865 had no effect on normal automaticity in canine Purkinje fibers at 1 microM, but 10 microM significantly slowed it. R 56865 at 10 microM did not affect isoproterenol-enhanced automaticity and only slightly reduced barium-induced abnormal automaticity that occurred at reduced membrane potentials. These results demonstrate that R 56865 reverses cardiac glycoside-induced arrhythmias in anesthetized dogs at doses that do not significantly affect conduction or refractoriness. Suppression of ouabain-induced DAD and triggered activity in isolated Purkinje fibers, at concentrations not affecting normal or abnormal automaticity, may be the mechanism of R 56865's antiarrhythmic actions in vivo. Suppression of DAD does not appear to be associated with blockade of voltage-dependent calcium channels, but R 56865 may prevent intracellular sodium overload by limiting excessive sodium entry during ouabain intoxication.

Action Potentials↗
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↗
PubMed1992

[Renal aging in man].

Renal morphological and functional changes occur in the elderly. Between the ages of 50 and 80 years the renal mass diminishes by a mean of 20 percent, to the expense of the renal cortex. Glomerular sclerosis results in a gradual fall in the number of functioning glomeruli. Simultaneously, a decrease of about 7 percent in glomerular filtration rate per decade after the age of 40 years and a 10 percent decrease in renal plasma flow per decade, and therefore an increase in filtration fraction, are observed. These haemodynamic abnormalities are accompanied by changes in tubular function, including a delay in renal adjustment to sodium overload, and above all to sodium restriction, together with a decrease in concentrating and, to a lesser extent, diluting capacity. In actual fact, the intensity of glomerular sclerosis varies considerably from one subject to another, and the decrease in glomerular filtration rate is far from being constant. These changes are perhaps not ineluctably associated with aging; they might result from pathological processes that have gone unnoticed.

Adult↗
PubMed2006

Inhibition of sodium-dependent calcium overload to treat myocardial ischemia.

Because intracellular sodium and calcium overload play a key role in both mechanical and electrical dysfunction during myocardial ischemia, inhibition of the late sodium current would be expected to decrease the intracellular sodium and calcium overloads and thereby reduce their undesirable effects. Ranolazine selectively inhibits late sodium current relative to peak sodium current, and attenuates the abnormalities of ventricular repolarization and contractility associated with ischemia. This is the currently proposed mechanism (hypothesis) of action of the effects of ranolazine during myocardial ischemia.

Acetanilides↗
PubMed2004

Susceptibilities to and mechanisms of excitotoxic cell death of adult mouse inner retinal neurons in dissociated culture.

PURPOSE: To explore the susceptibilities of adult retinal neurons in dissociated culture to treatments with excitotoxic agonists and the mechanisms of the resultant retinal cell death. METHODS: C57B6 mice were used. Retinas were removed, dissociated, plated on a polylysine/laminin substrate, and maintained in vitro for 5 to 7 days. Excitotoxic agonists (glutamate, N-methyl-D-aspartate [NMDA], or kainic acid [KA]) were added for 30 minutes or 24 hours, sometimes in the presence of modified extracellular ion concentrations or potential blocking agents. The next day, cells were fixed and immunocytochemically stained to identify ganglion and amacrine cells. Surviving cells were counted. RESULTS: Ganglion cells from adult mouse retinas were much less susceptible to excitotoxic death than those prepared from neonatal retinas. Adult amacrine cells were killed by KA, NMDA, or glutamate. Experiments with selective blockers demonstrated that KA killed through AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors, whereas NMDA and glutamate exerted toxicity through a combination of AMPA and NMDA receptors. The KA-induced death of amacrine cells was not mediated by chloride ions. Removal of extracellular sodium, however, completely prevented the amacrine cell death, and removal of extracellular calcium prevented approximately 70% of the death. The path of calcium entry was investigated. Experiments with selective blockers indicated that the lethal calcium entry was via reverse operation of a sodium-calcium exchanger. CONCLUSIONS: There is a profound developmental regulation in the sensitivity of retina ganglion cells to excitotoxic insults. Excessive intracellular sodium and calcium are the proximal causes of amacrine cell death. The pathologic calcium entry is dependent on the sodium overload, which then drives a sodium-calcium exchanger to take up calcium.

Amacrine Cells↗
PubMed1992

[Studies on the sodium concentration of dialysate solution for continuous ambulatory peritoneal dialysis].

Overloaded sodium(Na) induces the expansion of extracellular volume in case with severe renal insufficiency. Accordingly, in patients undergoing CAPD, the Na balance via trans-peritoneum is the critical determinant of fluid state. This study was performed to clarify the trans-peritoneal Na kinetics in patients using standard dialysate (Na: 132mEq/1,2-1), and to explore the clinical effects of lower Na concentration solution. Peritoneal dialysis effluent obtained from 87 patients was analysed [1.5% dextrose dialysate (D): 33 bags, 2.5%D: 54 bags]. In terms of net-Na removal, no significant relation was found with serum Na level. Whereas, a significant positive relation was found with ultrafiltration (UF) volume (p < 0.01). Net-Na removal was 10.0 +/- 3.3mEq in 1.5%D and 30.2 +/- 1.8 mEq in 2.5%D (mean +/- SEM). On the other hand, ultra low sodium concentration dialysate (ULNaD, Na level: 98mEq/1, Osm:340mOsm/1, 2l) was effectively used for the purpose of increasing Na removal. Net-Na removal was 78.1 +/- 5. 6mEq after 4-hr dwelling (n = 18). ULNaD was applied to ten patients who showed signs of overhydration, using once a day consecutively instead of standard one. After 9 days (mean) in this regimen, signs of overhydration were disappeared. Significant reductions in their body weight and fall in blood pressure were found compared to the periods before commencement of ULNaD, showing remarkable increase in Na removal (p < 0.01, respectively). No significant changes were found in serum Na level or UF volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗