Dietary Chloride Research Articles

The role of SLC26A6‐mediated chloride/oxalate exchange in causing susceptibility to nephrolithiasis

The role of SLC26A6‐mediated chloride/oxalate exchange in causing susceptibility to nephrolithiasis

Nitrogen-15 Determination in Tissues of Laying Hens Fed on Different Levels of 15N-Chlorocholine Chloride (15N-CCC) Diets

An experiment was conducted to determine the distribution of nitrogen-15 in tissues of laying hens receiving different levels of 15 N-CCC in diets. Twenty brown laying hens were divided into four groups and randomly assigned into one of four dietary treatment groups consisting of 0, 5, 50 and 100 ppm 15 N-CCC inclusion. The hens were individually fed with the 15 N-CCC diets in battery cages for 11 days and then all hens restored to feeding on the control diet for 7 days. After eleven days, eight hens were slaughtered, and the others were slaughtered seven days after 15 N-CCC diets withdrawal. Samples of blood, liver, heart and meat were collected and their 15 N contents were determined. The δ 15 N excess (δ 15 N-ex) and atom percentage excess in 15 N were calculated. The δ 15 N-ex and atom percentage excess 15 N increased significantly (p<0.05) with increasing levels of 15 N-CCC in diets in all tissues after feeding 15 N-CCC diets for eleven days. The highest concentration of δ 15 N-ex and atom percentage excess 15 N were detected in blood, followed in order by liver, heart and thigh meat. The concentrations reduced significantly (p<0.05) after 15 N-CCC diets were withdrawn. Comparison between treatment groups showed that δ 15 N-ex and atom percentage excess 15 N were still higher in hens that had been fed diets with higher levels of 15 N-CCC. This study showed that nitrogen-15 was distributed in blood, liver, heart and meat of laying hens.

Effect of potato on acid–base and mineral homeostasis in rats fed a high-sodium chloride diet

Excessive dietary NaCl in association with a paucity of plant foods, major sources of K alkaline salts, is a common feature in Western eating habits which may lead to acid-base disorders and to Ca and Mg wasting. In this context, to evaluate the effects of potato, rich in potassium citrate, on acid-base homeostasis and mineral retention, Wistar rats were fed wheat starch (WS) or cooked potato (CP) diets with a low (0.5 %) or a high (2 %) NaCl content during 3 weeks. The replacement of WS by CP in the diets resulted in a significant urinary alkalinisation (pH from 5.5 to 7.3) parallel to a rise in citrate and K excretion. Urinary Ca and Mg elimination represented respectively 17 and 62 % of the daily absorbed mineral in rats fed the high-salt WS diet compared with 5 and 28 % in rats fed the high-salt CP diet. The total SCFA concentration in the caecum was 3-fold higher in rats fed the CP diets compared with rats fed the WS diets, and it led to a significant rise in Ca and Mg intestinal absorption (Ca from 39 to 56 %; Mg from 37 to 60 %). The present model of low-grade metabolic acidosis indicates that CP may be effective in alkalinising urine, enhancing citrate excretion and ameliorating Ca and Mg balance.

A Miso (Japanese Soybean Paste) Diet Conferred Greater Protection against Hypertension than a Sodium Chloride Diet in Dahl Salt-Sensitive Rats

The purpose of this study was to compare the effects of miso and sodium chloride (NaCl) on blood pressure in both sexes of Dahl and SD rats. The systolic and diastolic blood pressures (SBP/DBP) were measured at 2, 4, 8 and 12 weeks of treatment with a miso diet including 2.3% NaCl, a high-sodium diet including 2.3% or 1.9% NaCl, or a normal diet including 0.3% NaCl (MF diet; Oriental Yeast Co., Tokyo, Japan). The rats were autopsied after 12 weeks on a diet. DBP in male Dahl rats was significantly increased by the 2.3% NaCl diet as compared with that in the MF group (p < 0.01) or miso group (p < 0.05) from 4 weeks of treatment. Thereafter, SBP and DBP in both the high NaCl groups were significantly increased when compared with the MF or miso group. SBP in female Dahl rats on 2.3% NaCI was significantly increased from 8 weeks after treatment. Nephropathy was observed in both sexes of Dahl rats but not SD rats. These results show that blood pressure was not increased by the miso diet.

Contributions of Sodium and Chloride to NaCl-Induced Hypertension

The recommendation to avoid high dietary “salt” intake for the prevention and treatment of hypertension is often expressed in terms of dietary sodium. However, a consistent body of evidence suggests that the chloride component of salt is an important contributor to NaCl-induced elevations of blood pressure.1 In several rat models of salt-sensitive hypertension (Dahl salt-sensitive [S] rat, DOCA-salt hypertension, stroke-prone SHR [SHRSP], angiotensin II-induced salt-sensitive hypertension), selective dietary sodium loading, in the absence of chloride, fails to produce hypertension. In various feeding protocols, anions provided with sodium included various combinations of bicarbonate, phosphate, aspartate, glutamate, and glycinate. Overall, the failure of selective dietary sodium loading to produce hypertension in these studies was not related to group differences of body weight, net sodium balance, blood pH, or serum concentrations of sodium, potassium, or chloride. Similarly, a limited number of clinical observations also indicate that blood pressure is not increased in humans by high dietary sodium intakes in the absence of chloride. In 1929, Berghoff et al reported that blood pressure increased in 7 hypertensive individuals on a high NaCl intake, but not on a high sodium bicarbonate intake.2 This observation was subsequently confirmed.3 Similarly, other investigators have also observed that in contrast to the increase of blood pressure induced by a high NaCl intake in hypertensive patients, blood pressure is not increased by a high sodium intake provided as sodium phosphate or sodium citrate.1 Further suggesting a modulating effect of dietary chloride on blood pressure, in hypertensive and normotensive subjects, substitution of dietary NaCl with equimolar sodium bicarbonate leads to a reduction of blood pressure.4,5 Additionally, in hypertensive humans, the reduction of blood pressure by dietary potassium is attenuated by potassium chloride compared with that of potassium citrate.6 Because the blood pressure increment in response …

Interaction of dietary sodium chloride and waterborne copper in rainbow trout (Oncorhynchus mykiss): copper toxicity and sodium and chloride homeostasis

Juvenile rainbow trout (Oncorhynchus mykiss) maintained on either low sodium chloride (LS (control), 1.4% NaCl) or high sodium chloride (HS, 11% NaCl) diet were exposed to 55 µg·L–1waterborne copper (Cu) for 28 days. Cu-exposed fish maintained on the LS diet exhibited 26% mortality, more than double (11%) that in fish maintained on the HS diet. Waterborne Cu exposure inhibited growth by 56% in fish maintained on the LS diet and by 35% in those maintained on the HS diet. Whole-body and tissue Na+levels, measured 6 h after feeding, were increased by exposure to HS diet and reduced by waterborne Cu exposure. Exposure to elevated waterborne Cu increased whole-body and tissue Cu levels, whereas exposure to HS diet decreased these levels. Moreover, whole-body and tissue Cu concentrations were consistently lower in Cu-exposed fish maintained on HS diet relative to those maintained on LS diet. Plasma Na+and Cl–levels were elevated by HS diet exposure and reduced by waterborne Cu exposure, whereas plasma Cu levels were decreased and increased by exposure to HS diet and waterborne Cu, respectively. These results demonstrate that elevated dietary NaCl modulates Na+and Cl–homeostasis and reduces accumulation and toxicity of waterborne Cu.

Pharmacokinetics and toxicity of bromide following high-dose oral potassium bromide administration in healthy Beagles.

The pharmacokinetics of a multidose regimen of potassium bromide (KBr) administration in normal dogs was examined. KBr was administered at 30 mg/kg p.o. q 12 h for a period of 115 days. Serum, urine, and cerebrospinal fluid (CSF) bromide (BR) concentrations were measured at the onset of dosing, during the accumulation phase, at steady-state, and after a subsequent dose adjustment. Median elimination half-life and steady-state serum concentration were 15.2 days and 245 mg/dL, respectively. Apparent total body clearance was 16.4 mL/day/kg and volume of distribution was 0.40 L/kg. The CSF:serum BR ratio at steady-state was 0.77. Dogs showed no neurologic deficits during maintenance dosing but significant latency shifts in waves I and V of the brainstem auditory evoked response were evident. Following a subsequent dose adjustment, serum BR concentrations of approximately 400 mg/dL were associated with caudal paresis in two dogs. Estimated half-life during the accumulation phase was shorter than elimination half-lives reported in other studies and was likely related to dietary chloride content. The range of steady-state concentrations achieved suggests individual differences in clearance and bioavailability between dogs. The described protocol reliably produced serum BR concentrations that are required by many epileptic patients for satisfactory seizure control.

Potassium Citrate Prevents Increased Urine Calcium Excretion and Bone Resorption Induced by a High Sodium Chloride Diet

The amount of sodium chloride in the diet of industrialized nations far exceeds physiological requirements. The impact of abundant dietary salt on skeletal health has yet to be established, but is potentially detrimental through increased urinary calcium losses. We examined the effect of increased dietary sodium chloride on urine calcium excretion and bone turnover markers in postmenopausal women and, further, whether potassium citrate attenuates the effects of increased dietary salt. Postmenopausal women (n = 60) were adapted to a low-salt (87 mmol/d sodium) diet for 3 wk, then randomized to a high-salt (225 mmol/d sodium) diet plus potassium citrate (90 mmol/d) or a high-salt diet plus placebo for 4 wk. Urine calcium, urine N-telopeptide, urine cAMP, serum osteocalcin, and fasting serum PTH were measured at the end of the low- and high-salt diets. On the high salt plus placebo diet, urine calcium increased 42 ± 12 mg/d (mean ± sem), but decreased 8 ± 14 mg/d in the high salt plus potassium citrate group (P = 0.008, potassium citrate vs. placebo, unpaired t test). N-telopeptide increased 6.4 ± 1.4 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus placebo group and 2.0 ± 1.7 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus potassium citrate group (P < 0.05, potassium citrate vs. placebo, unpaired t test). Osteocalcin, PTH, and cAMP were not significantly altered. The addition of oral potassium citrate to a high-salt diet prevented the increased excretion of urine calcium and the bone resorption marker caused by a high salt intake. Increased intake of dietary sources of potassium alkaline salts, namely fruit and vegetables, may be beneficial for postmenopausal women at risk for osteoporosis, particularly those consuming a diet generous in sodium chloride.

Echo doppler assessment of left ventricular function in rats with hypertensive hypertrophy

Objective: This study attempted to establish echocardiographic measurements of left ventricular (LV) mass and LV systolic and diastolic function, particularly in rats with hypertensive heart. Methods: M-mode LV echograms and Doppler mitral flow were obtained in Dahl salt-sensitive rats placed on 0.3% or 8% sodium chloride diet. Echo Doppler measurements were compared with catheterization and pathologic measurements in 54 rats for LV mass and in 45 rats for LV systolic and diastolic function. Results: Echocardiographic measurement of LV mass correlated well with pathologic measurement (r = 0.94, P <.01, n = 54, SEE = 0.08 mg), independent of LV size, aging, and therapeutic intervention. Endocardial fractional shortening (FS) correlated with LV peak + dP/dt (r = 0.56, n = 45, P <.01), and the correlation was improved to r = 0.71 if 11 rats with marked LV hypertrophy were excluded. Midwall FS correlated well with LV peak + dP/dt (r = 0.72, n = 45, P <.01) even if rats with extremely thickened ventricular wall were included. If midwall FS was lower than 14%, LV systolic dysfunction was very likely (sensitivity 67%, specificity 91%). Association of mitral E/A ratio of 2.0 or greater with deceleration time of shorter than 35 ms was an accurate indicator of elevated LV end-diastolic pressure (sensitivity 82%, specificity 86%) and increased lung weight because of congestive heart failure (sensitivity 89%, specificity 96%) in rats with hypertension. Conclusion: LV mass, LV systolic function, and LV end-diastolic pressure were assessable with echo Doppler in rats with hypertensive heart. (J Am Soc Echocardiogr 2002;15:109-17.)

The effect of dietary chloride and bicarbonate on blood pH, haematological variables, pulmonary hypertension and ascites in broiler chickens

1. The effect of supplementing grower diets with bicarbonate or chloride on haematological variables, pulmonary hypertension syndrome and ascites in broilers exposed to cold temperature was investigated. 2. High concentrations of dietary chloride had no effect on the pH of the venous blood but a low chloride/high bicarbonate diet significantly increased blood pH. There was no consistent effect of dietary chloride or bicarbonate concentrations on growth performance, although in 1 experiment birds given a low chloride/high bicarbonate diet consumed less food and gained less weight than controls. 3. Birds fed on high-chloride diets tended to have a higher incidence of ascites and pulmonary hypertension than controls. Birds fed on low-chloride and high-bicarbonate diets had significantly lower pulmonary hypertension and lower heart weights, which may have indicated a decrease in pulmonary and systemic blood pressure. 4. We conclude that increasing dietary bicarbonate and reducing dietary chloride has potential as a low cost and effective method to reduce the pulmonary hypertension which leads to ascites in broiler chickens.

Central AT1 and AT2 receptors mediate chronic intracerebroventricular angiotensin II-induced drinking in rats fed high sodium chloride diet from weaning.

Intracerebroventricular (ICV) angiotensin (AIl) administration stimulates central AII receptors to induce water consumption in rats. The aim of this study was to determine the role of brain AT1 and AT2 receptors in mediating chronic ICV AII-induced drinking in rats raised on normal or high sodium chloride diets from weaning. Rats were weaned at 21 days of age and placed on normal or high sodium chloride diet for 10-12 weeks. At adulthood, the animals were instrumented with brain lateral ventricular cannulas and femoral arterial catheters. Low dose chronic central AII infusion (20 ng min(-1)) significantly (P < 0.05) increased water intake in both groups of rats when compared with their respective controls of 24 h artificial cerebrospinal fluid infusions. In a separate group of high sodium fed rats, coinfusion of AII with the AT1 receptor antagonist, losartan (0.25 microg min(-1)) or the AT2 receptor blocker, PD 123319 (0.50 microg min(-1)) blocked chronic ICV AII-induced drinking. Upon reinfusion of AII water intake increased above control. Following the cessation of AII infusions, water intake returned to values not significantly different from control (P > 0.05). In contrast, in the normal sodium fed rats losartan, but not PD 123319, blocked the AII-mediated water intake. The data demonstrate that in high sodium chloride fed rats AII stimulates both central AT1 and AT2 receptors to induce drinking, while in the normal sodium chloride fed rats the peptide activates the drinking response primarily by stimulation of central AT1 receptors.

Dietary manipulation to reduce aerial ammonia concentrations in nursery pig facilities.

Two 4-wk trials (preliminary study) and three 5-wk trials (major study) were conducted to determine the effects of adding Yucca schidigera extract or anhydrous calcium chloride to nursery diets on the growth performance of nursery pigs and aerial ammonia concentration. The pigs were weaned between 13 and 15 d of age and had an initial BW of 3 to 6 kg. In each trial, pigs were allotted to three identical pig nursery rooms that were environmentally regulated. There were three diets (one diet per room): 1) control, containing 23% CP; 2) control plus 125 ppm of Yucca schidigera extract; and 3) control plus 1.95% anhydrous calcium chloride. Growth performance was recorded weekly. Aerial ammonia concentration was measured daily using aspiration detector tubes and during the last week of each trial using diffusion tubes. Manure samples were collected twice a week during the experimental period to determine ammonia and N concentrations and pH. Plasma urea concentration was determined in blood samples collected from the pigs at the end of each trial. Data were analyzed using split-plot and Latin square designs for the preliminary and major studies, respectively. Feed intake was similar among pigs fed all three diets. There were no differences in ADG and ADG/ADFI (G/F) between pigs fed the control diet and pigs fed the yucca extract diet (P > or = 0.41). In all trials, pigs fed the calcium chloride diet had lower ADG and G/F than pigs fed the other two diets (P < 0.05). In the preliminary study, aerial ammonia tended to be greater in the rooms in which pigs were fed the control diet than in the rooms with pigs fed the yucca extract diet (P = 0.08) and the calcium chloride diet (P = 0.11). In the major study, aerial ammonia increased weekly (diet x week; P < 0.001) in all rooms. In the 4th wk, ammonia concentrations were greater (P < 0.001) in the rooms in which pigs were fed the control diet than in the rooms in which the other two diets were fed. Dietary treatment had no effect on plasma urea concentration (P > or = 0.10), manure ammonia and N concentrations (P > or = 0.50), and manure pH (P > or = 0.78). Although aerial ammonia concentrations were relatively low, the addition of Yucca schidigera extract or calcium chloride to the diet of nursery pigs reduced ammonia concentrations in the nursery rooms.

Evaluation of the Chloride Requirement of the Broiler Breeder Hen

Two experiments wore conducted to evaluate the chloride requirement of the broiler breeder hen. Experiments were conducted for a twelve-week period and seven experimental diets wore fed. The diets contained the following dietary chloride levels: 0. 040, 0. 047, 0. 054, 0.060, 0.073, 0.09g, and 0. 174%. Sodiam bicarbonate was used to maintain a constant level of sodium. Levels of dietary chloride below 0.054% reduced EF; EW, &amp; EC (ED X (EW-shell wt). Also, the highest level of dietary chloride reduced all characteristics. Dietary chloride did not have a significant effect on body weight gain or fertility and hatchability of eggs. The Nationa/ Research Council (1994) suggests that the broller breeder hen have daily chloride intake of 185 milligrams per hen per day. In Experiments 1 and 2 the requirement was 96.1 mg/hen/day and 101. 1 mg/hen/day for EP, 116.1 mg/hen/day and 148.3 mg/hen/day for maximum EW, and 95.9 mg/hen/day and 109. 5 mg/hen/day for EC, respectively.

Dietary chloride does not correlate with urinary thromboxane in deoxycorticosterone acetate–treated rats

Renal vascular resistance in deoxycorticosterone acetate (DOCA) salt–treated uninephrectomized rats is increased by high dietary chloride. Because DOCA salt–hypertensive rats exhibit an increased urinary excretion of thromboxane B2 (TXB2), a metabolite of thromboxane A2 (TXA2), the increased TXB2 excretion by DOCA salt–treated rats could relate to elevated dietary chloride, increased blood pressure, and/or the presence of intact renal tubules. We hypothesized that high NaCl intake, resulting in an elevated tubular chloride excretion, stimulates TXA2 production. A result of that production could be renal vasoconstriction. Baseline blood pressures were measured for 10 days, and then the rats were treated with DOCA (30 mg/kg) and fed (1) normal NaCl, (2) normal sodium with high chloride, or (3) high sodium chloride (NaCl) for 4.5 weeks. Next, the rats were uninephrectomized (1K) or unihydronephrectomized (1KHK) to yield one kidney without an intact tubular system and therefore no macula densa. Two and a half weeks later, urinary excretion of TXB2 was determined. DOCA-high NaCl-fed 1KHK or 1K rats had significant increases in systemic blood pressure to 172 ± 12 and 190 ± 5 mm Hg, respectively, compared with no significant increase in blood pressure among the other groups. Urinary TXB2 excretion was increased to 29 ± 4 pg per 24 hours per gram of body weight in all DOCA-treated 1KHK and 1K animals regardless of diet compared with DOCA-treated animals with two intact kidneys (13 ± 2 pg per 24 hours per gram of body weight). DOCA treatment in rats with one functional kidney results in the excretion of high levels of urinary TXB2 unrelated to dietary chloride load, blood pressure, or intact renal tubules. (J Lab Clin Med 2000;135:493-7)

Hypocalcemia induced by intravenous administration of disodium ethylenediaminotetraacetate and its effects on excretion of calcium in urine of cows fed a high chloride diet.

Evidence supports the theory that a diet that is rich in nonmetabolizable anions fed to dairy cows during the dry period reduces the risk of hypocalcemic paresis puerperalis. When cows are fed a diet that is rich in anions instead of cations, more Ca is absorbed in the intestine and excreted in urine. We hypothesized that, in cows fed a diet that was rich in anions, the increased flow of Ca through the body could be drained to support the maintenance of plasma Ca concentration around parturition. The hypothesis was tested by binding plasma Ca through intravenous administration of Na2-EDTA and measuring excretion of Ca in urine. In a 2-period x 14-d crossover study, six, nonpregnant, nonlactating, multiparous cows were fed either a diet that was rich in cations (dietary cation-anion difference = +332 meq/kg of dry matter) or rich in anions (dietary cation-anion difference = -230 meq/kg of dry matter). On the last day of each feeding period, Na2-EDTA was infused intravenously until the amount of plasma Ca that was not bound to EDTA reached approximately 1 mmol/L. The amount of EDTA that could be infused was significantly greater when the cows were fed the diet that was rich in anions. During the infusion of Na2-EDTA the rate of Ca excretion in urine dropped to almost 0 when the diet that was rich in anions was fed. After feeding the diet that was rich in cations, excretion of Ca in urine was negligible and was not reduced further by Na2-EDTA infusion. Thus, in cows fed a diet that was rich in anions, the Ca intended for excretion with urine can be used when plasma Ca is under stress as would occur at the onset of lactation. However, the amount of Ca derived from plasma, interstitial fluid, and the skeleton during Na2-EDTA infusion was quantitatively much more important to the supply of Ca than was the reduction in excretion of Ca in urine. Most likely, this relationship would also be true when the production of colostrum begins.

α-Adrenergic systems mediate chronic central AII hypertension in rats fed high sodium chloride diet from weaning

Hypertension is elicited by chronic, low dose intracerebroventricular (ICV) angiotensin II (AII) infusion in rats raised from weaning on relatively high sodium chloride diet (250 mEq kg −1 food). This experimental model of hypertension is dependent upon renal innervation and associated with neurogenic sodium retention. The present study determined whether this neurogenic ICV AII hypertension is mediated by central α-adrenoceptors. Rats were weaned at 21 days of age and fed a 1.5% (250 mg kg −1 food) sodium chloride diet for 10–12 weeks. At adulthood, animals were instrumented with central nervous system (CNS) lateral ventricular cannulas, femoral artery and vein catheters and housed in metabolic pens for chronic study. Low dose ICV AII infusion (20 ng min −1) increased mean arterial pressure (MAP) from 121±4 to 140±6 mm Hg on the day of ICV infusion. This increase in arterial pressure was associated with 3 consecutive days of decreased urinary sodium excretion. Subsequent ICV α-adrenoceptor blockade with phentolamine (AII+phentolamine) abolished the pressor and antinatriuretic responses to low dose chronic ICV AII infusion. Resumption of ICV AII infusion alone increased in MAP toward pre-α-adrenergic blockade values (133±5 mm Hg) on day 8. Following cessation of ICV AII infusion, arterial pressure and sodium excretion returned to values not significantly different from control. This model of hypertension was not dependent on circulating plasma renin activity (PRA), since PRA decreased during ICV AII infusion. These data confirm that low dose ICV AII causes hypertension and sodium retention in rats raised from weaning on moderately elevated sodium intake. We conclude that AII mediated neurogenic hypertension and antinatriuresis is elicited by stimulation of AT 1 receptors on neurons which interact with noradrenergic cell bodies in cardiovascular and autonomic centers that may modulate renal sympathetic outflow via α-adrenoceptors.

Salt induces myocardial and renal fibrosis in normotensive and hypertensive rats.

The detrimental effects of high dietary salt intake may not only involve effects on blood pressure and organ hypertrophy but also lead to tissue fibrosis independently of these factors. The effect of a normal (1%) or high (8%) sodium chloride diet on myocardial and renal fibrosis was assessed by quantitative histomorphometry in spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto rats (WKYs). The effect of salt on transforming growth factor-beta1 (TGF-beta1) gene expression was assessed by Northern blot hybridization. A high-salt diet from 8 to 16 weeks of age resulted in increased blood pressure and left ventricular and renal hypertrophy in both WKYs and SHRs. Marked interstitial fibrosis was demonstrated in the left ventricle (LV), glomeruli, and renal tubules and in intramyocardial arteries and arterioles but not in the right ventricle. The collagen volume fraction increased significantly after high-salt diet in the LV, intramyocardial arteries and arterioles, glomeruli, and peritubular areas in both WKYs and SHRs. In the kidneys, glomerular and peritubular type IV collagen was also increased. There was overexpression of TGF-beta1 mRNA in the LV and kidneys in both rat strains after a high-salt diet (all P<0.001). High dietary salt led to widespread fibrosis and increased TGF-beta1 in the heart and kidney in normotensive and hypertensive rats. These results suggest a specific effect of dietary salt on fibrosis, possibly via TGF-beta1-dependent pathways, and further suggest that excessive salt intake may be an important direct pathogenic factor for cardiovascular disease.

AT 1 receptors mediate chronic central nervous system AII hypertension in rats fed high sodium chloride diet from weaning

CNS angiotensin II (AII) hypertension is induced by chronic, low dose intracerebroventricular (ICV) AII infusion only in rats raised on a relatively high sodium chloride diet (250 meq kg −1 food) from weaning. This experimental model of hypertension is dependent upon renal sympathetic innervation and associated with neurogenic sodium retention. This study determined whether AT 1 and/or AT 2 receptor subtypes in the CNS mediate this neurogenic ICV AII hypertension. Rats were weaned at 21 days of age and fed a 1.5% sodium chloride diet for 10–12 weeks. At adulthood, animals were instrumented with CNS lateral ventricular cannulas, femoral arterial and vein catheters and housed in metabolic pens for chronic study. Low dose ICV AII infusion (20 ng min −1) increased mean arterial pressure by 12±2 mm Hg and decreased urinary sodium excretion for three consecutive days. Subsequent ICV AT 1 blockade with losartan abolished both the pressor and antinatriuretic responses to low dose ICV AII. In contrast, ICV AT 2 receptor blockade with PD 123319 did not affect either angiotensin induced pressor or antinatriuretic responses. Following cessation of ICV AII infusion, arterial pressure and sodium excretion returned to values not significantly different from control in both groups of rats. These data confirm that low dose ICV AII causes hypertension and sodium retention in rats raised from early age on moderately elevated sodium intakes. This AII mediated neurogenic hypertension and antinatriuresis is transduced by activation of CNS AT 1 receptors and not by activation of central AT 2 receptors.

The Use of Diets Containing High Levels of Zinc for Controlling Early Growth in Female Broiler Chicks

A study was carried out with White Rock female chicks to evaluate the possibility of using dietary Zn supplied as ZnO, to control feed intake and weight gain during the period of 1 to 3 wk of age. The levels of supplemental Zn tested were 0, 0.25, 0.50, and 1.0% (Experiment 1); 0, 0.65, 0.75, and 0.85% (Experiment 2); 0.7 and 0.8% (Experiment 3). The effect of Zn supplementation was compared with that of a low sodium chloride diet (L-NaCl-D) and of severe feed restriction (SFR), which was calculated to supply energy only for maintenance (Experiments 1 and 3, respectively). The compensatory growth of the chicks from 3 to 4 wk of age was also evaluated.Feed intake and weight gain were negatively proportional to the levels of dietary Zn supplementation and there were significant (P < 0.02 and P < 0.01, in Experiments 1 and 2, respectively) negative correlations between supplemental dietary Zn levels and relative weight gains (values observed in the unsupplemented diet = 100%). The effects of L-NaCl-D and SFR on decreasing weight gain were calculated, according to the equations obtained in Experiments 1 and 2 to be equivalent to these of 0.58 to 0.65% and 0.78 to 0.87% Zn supplementation, respectively.Relative weight gain and feed efficiency of the chicks from 3 to 4 wk of age, after withdrawal of the growth-depressing factors, were positively related to the degree of growth depression during 1 to 3 wk of age; however, the intensity of recovery from a similar degree of growth depression induced by L-NaCl-D, SFR, or dietary Zn was least in the last mentioned treatment. It is concluded that dietary Zn supplementation can be used as an efficient tool for controlling early growth of young broiler breeder chicks.

High dietary chloride content associated with loss of therapeutic serum bromide concentrations in an epileptic dog

High dietary chloride content associated with loss of therapeutic serum bromide concentrations in an epileptic dog