OBJECTIVE: To investigate the effects of central nucleus of amygdala (CeA) lesion on the initiation and expression of sodium appetite in sodium-deficient rats. METHODS: Three groups of SD rats (n=6 in each group) were treated with bilateral CeA lesion, sham lesion or no lesion. After the recovery, the rats were fed with low-sodium diets for 14 days to establish a sodium-deficient rat model. The double-bottle selection in single cage test was used to observe the intake of 0.3 mol/L NaCl and DW in 5 timepoint with 24 hours in sodium-deficient rats. Immunofluorescence staining of aldosterone-sensitive neurons in the nucleus tractus solitarii (NTS)was used to investigate the effect of CeA lesion or not on the activity of aldosterone-sensitive neurons in rats with or without sodium deficiency. RESULTS: After fed with low-sodium diet for14 days, the volume and preference rate of 0.3 mol/L NaCl intake of the rats within 24 h were significantly increased compared with those before low-sodium diet (P＜0.01). The intake volume and the preference rate of 0.3 mol/L NaCl in CeA lesion rats were significantly decreased than those in CeA sham lesion rats and normal rats in the sodium-deficient condition (P＜0.01). The CeA lesion had no effects on the activity of aldosterone-sensitive neurons in NTS in rats with low-sodium diet. CONCLUSION Low-sodium diet induces an increase in the expression of sodium appetite in rats. CeA lesions inhibit the behavioral expression of sodium appetite in sodium-deficient rats but have no effects on the initiation of sodium appetite in rats with sodium-deficient rats.
Amygdala ; pathology ; Animals ; Appetite ; Diet, Sodium-Restricted ; Neurons ; Rats ; Rats, Sprague-Dawley ; Sodium ; Sodium, Dietary ; pharmacology

OBJECTIVETo explore a sampling method which could reflect iodine deficiency disorders (IDD) status at provincial level and discover risk areas with non-iodized salt problem.

METHODBaseline data of Iodized salt from Gansu and Fujian provinces were analyzed with Monte Carlo method both at county and prefecture levels respectively. True positive rate and false positive rate were also calculated.

RESULTSWith data from 7 - 8 villages or 4 - 5 townships counties at risk could be discovered. The true positive rate was around 80% and false positive rate was around 20%. At prefecture level, when randomly selecting and checking 3 counties, the samples would satisfy the discovery of all the risk areas with non-iodized salt problem.

CONCLUSIONSWe suggested that the sampling method of iodized salt investigation in national IDD surveillance as follows: to randomly choose 3 counties at each prefecture, 4 townships at each county, 2 villages at each township and 10 salt samples by household survey. The coverage rate of iodized salt in a province could be calculated by post-weighted method with population number.

China ; Drug Monitoring ; methods ; Humans ; Iodine ; deficiency ; pharmacology ; Monte Carlo Method ; Sodium Chloride, Dietary ; pharmacology

The present study evaluated the response of blood pressure (BP) by dietary sodium in sodium resistant (SR) subjects. One hundred one subjects (mean age, 46.0 yr; 31 hypertensives) were admitted and given low sodium-dietary approaches to stop hypertension (DASH) diet (LSD, 100 mM NaCl/day) for 7 days and high sodium-DASH diet (HSD, 300 mM NaCl/day) for the following 7 days. On the last day of each diet, 24 hr ambulatory BP was measured. Morning systolic BP (SBP) and diastolic BP (DBP) were elevated after HSD in all subjects (P < 0.01), but daytime SBP and DBP were not changed (P > 0.05). In hypertensive subjects, morning DBP elevation was greater than daytime DBP elevation (P = 0.036), although both DBPs were significantly elevated after HSD. The augmented elevation of morning DBP in hypertensive subjects was contributed by the absolute elevation of morning DBP (P = 0.032) and relative elevation to daytime DBP (P = 0.005) in sodium resistant (SR) subjects, but not by sodium sensitive subjects. Although there was no absolute elevation, SR subjects with normotension showed a relative elevation of morning SBP compared to daytime SBP change after HSD (P = 0.009). The present study demonstrates an absolute and relative elevation of morning BP in SR subjects by HSD.
Adult ; Blood Pressure/*drug effects ; Diet, Sodium-Restricted ; Humans ; Hypertension/*physiopathology ; Middle Aged ; Sodium, Dietary/*pharmacology ; Time Factors

OBJECTIVETo evaluate the effectiveness of universal salt iodization (USI) for the control of IDD in Hebei province since it was implemented in 1995, identify the problems currently encountered in the implementation of USI and provide practical proposals for addressing these problems.

METHODSProbability proportionate to size sampling (PPS) was employed in the surveillance of IDD, for which a total of 1200 school children aged 8-10 years were randomly selected from 30 counties around the whole province during each IDD survey. The iodine content of salt was determined quantitatively with the titration method. The iodine content of urinary samples was measured by the method of ammonium persulfate oxidation.

RESULTSThe coverage of iodized salt increased from 65.0% in 1995 to 98.0% in 1999, then decreased to 88.1% in 2005 which was below the national standard of 90%. The median urinary iodine of children aged 8-10 years varied between 160.1 microg/L and 307.4 microg/L, which was above the national standard. The proportion of urinary samples with iodine content above 300 microg/L was over 30% in 2005, implying exorbitant iodine nutrition among the children. The goiter rate (TGR) among children aged 8-10 years dropped from 11.8% in 1995 to 2.7% in 2005, indicating that the spread of endemic goiter was under control.

CONCLUSIONPreliminary elimination of IDD was achieved by USI in Hebei province. Nevertheless, some problems still existed in USI such as non-iodized salt competition, over iodization and un-standardized iodization. In order to address these problems, the management and supervision of salt market needs to be strengthened to prevent non-iodized salt from reaching households; updating equipment and modifying techniques are also necessary to ensure the quality of iodized salt; to clarify the causes of excessive urinary iodine content, the various sources of iodine from the diet need to be investigated in the future.

Child ; China ; epidemiology ; Female ; Goiter ; epidemiology ; prevention & control ; Humans ; Hypothyroidism ; epidemiology ; prevention & control ; Iodine ; deficiency ; pharmacology ; urine ; Male ; Nutrition Policy ; Nutritional Status ; Sodium Chloride, Dietary ; pharmacology ; Time Factors

OBJECTIVETo evaluate the influence of different salt iodine concentration on urinary iodine excrition among the target population and to determine the appropriate level of salt iodization to the local people.

METHODSIn the 31-day random control trial, 1099 subjects from 399 families were randomly distributed into four groups and were supplied with iodized-salt with different iodine concentration of (6 +/- 2)mg/kg, (15 +/- 2)mg/kg, (24 +/- 2)mg/kg and (34 +/- 2)mg/kg, respectively. The original family salt was retrieved, whose iodine content was determined in those subjects' families with single-blind method. Baseline survey was conducted including salt and urinary iodine of the subjects. From the 27th day after the intervention, the urinary samples of the subjects were continuously collected for 5 days and urinary iodine was tesed respectively. Meanwhile, daily meal investigation was conducted to evaluate the influences originated from food.

RESULTSThe median of local water iodine content was 3.05 microg/L and the average salt iodine concentration was (36.4 +/- 5.4)mg/kg while 98.8% of the household consumed sufficient iodized-salt. The medians of baseline urinary iodine of the subjects were 293.6 microg/L in city, and 508.8 microg/L in the countryside. The urinary iodine medians of four groups in the day of 28th after intervention were 97.2 microg/L, 198.6 microg/L, 249.4 microg/L, and 330.7 microg/L respectively in the city group, while they were 100.5 microg/L, 193.0 microg/L, 246.3 microg/L and 308.3 microg/L seperately in the countryside group. There was no statistically significant differences among the medians of urine iodine in the 27th, 28th, 29th, 30th and 31st day after intervention (P > 0.05).

CONCLUSIONSThe target areas were with iodine deficiency which possessed high coverage of qualified iodized-salt at household level. The average urinary iodine level of the subjects was slightly higher than the standard level, according to the baseline survey. The intervetion trail showed that the salt iodine concentration of 15-24 mg/kg was sufficient to the local people.

Adolescent ; Adult ; Child ; Child, Preschool ; Dose-Response Relationship, Drug ; Female ; Housing ; Humans ; Iodine ; deficiency ; pharmacology ; urine ; Male ; Pregnancy ; Sodium Chloride, Dietary ; pharmacology ; Time Factors

OBJECTIVETo investigate the effects of salt loading on blood pressure and the expression of arterial chloride channel in rats with elevated blood pressure induced by angiotensin II (AngII).

METHODSMale 12-week-old SD rats were randomly divided into AngII and control groups, and in the former group, the rats were exposed to subcutaneous AngII infusion delivered via a drug pump (at 100 ng. kg(-1). min(-1)) for 2 weeks. After the exposure, each group of the rats was further divided into 2 subgroups to receive a high-salt diet (4% NaCl) or normal salt diet (0.6% NaCl) for 12 weeks. The tail blood pressure and sodium metabolism of the rats were measured during the experiment. Since the commencement of salt loading, 6 rats were sacrificed every 4 weeks to obtain the artery samples, in which mCLCA(4) mRNA expression in the arterial smooth muscles was detected by in situ hybridization using mCLCA(4) oligonuclear probe.

RESULTSThe blood pressure of rats in AngII group was significantly higher than that of the control rats (P<0.05), but AngII did not produce significant effects on the expression of mCLCA(4). mCLCA4 mRNA expression was significantly increased in the arterial smooth muscle cells of the rats in high salt groups as compared with those in normal salt groups (P<0.05).

CONCLUSIONA sub-pressor dose of AngII can result in blood pressure elevation, but the mechanism of which does not seem to involve mCLCA(4) expression. mCLCA(4) mRNA expression is up-regulated in normal SD rats after high salt feeding, but salt loading does not obviously affect blood pressure, suggesting the role of mCLCA(4) in antagonizing the pressure-elevating effect of salt loading.

Angiotensin II ; pharmacology ; Animals ; Blood Pressure ; drug effects ; Chloride Channels ; biosynthesis ; genetics ; In Situ Hybridization ; Male ; Muscle, Smooth, Vascular ; drug effects ; metabolism ; RNA, Messenger ; biosynthesis ; genetics ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sodium Chloride, Dietary ; administration & dosage ; pharmacology

Metformin (MET), an antidiabetic agent, also has antioxidative effects in metabolic-related hypertension. This study was designed to determine whether MET has anti-hypertensive effects in salt-sensitive hypertensive rats by inhibiting oxidative stress in the hypothalamic paraventricular nucleus (PVN). Salt-sensitive rats received a high-salt (HS) diet to induce hypertension, or a normal-salt (NS) diet as control. At the same time, they received intracerebroventricular (ICV) infusion of MET or vehicle for 6 weeks. We found that HS rats had higher oxidative stress levels and mean arterial pressure (MAP) than NS rats. ICV infusion of MET attenuated MAP and reduced plasma norepinephrine levels in HS rats. It also decreased reactive oxygen species and the expression of subunits of NAD(P)H oxidase, improved the superoxide dismutase activity, reduced components of the renin-angiotensin system, and altered neurotransmitters in the PVN. Our findings suggest that central MET administration lowers MAP in salt-sensitive hypertension via attenuating oxidative stress, inhibiting the renin-angiotensin system, and restoring the balance between excitatory and inhibitory neurotransmitters in the PVN.
Animals ; Antioxidants ; therapeutic use ; Arterial Pressure ; drug effects ; Hypertension ; chemically induced ; drug therapy ; Infusions, Intraventricular ; Male ; Metformin ; administration & dosage ; pharmacology ; Neurotransmitter Agents ; metabolism ; Oxidative Stress ; drug effects ; Paraventricular Hypothalamic Nucleus ; drug effects ; Rats ; Reactive Oxygen Species ; metabolism ; Sodium Chloride, Dietary ; pharmacology

Angiotensin (Ang)-(1-7) is an important biologically-active peptide of the renin-angiotensin system. This study was designed to determine whether inhibition of Ang-(1-7) in the hypothalamic paraventricular nucleus (PVN) attenuates sympathetic activity and elevates blood pressure by modulating pro-inflammatory cytokines (PICs) and oxidative stress in the PVN in salt-induced hypertension. Rats were fed either a high-salt (8% NaCl) or a normal salt diet (0.3% NaCl) for 10 weeks, followed by bilateral microinjections of the Ang-(1-7) antagonist A-779 or vehicle into the PVN. We found that the mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and plasma norepinephrine (NE) were significantly increased in salt-induced hypertensive rats. The high-salt diet also resulted in higher levels of the PICs interleukin-6, interleukin-1beta, tumor necrosis factor alpha, and monocyte chemotactic protein-1, as well as higher gp91 expression and superoxide production in the PVN. Microinjection of A-779 (3 nmol/50 nL) into the bilateral PVN of hypertensive rats not only attenuated MAP, RSNA, and NE, but also decreased the PICs and oxidative stress in the PVN. These results suggest that the increased MAP and sympathetic activity in salt-induced hypertension can be suppressed by blockade of endogenous Ang-(1-7) in the PVN, through modulation of PICs and oxidative stress.
Angiotensin I ; antagonists & inhibitors ; metabolism ; Animals ; Antioxidants ; pharmacology ; Blood Pressure ; drug effects ; Hypertension ; chemically induced ; drug therapy ; Male ; Oxidative Stress ; drug effects ; Paraventricular Hypothalamic Nucleus ; drug effects ; Peptide Fragments ; antagonists & inhibitors ; metabolism ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; metabolism ; Sodium Chloride, Dietary ; pharmacology