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PubMed1997

A calcium-dependent chloride current in insulin-secreting beta TC-3 cells.

Ca(2+)-dependent conductances have been hypothesized to play a role in the bursting pattern of electrical activity of insulin-secreting beta cells in response to high plasma glucose. A Maxi K+ channel has received the most attention, while a low-conductance Ca(2+)-activated K+ current has also been identified. We used an increasingly popular beta cell model system, the beta TC-3 cell line, and the perforated-patch technique to describe the properties of a novel Ca(2+)-dependent Cl- current [ICl(Ca)] in insulin-secreting pancreatic beta cells. The reported ICl(Ca) could be activated under physiological Ca2+ concentrations and is the first of its kind to be described in pancreatic insulin-secreting cells. We found that long depolarizing steps above -20 mV elicited an outward current which showed slow inward relaxation upon repolarization to negative membrane potentials. Both the outward currents and the inward tails showed dependence on Ca2+ influx: their current/voltage (I/V) relations followed that of the "L-like" Ca2+ current (ICa) present in these cells; they were blocked completely by the removal of external Ca2+ or application of Cd2+ at concentrations sufficient for complete block of ICa; and their magnitude increased with the depolarizing step duration. Moreover, the inward tail decayed monoexponentially with a time constant which at voltages negative to activation of ICa showed a weak linear voltage dependence, while at voltages positive to activation of ICa it followed the voltage dependence of ICa. This Ca(2+)-dependent current reversed at -21.5 mV and when the external Cl- concentration was reduced from 159 mM to 62 mM the reversal potential shifted by approximately +20 mV as predicted by the Nernst relation for a Cl(-)-selective current. Cl- channel blockers such as DIDS (100 microM) and niflumic acid (100 microM) blocked this current. We concluded that this current was a Ca(2+)-dependent Cl- current [ICl(Ca)]. From substitution of the external Cl- with various monovalent anions and from the reversal potentials we obtained the following permeability sequence for ICl(Ca): I- > NO3- > Br- > Cl- > Acetate.

Animals↗
PubMed2000

Perturbation by the PCB mixture aroclor 1254 of GABA(A) receptor-mediated calcium and chloride responses during maturation in vitro of rat neocortical cells.

GABA(A) receptors are targets of highly chlorinated environmental chemicals and have important roles in developing neurons. As such, we examined effects of polychlorinated biphenyls (PCBs) on GABA(A) receptor responses in primary cultures of rat neocortical cells using fluorescence imaging techniques. Between days in vitro (DIV) 5 and 8, the effect of GABA(A) receptor stimulation switched from excitatory (Ca(2+) entry following a Cl(-) efflux; DIV </=6) to inhibitory (Cl(-) influx without a Ca(2+) rise; DIV >/=7). GABA(A)-receptor-stimulated increases in [Ca(2+)](i) were diminished in a concentration-dependent (1-20 microM) manner following 1 h of exposure to the PCB mixture Aroclor 1254 (A1254), with significant reductions at concentrations as low as 2 microM. A1254 (1-20 microM) also led to concentration-dependent increases in basal [Ca(2+)](i), irrespective of DIV. A1254 (10 and 20 microM) significantly increased basal Ca(2+)(i); the Ca(2+)(i) was elevated to 426 +/- 39 nM by 20 microM A1254 but this concentration was not cytotoxic at 1 h. In addition, the mixture, A1254, as well as ortho- and non-ortho-chlorinated PCB congeners (IUPAC Nos. 4, 15, 126, and 138; 5-10 microM) individually decreased GABA(A)-stimulated Ca(2+)(i) responses and this tended not to depend on increases in basal Ca(2+)(i). In cultures DIV 7 and older, A1254 (20 microM) also impaired inhibitory GABA(A) responses as evidenced by an approximately 50% reduction of GABA(A)-stimulated Cl(-) influx (from approximately 6 to 8 mM net accumulation in controls). The results demonstrate that: (1) GABA(A) receptor increases in Ca(2+)(i) and Cl(-)(i) are inhibited by 2-20 microM A1254, regardless of whether the responses are at excitatory or inhibitory stages of development; (2) Ca(2+)(i) homeostasis in cortical cells is disrupted by 10 microM A1254; yet (3) disruption of excitatory GABA(A) responses by A1254 or PCB congeners does not necessarily depend on impaired Ca(2+) homeostasis. These novel observations suggest that GABA(A) receptor responses are a sensitive target for PCB effects in the rat developing nervous system.

Animals↗
PubMed1986

Calcium-dependent chloride currents in isolated cells from rat lacrimal glands.

Isolated cells from rat lacrimal glands were studied with the tight-seal whole-cell recording technique. Cells were dialysed with K-free solutions containing a high concentration of Ca2+ buffer in order to record Ca-dependent Cl- currents at a Ca2+ level fixed between 0.1 and 10 microM. HEDTA was preferable to EGTA as a Ca2+ buffer, even under conditions of equivalent equilibrium buffering power. After replacement of all internal K+ with Na+, the cells displayed a small conductance component which could be abolished by removal of external K+ or by external application of 2 mM-tetraethylammonium. It is suggested that this conductance is due to Ca-dependent K+ channels. The main part of the cell current was Cl selective. The Cl- conductance was negligible at 0.5 microM-Ca2+, and fully activated at 2 microM-Ca2+. The dose-response curve relating Cl- currents to the internal Ca2+ concentration, [Ca]i, was steeper than predicted by a simple binding isotherm reaction. Relaxations observed in response to voltage jumps could, in most cases, be fitted with single exponentials. At [Ca]i 0.5 microM, the curve relating the relaxation time constant, tau, to the membrane potential, displayed a maximum near +20 mV and 250 ms. At hyperpolarized potentials, tau varied by an e-fold factor in 130 mV. At [Ca]i 1 microM, tau decreased from 100 ms at -120 mV to 60 ms at +60 mV. Relaxation analysis gave an estimate of the variation of the channel open state probability, Po, with potential. At [Ca]i 0.5 microM, Po varied by an e-fold factor in 50-70 mV at hyperpolarized potentials, and saturated above +60 mV. At [Ca]i 1 microM, Po varied e-fold in 100 to 110 mV at hyperpolarized potentials, and saturated near +20 mV. External Cl- was substituted with various anions. From reversal potential measurements, the following permeability sequence was obtained: I- greater than NO3- greater than Br- greater than Cl- greater than F- greater than isethionate, methanesulphonate greater than glutamate. The corresponding normalized permeability coefficients were 2.7, 2.4, 1.6, 1, 0.2, 0.1, 0.1, 0.05. Replacement of external Cl- with Br-, isethionate, methanesulphonate or glutamate did not alter current kinetics as obtained during or after a depolarizing voltage jump.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1991

Obligatory role of Ca2+ in the cytotoxic activity of dengue virus-induced cytotoxin.

The role of calcium ions (Ca2+) in the cytotoxic activity of the dengue type 2 virus (DV)-induced macrophage (M phi) cytotoxin (CF2) was investigated in the present study. The findings show that CF2 prepared in Ca(2+)-free medium had no cytotoxic activity on normal mouse spleen cells suspended in Ca(2+)-free medium but killed the cells suspended in the medium with Ca2+. Substitution with calcium chloride restored the cytotoxic activity of CF2 the optimal dose being 10(-4) M concentration. CF2 induced an influx of Ca2+, as assayed by uptake of radiolabelled calcium chloride (45Ca), in the susceptible target cells, viz. M phi and T lymphocytes. The cytotoxic activity of CF2 as well as the CF2-induced influx of 45Ca was inhibited by treatment of the target cell with the calcium channel blocking drugs verapamil and nifedipine. Thus, the presence of Ca2+ is obligatory for the cytotoxic activity of CF2 and cell death is associated with increased intracellular Ca2+.

Animals↗
PubMed1994

Thrombomodulin expression by human keratinocytes. Induction of cofactor activity during epidermal differentiation.

Thrombomodulin is an endothelial cell surface glycoprotein that inhibits the procoagulant activities of thrombin and accelerates activation of the anticoagulant protein C. Because protein C deficiency is associated with cutaneous thrombosis, we investigated the expression of thrombomodulin in human skin. Thrombomodulin was detected by immunohistochemical staining both in dermal endothelial cells and in epidermal keratinocytes. Within the epidermis, thrombomodulin staining was limited to keratinocytes of the spinous layer, suggesting that thrombomodulin is induced when basal keratinocytes begin to terminally differentiate. Thrombomodulin expression also correlated with squamous differentiation in epidermal malignancies; little or no thrombomodulin staining was seen in five basal cell carcinomas, whereas strong thrombomodulin staining was observed in each of five squamous cell carcinomas. Human foreskin keratinocytes cultured in medium containing 0.07 mM calcium chloride synthesized functional thrombomodulin with cofactor activity comparable to thrombomodulin in human umbilical vein endothelial cells. Stimulation of keratinocyte differentiation with 1.4 mM calcium chloride for 48 h produced 3.5-, 3.2-, and 5.6-fold increases in thrombomodulin cofactor activity, antigen, and mRNA, respectively. These observations suggest that thrombin is regulated by keratinocyte thrombomodulin at sites of cutaneous injury, and indicate a potential role for thrombomodulin in epidermal differentiation.

Cell Differentiation↗
PubMed2005

Extraction of milk-clotting enzyme produced by solid state fermentation of Aspergillus oryzae.

Studies on the extraction of milk-clotting enzyme after solid-state fermentation (SSF) of wheat bran by a local strain of Aspergillus oryzae LS1 were done. The extraction of the enzyme was found to be depended on different parameters like nature of extractant, soaking time, temperature etc. From different inorganic and organic extractants, calcium chloride (0.05%) and glycerol (40%) were found to be the best solvents for leaching out milk-clotting enzyme. The optimum volume of calcium chloride was 5 ml/g biomass. An extraction time of 180 min. at 30 degrees C and 100 rpm was sufficient to extract out nearly 28% of the enzyme (2666.7 U/g biomass). Most of the enzyme (about 98.71%) was recovered in four repeated extractions.

Aspartic Acid Endopeptidases↗
PubMed1988

A slow calcium-dependent chloride conductance in clonal anterior pituitary cells.

1. Whole cell voltage-clamp recordings were made from GH3 cells, a clonal cell line initially derived from a rat anterior pituitary tumor, using patch electrodes filled with CsCl or N-methylglucamine chloride (NMG Cl). The bathing medium contained tetraethylammonium chloride (TEA; 20 mM) and NaCl (120 mM) or NMG Cl (140 mM). These conditions resulted in substantial blockade of outward currents. 2. Depolarizing voltage steps from a holding potential of -50 mV activated transient (T-type) and sustained (L-type) inward Ca2+ currents. In addition, prolonged depolarization (greater than 1 s) invariably elicited a slowly activating inward current that persisted with maintained depolarization, and deactivated slowly on repolarization, resulting in a prominent inward tail current. 3. This tail current could be recorded under conditions where Ca2+ and Cl- were the only membrane-permeant ions (symmetrical NMG Cl). The tail current nulled near 0 mV with symmetrical Cl- and showed a negative reversal potential with nominally Cl--free internal solution. Ba2+ substituted for Ca2+ as a carrier of inward current, but no tail current was expressed. These observations indicate that Cl- is the charge carrier of the slow inward tail current. 4. The voltage dependence for activation of the slow tail current was U-shaped with a peak at approximately -10 mV. This closely paralleled the voltage dependency of the Ca2+ currents. Recordings with 5 mM internal ethylene glycol-bis(beta-aminoethylether)-N,N,N',N'-tetraacetic acid (EGTA) to buffer intracellular Ca2+ to low nM levels exhibited slow inward tail currents that were of lower peak amplitude than with the usual 1.1 mM EGTA-containing pipette solution, but the kinetics of the currents were similar in both cases. In addition, the slow tail current was eliminated on superfusion with the Ca2+ channel blocker Cd2+ or with Ca2+-free medium. These results demonstrate that the current is dependent on Ca2+ influx; it is, therefore, referred to as ICl(Ca). 5. Activation of ICl(Ca) required depolarization of at least 1 s. More prolonged depolarizations activated progressively greater current, to a maximum with 6-s depolarization. In most cases, the decay of the tail current was described by a single exponential function with time constant approximately 0.8-0.9 s within the potential range -80 to -30 mV. At more depolarized potentials the decay was slower (increasing e-fold/20-mV change in membrane potential). 6. In a high proportion of cells, ICl(Ca) rapidly diminished in amplitude on repeated activation. This "rundown" occurred more rapidly than the rundown of the Ca2+ currents.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2006

Alterations in the levels of ions in blood and liver of freshwater fish, Cyprinus carpio var. communis exposed to dimethoate.

The fingerlings of Cyprinus carpio var. communis were exposed to sublethal concentration of dimethoate for 7, 14 days to evaluate the impact of the pesticide dimethoate on different ions namely sodium, potassium, chloride, calcium, magnesium. The blood potassium, calcium, magnesium and liver chloride and magnesium levels were elevated under sublethal condition. The blood sodium, chloride and liver sodium, potassium, and calcium levels were found to be significantly decreased.

Animals↗
PubMed1987

Contributions of hippurate, indoxyl sulfate, and o-hydroxyhippurate to impaired ligand binding by plasma in azotemic humans.

We have evaluated pH, chloride, calcium and several endogenous aromatic acids as possible causes of the impaired binding of drugs by plasma albumin in renal failure. Changes in pH, chloride and calcium over the range found in renal failure had minimal or no effects on the binding of [14C]salicylate, a model probe which binds to both of the major drug-binding loci of human albumin. Hippurate and indoxyl sulfate were weak inhibitors of binding by normal plasma. Ortho-hydroxy-hippurate was undetectable or minimally elevated, except among patients with elevated plasma salicylate concentration. Although plasma hippurate and indoxyl sulfate concentrations were elevated markedly in patients with renal failure, inhibition of salicylate binding was significantly correlated only with the concentration of indoxyl sulfate. Addition of hippurate and indoxyl sulfate separately and together to normal plasma showed that these ligands could account for only 15% of the impaired binding of salicylate by azotemic plasma. The retained solutes which account for most of this binding defect remain to be identified. This uremic disorder (and perhaps others) is due not to a single chemical but to the additive effect of a family of chemicals.

Blood Proteins↗
PubMed1994

Effects of a change in phosphorus requirement on phosphorus kinetics in the sheep.

An experiment was carried out to examine the effects of a change in P requirement, achieved by intravenous calcium loading, on intestinal phosphorus absorption, salivary phosphorus secretion and faecal endogenous phosphorus loss in adult sheep fitted with a rumen and duodenal cannula. Isotope dilution was used to measure faecal endogenous phosphorus loss while 103ruthenium phenanthroline and 51chromium-ethylenediamine tetra-acetic acid were used to measure duodenal phosphorus flow. The infusion of calcium chloride led to an increase in calcium and phosphorus retention, the increase in phosphorus retention being due to a reduction in faecal phosphorus excretion as a result of enhanced intestinal phosphorus absorption and reduced faecal endogenous phosphorus excretion. There was, however, no change in duodenal phosphorus flow or in the amount of phosphorus estimated to have been added to the digesta via the saliva. These results suggest that the increase in phosphorus retention seen in response to an increase in phosphorus requirement is largely achieved through an increase in intestinal absorptive efficiency and not through any reduction in endogenous phosphorus secretion into the gut.

Animals↗
PubMed1987

Paradoxical effect of calcium on some cardiovascular effects of verapamil in the rat.

The ability of calcium infusions to reverse some cardiovascular effects of verapamil was tested in anesthetized rats and on isolated rat atria. Intravenous infusions of 1.88 mg/kg verapamil increased the cycle length (CL), lengthened the PR interval (PRi), and decreased the mean arterial pressure (Pa). After these effects were stabilized, a series of infusions of calcium chloride (338 mumol/kg each) were performed. Calcium on the one hand promoted the return of Pa to its basal value; on the other hand, it failed to reverse the effect of verapamil on AV conduction and the first infusion of calcium produced an additional increase in CL of 55 +/- 16 ms. This paradoxical effect of calcium was prevented by previous infusion of atropine (0.2 mg/kg). On isolated atria, the increase of calcium concentration in the media ([Ca2+]0) from 1.0 to 6.0 mM increased the concentration frequency by approximately 40 beats/min, both in atropinized and in nonatropinized preparations. After verapamil, however, the same increase in [Ca2+]0 decreased atrial rate in 50 +/- 15 beats/min in nonatropinized atria. The results obtained indicate that extra calcium can overcome the hypotensive effect of verapamil, whereas it paradoxically increases its negative chronotropic effect and fails to reverse its effect on AV conduction. This paradoxical effect of calcium can be prevented, both in vivo and in vitro, by atropine blockade of muscarinic receptors.

Animals↗
PubMed2006

Formulation, characterization and release studies of alginate microspheres encapsulated with tetanus toxoid.

Alginate is a safe, non-immunogenic and inexpensive natural polymer with high mucoadhesive properties. Alginate microspheres can be used as a delivery system for antigens to mucosal surfaces. In the present study alginate microspheres were prepared by an emulsification technique. The effects of sonication time, concentration of alginate, emulsifier and calcium chloride, and also the volume of calcium solution, were evaluated on mean size, size range, surface roughness and porosity, sphericity and clumping of microspheres using an optical microscope and particle size analyzer. The most desirable conditions were 90 s sonication, 3% alginate solution, 2% surfactant and 60 ml of 0.33% CaCl2 in octanol. The resulting microspheres had a mean size of 1.34 +/- 0.3 microm and size range of 0.3 +/- 2.0 microm, with no surface roughness and porosity, low clumping and high sphericity. The encapsulation efficiency was about 47.7%. All batches showed nearly the same release profiles with a low burst release. The stability of the model antigen (tetanus toxoid (TT)) extracted from microspheres was confirmed by SDS-PAGE; and the antigenicity of TT was studied by ELISA and found to be 91 +/- 5% of the original TT. It can be concluded that, with regard to the size and morphological characteristics of the prepared microspheres and their ability in preserving the antigenicity of the encapsulated TT, they could be used as a delivery system for mucosal delivery of TT.

1-Octanol↗
PubMed1989

Isolation of an acidic protein from cholesterol gallstones, which inhibits the precipitation of calcium carbonate in vitro.

In seeking to identify nucleating/antinucleating proteins involved in the pathogenesis of cholesterol gallstones, a major acidic protein was isolated from each of 13 samples of cholesterol gallstones. After the stones were extracted with methyl t-butyl ether to remove cholesterol, and methanol to remove bile salts and other lipids, they were demineralized with EDTA. The extracts were desalted with Sephadex-G25, and the proteins separated by PAGE. A protein was isolated, of molecular weight below 10 kD, which included firmly-bound diazo-positive yellow pigments and contained 24% acidic, but only 7% basic amino acid residues. The presence of N-acetyl glucosamine suggested that this was a glycoprotein. This protein at concentrations as low as 2 micrograms/ml, but neither human serum albumin nor its complex with bilirubin, inhibited calcium carbonate precipitation from a supersaturated solution in vitro. This protein could be precipitated from 0.15 M NaCl solution by the addition of 0.5 M calcium chloride. Considering that cholesterol gallstones contain calcium and pigment at their centers, and that small acidic proteins are important regulators in other biomineralization systems, this protein seems likely to play a role in the pathogenesis of cholesterol gallstones.

Amino Acids↗
PubMed1979

[Dissociation of human factor VIII and recombination of the fragments VIII-C and VIII-AG].

Human factor VIII has been dissociated into fragment VIII-C and fragment VIII-AG in the presence of calcium chloride (0.25 M). After removing the calcium, recombination of the molecule is obtained. Fragment VIII-C can be activated by thrombin in a similar manner to the coagulant activity of whole factor VIII. This activation is calcium-dependent. In rabbits immunized against purified F VIII, VIII-C and VIII-AG specific antisera against these three entities were obtained.

Blood Coagulation Tests↗
PubMedDate not supplied

Antagonistic effect of morphine on the positive inotropic response of ouabain on the isolated rabbit heart.

The antagonistic effect of morphine on the positive inotropic response of ouabain was studied in 96 isolated rabbit hearts, using a modified Langendorff preparation. Decreased calcium (Ca) in the perfusate resulted in increased depression of peak left ventricular dP/dt by morphine (10(-4) gm/ml), and the number of beats required to reach the depression was proportionally reduced with the reduction of calcium chloride from 2.16 mM to 0.54 mM. Likewise, the positive inotropic effect of ouabain (10(-6) gm/ml) was proportionally reduced by the same reduction of calcium chloride concentration in the perfusate, but the number of beats required to reach the cardiotonic effect was proportionally increased with Ca deficiency. The opposing effects of ouabain and morphine were mutually antagonistic regardless of the order of drug administration. When the hearts had been previously exposed to morphine, ouabain stimulation was no longer beat-dependent. Following prior exposure to ouabain, the beat-dependency of morphine depression on the heart also was partially antagonized. These results suggest that the level of maximal dP/dt during morphine depression or ouabain stimulation is directly related to the extracellular concentration of Ca. The number of beats required to attain the depression or stimulation is probably a reflection of the rate at which equilibrium is established between the mobile fraction of extracellular and intracellular Ca, since transmembrane movement of Ca is believed to occur during each beat. A possible common site of morphine and ouabain effect may be the cellular membrane, where ionic flux occurs.

Animals↗
PubMed1988

Ultrastructural study of hypervitaminosis D induced arterial calcification in Wistar rats.

Hypervitaminosis D produces extensive vascular alterations which are similar to Monckeberg's calcinosis. The present study was undertaken to examine early changes in vascular ultrastructure of rats receiving tap water supplemented with either calcium chloride or a relatively low dosage of irradiated ergocalciferol ad libitum for 21 days. Untreated rats received normal tap water ad libitum. A significant increase in serum calcium levels was obtained in hypervitaminosis D treated rats. Calcium deposits were seen near the internal elastic lamina, within new elastic elements and around degenerating smooth muscle cell fragments in the extracellular organic matrix of hypervitaminosis D treated rats. Calcium deposits were not detected in vascular sections from untreated rats or those receiving calcium chloride. A complex pathogenesis of vascular lesions produced by hypervitaminosis is suggested. One possible pathogenic mechanism for calcification of elastic matrix may be via altered microfibrils. Our data support this hypothesis and indicate that much lower levels of vitamin D administration, compared to other reports, produce considerable vascular calcinosis in this experimental preparation. Several hypotheses regarding possible mechanisms of pathologic calcification are discussed.

Animals↗
PubMed2003

Suppressive role of endogenous regucalcin in the enhancement of nitric oxide synthase activity in liver cytosol of normal and regucalcin transgenic rats.

The suppressive role of endogenous regucalcin, which is a regulatory protein of calcium signaling, in the enhancement of nitric oxide (NO) synthase activity in the liver cytosol of rats was investigated. The enzyme activity was measured in a reaction mixture containing either vehicle or calcium chloride (1-20 microM) in the absence or presence of regucalcin (0.1, 0.25, or 0.5 microM). NO synthase activity was significantly increased by the addition of calcium (5-20 microM). This increase was completely abolished in the presence of trifluoperazine (TFP; 10-50 microM), an antagonist of Ca(2+)/calmodulin. The addition of regucalcin (0.1-0.5 microM) caused a significant fall in the calcium-increased enzyme activity. The effect of regucalcin (0.25 microM) in decreasing NO synthase activity was seen in the presence of ethylene glycol bis-(2-aminoethylether) N,N,N',N'-tetraacetic acid (EGTA, 1 mM) or TFP (20 microM), indicating that regucalcin acts independent on Ca(2+)/calmodulin. NO synthase activity was significantly raised in the presence of anti-regucalcin monoclonal antibody (10-50 ng/ml) in the reaction mixture. The effect of the antibody (50 ng/ml) or calcium (10 microM) in elevating NO synthase activity in the liver cytosol of normal rats was not seen in the liver cytosol obtained from regucalcin transgenic rats. Moreover, the increase in NO synthase activity in the liver cytosol of normal rats induced by a single intraperitoneal administration of calcium (5.0 mg/100 g body weight) was significantly enhanced in the presence of anti-regucalcin monoclonal antibody (50 ng/ml) in the reaction mixture. The administration of calcium caused a significant increase in regucalcin level in the liver cytosol of normal rats. The present study demonstrated that endogenous regucalcin plays a suppressive role in the enhancement of NO synthase activity in the liver cytosol of rats.

Animals↗
PubMed1991

The interactive effects of dietary sodium chloride and calcium on cardiovascular stress responses.

Blood pressure increases associated with salt loading in the spontaneously hypertensive rat (SHR) are attenuated with increased dietary calcium. To assess the cardiovascular effects of these nutrients during stress, blood pressure and sympathoadrenal responses to stress were compared in salt-sensitive SHRs fed diets containing normal (0.73%) or high (8.0%) NaCl combined with either low (0.2%) or high (2.0%) calcium. NaCl-loaded rats showed increased blood pressure and exaggerated plasma epinephrine changes during restraint stress. Elevated blood pressure responses to exogenous NE were also observed with high salt intake. Supplementary calcium reduced blood pressure and attenuated the hypertensive effect of NaCl during restraint stress. Animals fed the high calcium diets had lower plasma epinephrine levels while vascular reactivity was not affected. The results indicate that increased sympathoadrenal activity and vascular reactivity contribute to elevated blood pressure and exaggerated pressor responses produced by NaCl loading in the salt-sensitive SHR. However, the hypotensive effects of dietary calcium appear to be related to sympathoadrenal activity but not vascular reactivity.

Analysis of Variance↗