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PubMed1994

Faecal dry weight and potassium are related to faecal sodium and plasma aldosterone in rats chronically fed on varying amounts of sodium or potassium chlorides.

Recent studies have shown that faecal residue (dry weight) and Na and K increase with increasing levels of dietary fibre, an effect which may be related to unstirred layers that slow absorption and the flow rate of chyme through the gastrointestinal tract. Salts of Na are the primary osmotic components of chyme and influence both retention of fluid in the bowel and transit of fluid from the small to the large intestine. The present study examines the chronic effects of dietary Na and K intake on faecal Na, K and residue excretion. Male Sprague-Dawley rats were given 12-13 g feed/d (control (g/kg): Na 4, K 8.5) for 1 week, followed by a 4-week period where Na or K intake was altered (0.01-3 times control levels). These diets altered chronic (> 1 week) faecal residue excretion and affected Na and K excretion by 8-, 310- and 2100-fold respectively. Low dietary Na reduced faecal Na and residue; K excretion was doubled during week 1, but fell over weeks 2-4 despite a 4-5-fold increase in plasma aldosterone. Chronic high dietary Na increased faecal Na, residue and K despite a 60% decrease in plasma aldosterone. Chronic low dietary K decreased faecal Na, K and residue and plasma aldosterone. Chronic high dietary K did not alter faecal Na and K despite increased faecal residue and a 4-5-fold increase in plasma aldosterone. Faecal water was unchanged by diet, paralleling changes in faecal residue. Analyses of the results provide systematic models of chronic regulation of faecal Na, K and residue excretions. When plasma aldosterone is low (< 160 ng/l), weekly faecal residue excretion is equal to 3.6 g (fibre intake was 2.6-2.7 g/week)+2.6 g/mmol Na, and K excretion is equal to 0.55 mmol/mmol Na. When plasma aldosterone is high (> 1500 ng/l) weekly faecal residue excretion is equal to 2.3 g + 2.6 g/mmol Na, and K excretion is equal to 0.7 mmol/week + 0.55 mmol/mmol Na.

Aldosterone↗
PubMed1991

Endothelial cell sodium-potassium-chloride cotransport. Evidence of regulation by Ca2+ and protein kinase C.

Previous studies have shown that vascular endothelial cells exhibit a highly active Na-K-Cl cotransport system that is regulated by a variety of vasoactive hormones and neurotransmitters, suggesting that the cotransporter may play an important role in endothelial cell function. In this study, the regulation of endothelial cell Na-K-Cl cotransport was further investigated by probing the stimulus-transfer pathway by which vasoactive agents stimulate the cotransporter. Specifically, three peptides previously shown to stimulate cotransport activity (angiotensin II, vasopressin, and bradykinin) were evaluated. Na-K-Cl cotransport was assessed in cultured bovine aortic endothelial cells as bumetanide-sensitive K+ influx. Stimulation of Na-K-Cl cotransport by angiotensin II, vasopressin, or bradykinin was found to be reduced either by removal of extracellular Ca2+ or by treatment of the cells with 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate or 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid. In addition, the calmodulin antagonist W-7 was found to prevent stimulation of endothelial cell Na-K-Cl cotransport by the three peptides. These findings suggest that regulation of endothelial cell cotransport by these vasoactive peptides may be both Ca(2+)- and calmodulin-dependent. Angiotensin II, vasopressin, and bradykinin were also found to elevate phosphatidylinositol hydrolysis in the cultured endothelial cells. Thus, the possibility that regulation of endothelial Na-K-Cl cotransport by these vasoactive peptides also involves diacylglycerol activation of protein kinase C was investigated. A 10-min exposure of the endothelial cells to low doses of phorbol 12-myristate 13-acetate was found to reduce Na-K-Cl cotransport whether in the presence or absence of angiotensin II, vasopressin, or bradykinin. However, down-regulation of protein kinase C by a 40-h exposure to higher doses of the phorbol ester was found to elevate Na-K-Cl cotransport activity under both control and agonist-stimulated conditions, indicating that activation of protein kinase C results in inhibition of endothelial cell Na-K-Cl cotransport. Thus, protein kinase C activation may serve as negative feedback in the stimulus-transfer pathway by which these agonists regulate endothelial cell Na-K-Cl cotransport.

Adenosine Triphosphate↗
PubMedDate not supplied

[The sodium-potassium-chloride cotransport of the cell membrane].

Discovery and active exploration of the furosemid-sensitive derived-active co-transport of sodium-potassium-chlorine ions took place in the end of 1970-es-1980-es. This transportation mechanism was discovered in various types of cells, both of plant and of animal origin. This review describes properties of the transportation process, which was most comprehensive explored in experiments with erythrocytes, epithelium cells and muscles. The review covers the following properties: anion and cation selectivity of the chlorine transportation, its sensitivity to the specific blocking agents (furocemid, bumetanid, etc.), stoichiometry of the transportation process, etc. For energy source, the chlorine transportation is based on transmembrane electrochemical gradient for sodium ions. The article provides the most recent results of investigation of the chemical nature of the molecule of the chlorine membrane transport. Based on various studies, the molecule of this protein weighs from 120 to 200 kD, includes about 1200 amino acid residua, and forms long cytoplasmatic NH2 and COOH-termini. The gene encoding the amino acid sequence has been cloned. The article discusses the issues of regulation of the chlorine transportation. Humoral control of intensity of the chlorine transportation has been mostly studied in experiments with plain muscles, the issues related to nervous regulation--with only skeleton muscle fibers. The article provides specific data on the mechanisms of the above types of the physiological regulation of active chlorine transportation. In general, the humoral factors, which increase the intracellular concentration of cAMF stimulate chlorine transportation. On the contrary, the hormones, which increase concentration of cGMF in cytoplasm reduce its activity in plain muscles. The discussion of the mechanisms of the nervous controls of the chlorine transportation in the skeleton muscles includes the original results of the author. These results indicate that the suppressive influence of the motor innervation on intensity of the chlorine transportation involves the non-quantum acetilcholine and glutamate secreted from the motor nerves. These agents produce Ca(2+)-dependent molecules of nitrogen oxide in sarcoplasm, which act in the retrograde mode on the nervous terminal and activate there the synthesis of cGMF. Disruption of this bilateral transsynaptic signalization resulting from cutting a nerve of blocking of its axoflow creates more active chlorine transportation and subsequent de-innervation changes in properties of the muscle fibers. The functions of chlorine transportation, which are best studies as of today and therefore, discussed in more detail in the review, include participation of this process in the regulatory rehabilitation of the volume of various cells in non-isotonic medium, and the role of chlorine transportation in development of a negative charge at the interior side of membrane of the skeleton muscle fibers. The former function essentially means that dehydration of a cell in the hypertonic medium increases activity of the sodium, potassium and chlorine co-transport directed to the cell, resulting in increase of the amount of the osmosis-active cytoplasm material, and inflow of water, which fully restores the cell volume in these conditions. Starting from the pioneer studies by Hodgkin and Horowicz [correction of Hojkin and Gorovits], the role of chlorine ions in forming a charge on the membrane of excited cells has been generally interpreted as exclusively passive. I.e., distribution of these ions over both sides of membrane was assumed as equilibrium with the existing values of the membrane potential in the non-excited state. The review provides data obtained in the recent decade, which have proved that the non-excited membrane potential in muscle fibers is co-created by the diffusional potassium and chlorine potential. (ABSTRACT TRUNCATED)

Animals↗
PubMed1994

Molecular cloning, primary structure, and characterization of two members of the mammalian electroneutral sodium-(potassium)-chloride cotransporter family expressed in kidney.

Electrically silent Na(+)-(K+)-Cl- transporter systems are present in a wide variety of cells and serve diverse physiological functions. In chloride secretory and absorbing epithelia, these cotransporters provide the chloride entry mechanism crucial for transcellular chloride transport. We have isolated cDNAs encoding the two major electroneutral sodium-chloride transporters present in the mammalian kidney, the bumetanide-sensitive Na(+)-K(+)-Cl- symporter and thiazide-sensitive Na(+)-Cl- cotransporter, and have characterized their functional activity in Xenopus laevis oocytes. Despite their differing sensitivities to bumetanide and thiazides and their different requirements for potassium, these approximately 115-kDa proteins share significant sequence similarity (approximately 60%) and exhibit a topology featuring 12 potential membrane-spanning helices flanked by long non-hydrophobic domains at the NH2 and COOH termini. Northern blot analysis and in situ hybridization indicate that these transporters are expressed predominantly in kidney with an intrarenal distribution consistent with their recognized functional localization. These proteins establish a new family of Na(+)-(K+)-Cl- cotransporters.

Amino Acid Sequence↗
PubMed1990

Potassium, chloride and non-selective cation conductances opened by noradrenaline in rabbit ear artery cells.

1. The action of noradrenaline on cells isolated from the rabbit ear artery was studied with the whole-cell configuration of the patch clamp technique. In normal potassium-containing solutions at a holding potential of -50 mV noradrenaline elicited either outward, inward or mixed outward and inward currents. These responses were blocked by the alpha-adrenoceptor antagonist, phentolamine (10(-6) M). 2. The outward current occurred as a consequence of an increase in membrane conductance and the reversal potential was close to the potassium equilibrium potential (EK). It was possible to record outward currents without external calcium but not when the concentration of EGTA in the pipette was increased to 10 mM or when potassium was absent from the pipette solution. It is concluded that the outward current evoked by alpha-adrenoceptor stimulation is produced by a calcium mediated increase in potassium conductance. 3. The ionic basis of the inward current was investigated in potassium-free external and pipette solutions. When sodium chloride was the major constituent of the external and pipette solutions the reversal potential (Er) of the noradrenaline-induced current was 0.63 mV, close to ENa and ECl. 4. When most of the external sodium chloride was replaced by sucrose Er was intermediate between ENa and ECl but had shifted significantly towards ENa. Further ion substitution experiments suggest that noradrenaline increased the membrane conductance to both anions and cations. 5. When the current was carried predominantly by anions, depolarizing steps (from -50 mV) produced outward current relaxations with a time constant of about 40 ms. Bath-applied caffeine also produced a membrane current which rectified in the outward direction. 6. When the response to noradrenaline was mediated mainly by cations, the relationship between the membrane current and clamp potential was non-linear and the amplitude of the currents at potentials positive to -50 mV became disproportionately smaller. In addition on repolarization to -50 mV the instantaneous current was followed by an inward relaxation. 7. In high external barium solution noradrenaline evoked a membrane current with a reversal potential much more positive than ENa or ECl. This current was recorded in the presence of 10(-5) M-nifedipine and diltiazem and in 10(-4) M-cadmium which suggests that the voltage-dependent calcium channel is not implicated in the generation of the non-selective cation current to noradrenaline.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗