scholarly journals Potassium-Dependent Mechanism for the Regulation of Angiotensin II Receptors in the Zona Glomerulosa of the Adrenal Gland during Chronic Extracellular Fluid Volume Depletion in Young Rats

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 336A-336A
Author(s):  
Patricio E Ray
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Extracellular Fluid ◽  
Zona Glomerulosa ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Angiotensin Ii Receptors ◽  
Volume Depletion ◽  
Young Rats ◽  
Dependent Mechanism

Different effects of sodium or chloride depletion on angiotensin II receptors in rats

1990 ◽  
Vol 258 (4) ◽  
pp. R1008-R1015
Author(s):  
P. E. Ray ◽  
E. Castren ◽  
E. J. Ruley ◽  
J. M. Saavedra
Keyword(s):  
Angiotensin Ii ◽  
Extracellular Fluid ◽  
Zona Glomerulosa ◽  
Subfornical Organ ◽  
Angiotensin Ii Receptors ◽  
Sodium Depletion ◽  
Angiotensin Ii Receptor ◽  
Young Rats ◽  
Chloride Depletion ◽  
Receptor Concentration

We studied the effects of selective chronic sodium or chloride depletion (0.005% in diet) on central and peripheral angiotensin II receptors in young rats. Chloride depletion produced the most significant increase in plasma renin activity and extracellular fluid volume contraction. In the brain, subfornical organ angiotensin II receptor concentration was decreased by sodium depletion and increased by chloride depletion. There were no significant changes in angiotensin II binding in the paraventricular nucleus. When sodium-depleted rats were water deprived for 3 days, subfornical organ angiotensin II receptor concentration increased, showing that normal sodium intake was not essential for increased numbers of angiotensin II receptors during dehydration. In the adrenal gland, chloride depletion decreased angiotensin II receptors in the medulla and zona glomerulosa. Conversely, sodium depletion increased angiotensin II receptors in the zona glomerulosa. In the kidney glomeruli and medulla, angiotensin II receptors were decreased by either sodium or chloride depletion. These results suggest different roles for sodium and chloride in the regulation of the peripheral and central renin-angiotensin system in young rats.

The Interrelationship between ECF Volume and ECF Anion Composition in the Regulation of Sodium Excretion

1970 ◽  
Vol 39 (4) ◽  
pp. 475-487
Author(s):  
J. J. Cohen ◽  
J. A. Chazan ◽  
S. Garella
Keyword(s):  
Hydrochloric Acid ◽  
Sodium Bicarbonate ◽  
Sodium Excretion ◽  
Extracellular Fluid ◽  
Progressive Increase ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Volume Depletion ◽  
Anion Composition ◽  
Bicarbonate Infusion

1. The interrelationship between extracellular fluid volume and extracellular anion composition as determinants of sodium excretion was studied in thirty-four dogs. In six, hypovolaemia, hypochloraemia and hyperbicarbonataemia were induced by the administration of ethacrynic acid and a low chloride diet. Isotonic sodium bicarbonate was then infused resulting in a progressive increase in sodium excretion. After 3 h while continuing the sodium bicarbonate infusion, an infusion of hydrochloric acid was given in order to return extracellular anion composition towards normal. This resulted in a prompt fall in sodium excretion without a change in GFR. 2. Ten studies were performed to determine whether this hydrochloric acid-induced enhancement of sodium conservation depends upon the presence of volume depletion and sodium avidity or whether it could also be demonstrated under circumstances of volume expansion. In these studies, hypervolaemia, hypochloraemia, hyperbicarbonataemia and a brisk natriuresis were induced by infusing isotonic sodium bicarbonate into normal dogs. The addition of hydrochloric acid returned anion composition to normal and, as before, resulted in a prompt suppression of sodium excretion despite continued sodium loading and enhanced glomerular filtration. 3. Results obtained from three related protocols (six animals each) confirmed that hypochloraemia and hyperbicarbonataemia were the necessary prerequisite conditions for this effect of hydrochloric acid in volume expanded animals. We interpret these findings as evidence that the response of the kidney to changes in extracellular fluid volume may be significantly affected by changes in the extracellular concentration of physiologic anions.

Angiotensin II receptors: protein and gene structures, expression and potential pathological involvements

1996 ◽  
Vol 134 (4) ◽  
pp. 403-411 ◽  
Author(s):  
E Clauser ◽  
KM Curnow ◽  
E Davies ◽  
S Conchon ◽  
B Teutsch ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Zona Glomerulosa ◽  
Expression Cloning ◽  
Angiotensin Ii Receptors ◽  
Angiotensin Ii Receptor ◽  
Receptor System ◽  
Physiological Importance ◽  
Increased Risk ◽  
Gene Structures

Clauser E, Curnow KM, Davies E, Conchon S, Teutsch B, Vianello B, Monnot C, Corvol P. Angiotensin II receptors: protein and gene structures, expression and potential pathological involvements. Eur J Endocrinol 1996;134:403–11. ISSN 0804–4643 Two distinct types of cell-surface angiotensin II receptors (AT1 and AT2) have been defined pharmacologically and cDNAs encoding each type have been identified by expression cloning. These pharmacological studies showed the AT1 receptors to mediate all the known functions of angiotensin II in regulating salt and fluid homeostasis. Further complexity in the angiotensin II receptor system was revealed when homology cloning showed the existence of two AT1 subtypes in rodents and in situ hybridization and reverse transcription-polymerase chain reaction analyses showed their level of expression to be regulated differently in different tissues: AT1A is the principal receptor in the vessels, brain, kidney, lung, liver, adrenal gland and fetal pituitary, while AT1B predominates in the adult pituitary and is only expressed in specific regions of the adrenal gland (zona glomerulosa) and kidney (glomeruli). Expression of AT1A appears to be induced by angiotensin II in vascular smooth-muscle cells but is inhibited in the adrenal gland. Preliminary analysis of the AT1 promoters is also suggestive of a high degree of complexity in their regulation. Investigation of a potential role for altered AT1 receptor function has commenced at a genetic level in several diseases of the cardiovascular system. No mutations affecting the coding sequence have been identified in Conn adenoma and no linkage has been demonstrated with human hypertension by sib-pair analysis. None the less, certain polymorphisms that do not alter the protein structure have been found to be associated with hypertension and to occur at an increased frequency in conjunction with specific polymorphisms in the ACE gene in individuals at increased risk for myocardial infarction. Further characterization of the regions of the AT1 gene that regulate its expression are therefore needed. The physiological importance of the AT2 gene product still remains a matter of debate. E Clauser, INSERM U36, Collège de France, 3 rue d'Ulm, 75005 Paris, France

Determinants of High Blood Pressure in Salt-Deprived Renal Hypertensive Rats: Role of Changes in Plasma Volume, Extracellular Fluid Volume and Plasma Angiotensin II

1978 ◽  
Vol 55 (1) ◽  
pp. 81-87 ◽  
Author(s):  
A. J. Mourant
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
High Blood Pressure ◽  
Plasma Volume ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Right Atrial ◽  
Free Access ◽  
Plasma Angiotensin

1. Rats with indwelling aortic and right atrial cannulae were maintained on a sodium-free diet before and after renal arterial constriction combined with contralateral nephrectomy. Control animals underwent the same protocol except that non-constricting clips were used. 2. Plasma volumes in the salt-deprived animals were lower than previously determined values in animals with free access to sodium. After clipping plasma volume increased in the hypertensive animals. Extracellular fluid volume was increased equally in both normotensive and hypertensive animals on the second postoperative day only. 3. Before clipping and contralateral nephrectomy plasma angiotensin II values were higher than normal. After the operation angiotensin II concentrations fell to normal over a period of 14 days without significant differences between experimental and control groups. 4. It is concluded that high blood pressure after clipping may be in part maintained by increases in plasma volume. However, the results strongly suggest that other renal mechanisms are likely to be of major pathogenic importance.

scholarly journals In SituDemonstration of Angiotensin-Dependent and Independent Pathways for Hyperaldosteronism During Chronic Extracellular Fluid Volume Depletion

2001 ◽  
Vol 15 (12) ◽  
pp. 2229-2235 ◽  
Author(s):  
Junji Takaya ◽  
Taiji Matsusaka ◽  
Hideyuki Katori ◽  
Masaaki Tamura ◽  
Yoichi Miyazaki ◽  
...  
Keyword(s):  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Volume Depletion

Dietary NaCl modulates Na(+)-H+ antiporter activity in renal cortical apical membrane vesicles

1991 ◽  
Vol 260 (1) ◽  
pp. F130-F137 ◽  
Author(s):  
O. W. Moe ◽  
A. Tejedor ◽  
M. Levi ◽  
D. W. Seldin ◽  
P. A. Preisig ◽  
...  
Keyword(s):  
Apical Membrane ◽  
Extracellular Fluid ◽  
Membrane Vesicles ◽  
Maximal Activity ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Volume Depletion ◽  
Orange Fluorescence ◽  
K Deficiency ◽  
Apical Membrane Vesicles

An apical membrane Na(+)-H+ antiporter mediates proximal tubule NaCl and NaHCO3 reabsorption. The present studies examined whether chronic changes in dietary NaCl intake lead to an adaptation of the Na(+)-H+ antiporter. Rats were maintained either on a low-salt (LS, 0% NaCl) or a high-salt (HS, 2% NaCl) diet for 4 days. Na(+)-H+ antiporter was assayed using the acridine orange fluorescence method in apical membrane vesicles prepared by Mg2+ aggregation. Rats on LS diet exhibited a higher maximal activity (Vmax) for antiporter activity (0.109 +/- 0.008 s-1) compared with rats on HS diet (0.090 +/- 0.008 s-1; P less than 0.01), whereas Na activity (KNa) was similar (13.1 +/- 1.5 and 14.2 +/- 0.8 mM in HS and LS groups, respectively). The modulation of Na(+)-H+ antiporter activity was amiloride sensitive. Proton permeability, Na(+)-dependent [3H]glucose uptake, and vesicle enrichments were similar in both groups. In addition, the dietary protocols were not associated with any systemic acid-base disturbances, K+ deficiency, or hyperfiltration, conditions that have previously been demonstrated to alter Na(+)-H+ antiporter activity. Acute differences in extracellular fluid volume, induced by 10% body weight isohydric expansion failed to affect Na(+)-H+ antiporter activity. Thus chronic alterations in dietary NaCl intake alter the maximal activity (Vmax) of the Na(+)-H+ antiporter. This adaptation may contribute to decreased NaCl reabsorption in extracellular fluid volume expansion, enhanced NaCl reabsorption in extracellular fluid volume depletion, and enhanced NaHCO3 reabsorption in chronic metabolic alkalosis associated with volume contraction.

scholarly journals Angiotensin-independent mechanism for aldosterone synthesis during chronic extracellular fluid volume depletion.

1997 ◽  
Vol 99 (5) ◽  
pp. 855-860 ◽  
Author(s):  
S Okubo ◽  
F Niimura ◽  
H Nishimura ◽  
F Takemoto ◽  
A Fogo ◽  
...  
Keyword(s):  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Volume Depletion ◽  
Independent Mechanism

Sodium appetite and thirst in cattle subjected to dehydration

1989 ◽  
Vol 257 (5) ◽  
pp. R1212-R1218 ◽  
Author(s):  
J. R. Blair-West ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
R. S. Weisinger
Keyword(s):  
Angiotensin Ii ◽  
Extracellular Fluid ◽  
Extracellular Fluid Volume ◽  
Angiotensin Ii Receptors ◽  
Free Access ◽  
Nacl Solution ◽  
Sodium Appetite ◽  
Site Of Action ◽  
Access To Water ◽  
The Brain

Cows having free access to water (hydrated) or deprived of water for 26.5 h (dehydrated) were infused for 3 h with angiotensin II or captopril solutions intravenously (iv) or intracerebroventricularly (icv) beginning 1 h before access to 0.3 M NaHCO3/NaCl solution for 2 h. The results agree with the results of the experiments with the same agents and doses in Na-deficient cows. Only iv infusion of angiotensin II stimulated Na appetite and only icv infusion of angiotensin II stimulated thirst. Therefore, barriers to the penetration of angiotensin II in the brain determined the particular site of action and elicited response. Dehydration did not stimulate Na appetite and, as shown previously, Na deficiency did not stimulate thirst, but both behaviors seem to be influenced by angiotensin-related mechanisms in the brain. The inability of iv angiotensin II to stimulate Na appetite in hydrated cows might be explained by the lack of a response caused by, and common to, Na deficiency and dehydration, e.g., upregulation of angiotensin II receptors, or reduced extracellular fluid volume.

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