Importance of chloride for the correction of chronic metabolic alkalosis in the rat

1987 ◽  
Vol 253 (5) ◽  
pp. F1031-F1039 ◽  
Author(s):  
B. M. Wall ◽  
G. V. Byrum ◽  
J. H. Galla ◽  
R. G. Luke
Keyword(s):  
Plasma Volume ◽  
Metabolic Alkalosis ◽  
Choline Chloride ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Volume Contraction ◽  
Chloride Depletion ◽  
Sprague Dawley Rats ◽  
Sodium And Potassium

To determine whether chloride repletion without sodium could correct chronic chloride depletion metabolic alkalosis (CDA) in Sprague-Dawley rats without volume expansion and without increasing glomerular filtration rate (GFR), CDA was generated by peritoneal dialysis (PD) against 0.15 M NaHCO3 and maintained for 7-10 days by a chloride-restricted diet supplemented with sodium and potassium salts. Control animals were dialyzed against Ringer bicarbonate. The maintenance period of chronic CDA, compared with control, was characterized by hypokalemic metabolic alkalosis (serum TCO2 31.9 +/- 0.6 vs. 23.1 +/- 0.5 meq/l, P less than 0.05), volume contraction (plasma volume 3.76 +/- 0.08 vs. 4.19 +/- 0.22 ml/100 g body wt, P less than 0.05), decreased GFR (838 +/- 84 vs. 1045 +/- 45 microliters.min-1.100 g body wt-1, P less than 0.05), increased plasma renin activity (PRA) (63 +/- 13 vs. 12 +/- 3 ng.ml-1.h-1, P less than 0.05), but unchanged plasma aldosterone concentrations (PAC) (4.1 +/- 1.0 vs. 3.4 +/- 1.6 ng/dl, P = NS). Complete correction of chronic CDA was accomplished by 24 h of ingestion of choline chloride drink, and despite negative sodium balance, neutral potassium balance, continued bicarbonate ingestion, and persistent volume contraction (plasma volume 3.76 +/- 0.08 vs. 3.73 +/- 0.12 ml/100 g body wt pre- and postcorrection, P = NS), GFR remained decreased (659 +/- 87 vs. 1,045 +/- 45 microliters.min-1.100 g body wt-1, P less than 0.05), PRA decreased (63 +/- 13 vs. 33 +/- 5 ng.ml-1.h-1, P less than 0.05), but PAC did not change (4.1 +/- 1.0 vs. 6.1 +/- 1.6 ng/dl, P = NS) after correction of CDA.(ABSTRACT TRUNCATED AT 250 WORDS)

Superficial distal and deep nephrons in correction of metabolic alkalosis

1989 ◽  
Vol 257 (1) ◽  
pp. F107-F113
Author(s):  
J. H. Galla ◽  
D. N. Bonduris ◽  
R. G. Luke
Keyword(s):  
Metabolic Alkalosis ◽  
Wistar Rats ◽  
Collecting Duct ◽  
Sprague Dawley ◽  
Chloride Depletion ◽  
Henle's Loop ◽  
Sprague Dawley Rats ◽  
Necessary And Sufficient ◽  
Distal Convolution

Chloride is necessary and sufficient to correct alkalosis induced by dialysis vs. 0.15 M NaHCO3. To determine the contribution of the cortical (SC) distal convolution (DCT) and juxtamedullary (JM) nephrons to correction, we examined Cl and total CO2 (tCO2) transport in alkalotic Sprague-Dawley rats infused with 5% dextrose (group DM) or with 5% dextrose and 80 mM Cl (group CC); in papillary studies in alkalotic Munich-Wistar rats, 6% albumin was added to the infusate. In cortical studies, changes in plasma Cl and tCO2 were 4.9 +/- 0.7 vs. 0.7 +/- 0.9 and -6.0 +/- 0.8 vs. 0.4 +/- 0.9 meq/l and in tCO2 excretion (133 +/- 28 vs. -8 +/- 10 mueq/min) in groups CC and DM, respectively; results in papillary studies were similar. Delivery of tCO2 out of late SC DCT (CC 146 +/- 20 and DM 146 +/- 23 pmol/min) and Henle's loop (CC 145 +/- 18 and DM 202 +/- 56 pmol/min) and reabsorption within DCT (CC 15 +/- 24 and DM 45 +/- 19 pmol/min) did not differ. During correction of chloride-depletion alkalosis, the increment in bicarbonate excretion does not emanate from DCT of SC nephrons or JM nephrons but rather from the collecting duct.

scholarly journals Sodium, potassium and chloride utilization by rats given various inorganic anions

1991 ◽  
Vol 66 (3) ◽  
pp. 523-532 ◽  
Author(s):  
Susan M. Kaup ◽  
Alison R. Behling ◽  
J. L. Greger
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Basal Diet ◽  
Renin Activity ◽  
Sprague Dawley ◽  
Sodium Potassium ◽  
Sprague Dawley Rats ◽  
Blood Pressures ◽  
Sodium And Potassium

The purpose of the present studies was to examine the effect of ingestion of sodium and potassium salts of various fixed anions on blood pressure, and to assess interactions among electrolytes. In the first study, Sprague-Dawley rats fed on purified diets supplemented with Na salts of chloride, sulphate, bisulphate, carbonate and bicarbonate for 7 weeks developed higher blood pressures than rats fed on the basal diet. In a second study, rats fed on Na or K salts of HSO4, HCO3 or Cl had higher blood pressures than rats fed on the basal diet. Blood pressure measurements were not correlated with plasma volume, plasma renin activity, or plasma atrial natriuretic peptide concentrations at 7 weeks. Plasma renin activity was depressed in rats fed on supplemental Na and even more in rats fed on supplemental K salts rather than the basal diet. Generally, rats fed on supplemental Na excreted Na in urine and absorbed Na in the gut more efficiently than rats fed on the basal diet or diets supplemented with K, but the anions fed also altered Na absorption and excretion. In a third study, rats fed on diets supplemented with any Cl salt, but especially KCI, absorbed K more efficiently than those fed on the basal diet. In studies 1 and 2, the efficiency of urinary excretion of K was greatest when HCO3 and CO3 salts were fed and least when HSO4 salts were fed. Despite large variations in the efficiency of absorption and excretion of Na and K, tissue levels of the electrolytes remained constant.

Failure of Loading with Sodium Bicarbonate to Protect against Acute Renal Failure Induced by Mercuric Chloride in the Rat

1977 ◽  
Vol 53 (2) ◽  
pp. 149-154 ◽  
Author(s):  
J. E. Beaumont ◽  
T. A. Kotchen ◽  
J. H. Galla ◽  
R. G. Luke
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Balance ◽  
Control Group ◽  
Sprague Dawley ◽  
Urinary Volume ◽  
Sprague Dawley Rats

1. To investigate the mechanism by which sodium loading protects against acute renal failure we compared the effects of prior chronic loading with NaCl, or with NaHCO3, on renal function after injection of HgCl2. 2. Twenty-four male Sprague-Dawley rats were divided into three groups of eight rats. One group drank isotonic NaCl solution, a second drank isotonic NaHCO3 solution and the third control group drank deionized water. Acute renal failure was induced by HgCl2 on day 9, and the rats were killed 48 h after injection. 3. Net sodium balances and plasma volumes were similar in both groups of sodium-loaded rats. After HgCl2 serum creatinine was significantly less and urinary volume was greater in NaCl-loaded than in both NaHCO3-loaded and water-drinking animals. 4. Plasma renin activity of both NaCl- and NaHCO3-loaded animals was less than that of control rats. However, renal renin content was suppressed by NaCl but not by NaHCO3 loading. 5. Loading with NaCl afforded greater protection against HgCl2-induced acute renal failure than NaHCO3. Since this difference was not related to changes in sodium balance or plasma volume before HgCl2, or plasma renin activity after HgCl2, the results support the hypothesis that intrarenal renin plays a role in the pathogenesis of HgCl2-induced acute renal failure in the rat.

scholarly journals Intrarenal ghrelin receptor inhibition ameliorates angiotensin II-dependent hypertension in rats

2018 ◽  
Vol 315 (4) ◽  
pp. F1058-F1066 ◽  
Author(s):  
Brandon A. Kemp ◽  
Nancy L. Howell ◽  
Shetal H. Padia
Keyword(s):  
Angiotensin Ii ◽  
Collecting Duct ◽  
Sodium Balance ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Sprague Dawley ◽  
Systemic Delivery ◽  
Ghrelin Receptor ◽  
Receptor Inhibition ◽  
Sprague Dawley Rats

The intrarenal ghrelin receptor (GR) is localized to collecting duct (CD) cells, where it increases epithelial Na+ channel (αENaC)-dependent sodium reabsorption in rodents. We hypothesized that chronic GR inhibition with intrarenal GR siRNA lowers blood pressure (BP) in angiotensin II-dependent hypertension via reductions in αENaC-dependent sodium reabsorption. Uninephrectomized Sprague-Dawley rats ( n = 121) received subcutaneous osmotic pumps for chronic systemic delivery of angiotensin II or vehicle (5% dextrose in water). Rats also received intrarenal infusion of vehicle, GR siRNA, or scrambled (SCR) siRNA. In rats receiving intrarenal vehicle or intrarenal SCR siRNA, systemic angiotensin II infusion increased sodium retention and BP on day 1, and BP remained elevated throughout the 5-day study. These rats also demonstrated increased CD GR expression after 5 days of infusion. However, intrarenal GR siRNA infusion prevented angiotensin II-mediated sodium retention on day 1, induced a continuously negative cumulative sodium balance compared with angiotensin II alone, and reduced BP chronically. Glomerular filtration rate and renal blood flow remained unchanged in GR siRNA-infused rats. Systemic angiotensin II infusion also increased serum aldosterone levels, CD αENaC, and phosphorylated serum and glucocorticoid-inducible kinase 1 expression in rats with intrarenal SCR siRNA; however, these effects were not observed in the presence of intrarenal GR siRNA, despite exposure to the same systemic angiotensin II. These data demonstrate that chronic inhibition of intrarenal GR activity significantly reduces αENaC-dependent sodium retention, resulting in a negative cumulative sodium balance, thereby ameliorating angiotensin II–induced hypertension in rats. Renal GRs represent a novel therapeutic target for the treatment of hypertension and other sodium-retaining states.

RENIN, CORTISOL AND PLASMA VOLUME IN MARINE TELEOST FISHES ADAPTED TO DILUTE MEDIA

1976 ◽  
Vol 70 (1) ◽  
pp. 47-59 ◽  
Author(s):  
HIROKO NISHIMURA ◽  
W. H. SAWYER ◽  
R. F. NIGRELLI
Keyword(s):  
Fresh Water ◽  
Plasma Volume ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Teleost Fishes ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
American Eels

SUMMARY The renin–angiotensin system has been found in teleost fishes from both marine and freshwater environments. In an attempt to define whether activity of the renin–angiotensin system is related to sodium balance in fishes, we transferred two euryhaline teleosts from seawater to hypo-osmotic media. Plasma renin activity decreased in American eels, Anguilla rostrata, after they were transferred from seawater to fresh water, and it did not change in the aglomerular toadfish, Opsanus tau, after transfer from 50% seawater to 5% seawater. Plasma sodium concentrations decreased significantly in toadfish in 5% seawater and in one group of eels in fresh water. Plasma levels of cortisol, a major mineralocorticoid in teleosts, and plasma volume, measured in eels, remained relatively constant. There are no clear correlations between plasma renin levels and those of plasma sodium or plasma cortisol. These results provide no evidence that the need of these fishes to conserve sodium when in hypo-osmotic media stimulates the renin–angiotensin system.

Effects of naloxone on renin and pressor responses to acute renal hypotension in rats.

1990 ◽  
Vol 259 (3) ◽  
pp. E432
Author(s):  
C J Weaver ◽  
M D Johnson
Keyword(s):  
Arterial Pressure ◽  
Abdominal Aorta ◽  
Pressor Response ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Opiate Antagonist ◽  
Sprague Dawley ◽  
Aortic Constriction ◽  
Sprague Dawley Rats ◽  
Pressor Responses

Reduction of renal perfusion is followed by increases in plasma renin activity (PRA) and arterial pressure. The present experiments were designed to determine if an opiate antagonist would alter pressor or renin responses to acute reduction of renal arterial pressure (RAP) in anesthetized rats. Male Sprague-Dawley rats were anesthetized with Inactin, and an adjustable constrictor device was placed around the abdominal aorta proximal to the renal arteries. One-half of the animals were pretreated with the opiate antagonist naloxone (2 mg/kg iv), and the other one-half were pretreated with saline vehicle. The abdominal aorta was then constricted to reduce RAP by 25% (measured as femoral arterial pressure) in one-half of the animals in each pretreatment group. Compared with vehicle pretreatment, naloxone pretreatment did not alter the PRA response to aortic constriction; however, naloxone did attenuate the pressor response. We conclude that 1) the PRA response to acute reduction of renal arterial pressure is not dependent on an opiate mechanism in the rat, and 2) attenuation of the pressor response to aortic constriction by naloxone in intact rats is not secondary to a suppression of the PRA response.

Area postrema: essential for support of arterial pressure after hemorrhage in rats

1990 ◽  
Vol 258 (6) ◽  
pp. R1472-R1478 ◽  
Author(s):  
K. M. Skoog ◽  
M. L. Blair ◽  
C. D. Sladek ◽  
W. M. Williams ◽  
M. L. Mangiapane
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Data Acquisition ◽  
Area Postrema ◽  
Plasma Renin ◽  
Base Line ◽  
Sprague Dawley ◽  
Time Period ◽  
Sprague Dawley Rats

Previous studies have indicated that the area postrema (AP) of the rat is necessary for the development of chronic angiotensin-dependent hypertension. The present study assesses the role of the AP in the maintenance of arterial pressure during hemorrhage. Sprague-Dawley rats were given sham or AP lesions 1 wk before the experiment. They were instrumented with femoral arterial and venous catheters 2 days before the experiment. On the day of the experiment, base-line mean arterial pressure (MAP) was measured for 1 h before hemorrhage. During the following 45 min, each rat was subjected to one 7-ml/kg hemorrhage every 15 min for a total of three hemorrhages. MAP was monitored by computerized data acquisition. As shown previously, MAP was slightly but significantly lower in AP-lesion rats compared with sham-lesion rats before the hemorrhage procedure. In AP-lesion rats, hemorrhage resulted in a significantly greater fall in arterial pressure than in sham-lesion rats. In spite of larger drops in pressure in AP-lesion rats, hemorrhage caused equivalent increases in plasma renin and vasopressin in both groups. In AP-lesion rats compared with sham-lesion rats, significant bradycardia was present before hemorrhage. Hemorrhage caused bradycardia in both sham- and AP-lesion rats relative to the prehemorrhage heart rates, but AP-lesion rats showed greater bradycardia than did sham-lesion rats during every time period. We conclude that the AP may play an important role in the defense of arterial pressure against hemorrhage.

Obesity-Induced Hypertension Develops in Young Rats Independently of the Renin-Angiotensin-Aldosterone System

2006 ◽  
Vol 231 (3) ◽  
pp. 282-287 ◽  
Author(s):  
Anita D. Smith ◽  
Michael W. Brands ◽  
Mong-Heng Wang ◽  
Anne M. Dorrance
Keyword(s):  
Blood Pressure ◽  
Blood Glucose ◽  
Vascular Reactivity ◽  
Fasting Blood Glucose ◽  
Plasma Renin ◽  
Diet Group ◽  
Sprague Dawley ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Induced Hypertension

A correlation exists between obesity and hypertension. In the currently available models of diet-induced obesity, the treatment of rats with a high fat (HF) diet does not begin until adulthood. Our aim was to develop and characterize a model of pre-pubescent obesity-induced hypertension. Male Sprague-Dawley rats were fed a HF diet (35% fat) for 10 weeks, beginning at age 3 weeks. Blood pressure was measured by tail-cuff, and a terminal blood sample was obtained to measure fasting blood glucose, insulin, plasma renin, aldosterone, thiobarbitutic acid reactive substances (TBARS), and free 8-isoprostanes levels. The vascular reactivity in the aorta was assessed using a myograph. Blood pressure was increased in rats fed the HF diet (HF, 161 ± 2 mm Hg vs. control, 137 ± 2 mm Hg, P < 0.05). Blood glucose (HF, 155 ± 4 mg/dL vs. control, 123 ± 5 mg/dL, P < 0.05), insulin (HF, 232 ± 63 pM vs. control, 60 ± 11 pM, P < 0.05), TBARS (expressed as nM of malondialdehyde [MDA]/ml [HF, 1.8 ± 0.37 nM MDA/ml vs. control 1.05 ± 0.09 nM MDA/ml, P < 0.05]), and free 8-isoprostanes (HF, 229 ± 68 pg/ml vs. control, 112 ± 9 pg/ml, P < 0.05) levels were elevated in the HF diet group. Interestingly, plasma renin and aldosterone levels were not different between the groups. The maximum vasoconstriction to phenylephrine (10−4 M) was increased in the HF diet group (HF, 26.1 ± 1.5 mN vs. control 22.3 ± 1.2 mN, P < 0.05). In conclusion, pre-pubescent rats become hypertensive and have increased oxidative stress and enhanced vasoconstriction when fed a HF diet. Surprisingly, this occurs without the increase in renin or aldosterone levels seen in the adult models of diet-induced obesity.

Failure of NaHCO3 and KHCO3 to inhibit renin in the rat

1976 ◽  
Vol 231 (4) ◽  
pp. 1050-1056 ◽  
Author(s):  
TA Kotchen ◽  
JH Galla ◽  
RG Luke
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Volume ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Balance ◽  
Renin Inhibition ◽  
Renin Content

To evaluate the contribution of chloride to NaCl- and KCl-induced renin inhibition, renin responses to NaCl or NaHCO3 and to KCl or KHCO3 loading were compared in NaCl-deprived rats. Sodium balance in animals drinking isotonic NaHCO3 and NaCl for 9 days did not differ (P greater than 0.40); K+ balance was less positive in NaHCO3-drinking animals (P less than 0.005). Plasma renin activity (PRA) in NaCl-loaded (16.5 ng/ml per h +/- 4.4 SE), but not in NaHCO3-loaded rats (57.2 +/- 9.8), was lower (P less than 0.005) than in NaCl-deprived controls (44.8 +/- 4.7). Renal renin content (RRC) of NaCl but not of NaHCO3-drinking animals was also decreased (P less than 0.02). Both PRA and RRC of KCl- but not of KHCO3-loaded rats (5 meq K+/10 g diet) were lower (P less than 0.01) than in NaCl-deprived controls. After acute intravenous expansion with isotonic NaCl or NaHCO3, increases of plasma volume and plasma K+ did not differ (P greater than 0.05). However, PRA of NaCl-expanded rats (11.8 +/- 3.8) was lower (P less than 0.05) than in NaHCO3-expanded animals (29.7 +/- 8.5). The failure of NaHCO3 and KHCO3 to inhibit renin suggests a role for chloride in mediating the renin responses to Na+ and K+.

Sign in / Sign up

Export Citation Format

Share Document