Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal haemodynamics, sodium excretion, and free-water clearance were evaluated at baseline and after acute frusemide administration in nine moderately volume-expanded healthy volunteers receiving a single administration of either 750 mg lithium carbonate or placebo. Lithium plasma concentration under 0.29 mmol/l exerted no significant effect on renal haemodynamics, on absolute, fractional, or cumulative sodium excretion, or on free-water and chloride clearances at baseline or after frusemide administration. Despite previous volume expansion and presumably depressed proximal reabsorption, frusemide decreased the fractional reabsorption of lithium significantly, suggesting that a small but significant part of lithium may be reabsorbed in the thick ascending limb of Henle's loop. By contrast, frusemide did not change renal haemodynamics or plasma renin activity. Using combined free-water and lithium clearances at baseline and after frusemide administration, fractional reabsorption of sodium in the (FRTAL) was calculated as delta CH2O/CLi, where delta CH2O, the difference in free water clearance before minus after frusemide, is taken as an index of sodium reabsorption in the thick ascending limb, and lithium clearance as an estimation of sodium delivery to the thick ascending limb. FRTAL was calculated in these volume-expanded subjects to lie from 11% to 20% depending on whether some lithium is assumed to be in the thick ascending limb.
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PMID:Does lithium affect renal sodium handling and renal haemodynamics in normal man? 212 49

1. alpha-Human atrial natriuretic peptide (7.5 pmol min-1 kg-1) was infused intravenously into eight healthy men after pretreatment with lithium carbonate (750 mg) or placebo. 2. Baseline sodium excretion was significantly increased after lithium, but the natriuresis during infusion of alpha-human atrial natriuretic peptide was attenuated. 3. Similar decreases in plasma renin activity with infusion of alpha-human atrial natriuretic peptide occurred on both days. 4. Administration of lithium may be associated with pharmacological effects and further work is required to validate the use of lithium clearance as a marker of proximal renal tubular sodium handling.
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PMID:Effect of lithium on the renal actions of alpha-human atrial natriuretic peptide in normal man. 216 Mar 54

To test the hypothesis that NaCl and NaHCO3 have divergent effects on blood pressure, we carried out a randomly allocated, placebo-controlled, crossover trial in 10 mildly hypertensive and 10 normal subjects. They ingested a fixed daily basal diet of 60 mmol sodium and chloride, 60 mmol potassium and 14 mmol calcium. After balance was achieved (4 days), the subjects were randomly assigned to drink 3 liters/day of a NaHCO3-containing mineral water (26.2 mmol/l sodium and 33.03 mmol/l HCO3) or a control solution containing equimolar amounts of cations as the chloride salt for 7 days (total daily sodium 138 mmol). All urine was collected. Blood pressure was determined by an automated device. One month later the opposite regimen was followed. NaCl did not influence blood pressure, whereas NaHCO3 decreased systolic blood pressure (by 5 mmHg) in the hypertensive subjects. Both regimens decreased plasma renin activity in the hypertensive subjects but did not consistently influence plasma aldosterone or catecholamines. However, urinary calcium excretion, which was greater in hypertensives than in normotensives, and greater in white than in black subjects, increased consistently with NaCl but not with NaHCO3. The excretion of urate was not influenced by the regimens; however, urate excretion was consistently greater in whites than in blacks. The data show that NaCl increases calcium excretion whereas NaHCO3 does not, even at modest levels of intake. NaCl and NaHCO3 may therefore differ in their effects on blood pressure.
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PMID:Sodium bicarbonate and sodium chloride: effects on blood pressure and electrolyte homeostasis in normal and hypertensive man. 216 57

A diet fortified with calcium carbonate has been reported to reduce blood pressure in low-renin and salt-sensitive hypertensive patients. We have therefore examined the effect of increased dietary calcium on the development of reduced renal mass-saline hypertension in rats, a classical, low-renin, volume, and sodium-dependent model of hypertension. Rats with 70-75% reduction in renal mass were divided into experimental and control groups. The experimental rats were fed a sodium-free diet supplemented with calcium carbonate (2.0% calcium) and drank 1% saline for 5 weeks. Control rats consumed the salt-free diet and drank 1% saline for the same period. In control rats, as previously observed, blood pressure progressive increased from a control value of 120.0 +/- 1.2 to 174.2 +/- 1.2 mm Hg by the fifth week. In contrast, in the calcium-supplemented rats the development of hypertension was significantly attenuated; the blood pressure only increased from 117.0 +/- 1.2 to 134.0 +/- 3.8 mm Hg by the fifth week. This was associated with a 30% decrease in saline intake by the fifth week, with proportionate decreases in urine volume and sodium excretion but not potassium excretion. Urinary magnesium excretion increased. No such changes were seen in control rats. At the end of the treatment period, plasma levels of sodium, potassium, calcium, creatinine, BUN, and protein were not different, but plasma chloride and magnesium were lower in experimental rats; vascular smooth muscle cell membrane potentials were also not different. These data show that dietary calcium carbonate can attenuate the development of reduced renal mass-saline hypertension in the rat, possibly in part by altering sodium and water intake.
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PMID:Effect of increased dietary calcium on the development of reduced renal mass saline hypertension in rats. 230 5

To assess a possible role for endogenous renal dopamine in sodium excretion, the dopa decarboxylase inhibitor carbidopa was given during intravenous salt loading. In addition, the effect of lithium on tubular sodium handling was separately determined. Nine males were studied randomly on three occasions, receiving placebo, lithium carbonate (1000 mg, 11 h prior to study) or carbidopa (100 mg x 2). On each day a baseline period was followed by infusion of isotonic saline (20 ml/kg per hour) over 3 h, and 6 h recovery. With placebo, sodium excretion increased markedly to a peak in the hour after infusion (0.15 +/- 0.03 to 0.73 +/- 0.12 mmol/min, P less than 0.01). Urine dopamine excretion increased modestly (1.33 +/- 0.12 to 1.67 +/- 0.13 mmol/min, P less than 0.01). Carbidopa effectively blocked dopamine output during the study. However, the natriuretic response was comparable to values on placebo at all time points. Fractional lithium clearance, a proposed measure of proximal tubular fluid rejection, increased significantly during saline infusion. However, baseline sodium excretion was greater in the presence of lithium, and plasma renin activity (PRA) was significantly elevated. In addition, the peak natriuretic response was smaller and cumulative sodium excretion reduced by 40% (P less than 0.01) compared to placebo. This study provides no evidence for a facilitatory role for dopamine in the natriuretic response to intravenous salt loading. Lithium, at subtherapeutic levels, cannot be presumed to be an inert marker, and clearance data must be interpreted with caution.
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PMID:The effect of carbidopa and lithium on the systemic and renal response to acute intravenous saline loading in normal man. 252 33

The purpose of this study was to investigate the renal handling of sodium and potassium in rats during an acute ethanol (ETOH) administration and to relate any observed changes to alterations in renin-aldosterone secretion. Eight male Wistar rats, 7 to 8 weeks of age, were injected intraperitoneally (IP) with 1.0 g/kg body wt. ETOH (15% v/v, 95% ETOH in saline, pH 6.98, osmolality 284 mOsm/kg). Blood ETOH levels were 159 +/- 16 (Mean +/- SEM) and 120 +/- 12 mg/dl, 10 and 30 min after the ETOH injection respectively (p less than 0.05). Control animals were given either an equal volume (1.77 ml/100 g body wt.) of 0.9% saline (n = 6) or 5% dextrose solution (n = 4) with similar pH and osmolality. Following ETOH administration blood pH, urine pH, plasma bicarbonate (HCO3) concentration declined significantly (p less than 0.01) while glomerular filtration rate (GFR) and hematocrit (Hct) remained unchanged (p = 0.1). Mean fractional sodium excretion (FENa), fractional potassium excretion (FEK), and osmolar clearance (Cosm) fell significantly despite an increase in plasma sodium (p less than 0.01), potassium (p less than 0.05) and osmolality concentrations (p less than 0.05). There was no significant change in plasma aldosterone concentration (PA) or plasma renin activity (PRA) following the ETOH administration. No difference in GFR, FENa, FEK, Cosm, blood pH, urine pH, plasma electrolytes, PA, or PRA was observed following the saline or dextrose injections. In conclusion, acute ETOH administration in rats alters renal sodium and potassium excretion independent of changes in GFR, PA, PRA or plasma volume as reflected by Hct.
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PMID:Acute effect of ethanol on renal electrolyte excretion in rats. 266 Aug 49

Juxtaglomerular cells in vitro are sensitive to changes in osmolality, but it is unknown whether volume-regulatory changes in cellular ion fluxes are important for the renin secretory process. The sensitivity of renin release to increases in osmolality by NaCl was therefore tested on superfused rat glomeruli treated with bicarbonate/chloride exchange inhibitor (DNDS), NaCl/KCl cotransport inhibitor (bumetanide), or Na+/H+ antiport inhibitor (amiloride) in the presence or absence of bicarbonate. In addition, the sensitivity to increases in osmolality by addition of sucrose was tested in the presence or absence of bicarbonate. Renin release from time controls superfused with a bicarbonate-free Ringer was identical to release from glomeruli superfused with a bicarbonate Ringer. DNDS (0.11 or 1.1 mM) had no effect on renin release in a bicarbonate Ringer. 30 mM sucrose inhibited renin release independently of bicarbonate. 15 mM NaCl stimulated renin release when bicarbonate was absent, while it caused an inhibition in the presence of bicarbonate. When bicarbonate/chloride exchange was inhibited, addition of NaCl stimulated renin release even when bicarbonate was present. The effect of NaCl on renin release was not affected by amiloride (1 mM) or bumetanide (10 microM). Thus, volume regulatory mechanisms as known from other cells are not involved in the renin secretory response to small increases in NaCl concentration. Furthermore, the sensitivity of renin release to changes in NaCl concentrations is modulated by bicarbonate in a way that depends on a functioning anion-exchange mechanism. The results are compatible with the existence in the membrane of the secretory granule of a Cl-/HCO3- exchange mechanism which mediates exit of Cl-, and thereby attenuates granular swelling and exocytotic release.
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PMID:Influence of bicarbonate on the sensitivity of renin release to sodium chloride. 268 21

1. To test the hypothesis that NaCl increases blood pressure, while NaHCO3 does not, we measured the effect of an NaHCO3-containing mineral water on blood pressure in stroke-prone spontaneously hypertensive (SHR-SP) and Wistar-Kyoto (WKY) rats. We compared mineral water with equimolar amounts of NaCl and demineralized drinking water in six groups of 20 rats each over 24 weeks. 2. NaCl consistently increased blood pressure in both SHR-SP and WKY compared with demineralized water, while mineral water did not. 3. We studied the possible role of sodium-regulating hormones. Sodium, potassium-dependent adenosine triphosphatase activity was decreased by NaCl and by age, but not by mineral water. The concentration of atrial natriuretic peptide was greater in SHR-SP, but was not influenced by the two regimens. Components of the renin-angiotensin-aldosterone system and 18-hydroxydeoxycorticosterone tended to decrease with NaCl, but not with mineral water. 4. Plasma pH values in the six groups of rats were not different; however, SHR-SP had consistently lower PCO2 and HCO3- values and higher anion gap values than WKY rats. These values were not influence by the two regimens. 5. NaCl elevates blood pressure in SHR-SP while NaHCO3 does not. The changes in hormones regulating sodium homoeostasis suggest that NaCl induces volume expansion while NaHCO3 does not. The effect may be related to influences on renal sodium reabsorption by chloride and bicarbonate. The possible role of increased proton excretory activity in SHR-SP remains to be determined.
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PMID:Effect of sodium chloride and sodium bicarbonate on blood pressure in stroke-prone spontaneously hypertensive rats. 284 Feb 35

Current information suggests that alpha 2-adrenoceptors do not directly influence vascular resistance or Na reabsorption in the rat kidney. To reexamine the effects of alpha 2-agonists we used isolated rat kidneys perfused at 37.5 degrees C with precise measurement of renal artery pressure and flow. The recirculating perfusate contained pyruvate as the sole metabolic substrate which enabled us to use gluconeogenesis as an index of proximal tubular alpha 1-responses. Clonidine and guanfacine in 100 nM concentrations decreased phosphate excretion without altering Na, Cl, or K reabsorption or gluconeogenesis; 500 nM concentrations increased vascular resistance and decreased glomerular filtration rate and Na, Cl, and K excretion with no significant effect on gluconeogenesis. Prior thyroparathyroidectomy prevented the antiphosphaturic but not the antinatriuretic or vascular responses. Clonidine, an alpha 2-agonist with some alpha 1-activity, was a more potent vasoconstrictor than methoxamine or guanfacine. In the presence of prazosin (1 microM), norepinephrine (60 nM) stimulated phosphate reabsorption; norepinephrine alone did not stimulate phosphate reabsorption which indicates alpha 1-antagonism of this alpha 2-response to NE. These results and a literature review suggest that increased renal alpha 2-adrenoceptors could raise renal vascular resistance, reduce renin secretion, and antagonize parathyroid hormone effects on Pi, Ca, HCO3, and Na reabsorption to produce a low renin type of hypertension with increased proximal Na reabsorption and abnormal Ca and Pi excretion.
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PMID:Is there a role for renal alpha 2-adrenoceptors in the pathogenesis of hypertension? 289 22

1. The effect of renal arterial infusion of synthetic human atrial natriuretic factor (ANF (99-126] on renal function in the conscious euvolaemic sheep was characterized. ANF (99-126) was infused for 2 h at 5 and 50 micrograms/h into the renal artery of crossbred Merino ewes with chronically indwelling cannulae inserted in the renal artery. The effect on absolute and fractional excretion of Na, K, Ca, Cl and HCO3, glomerular filtration rate (GFR), effective renal plasma flow (ERPF) and free water clearance (CH2O) were measured. 2. Infusion at 50 micrograms/h produced a fourfold increase in Na and Cl excretion. Ca excretion increased eightfold, while K and HCO3 increased by small amounts. At the lower dose only Na, Cl and Ca excretion increased significantly. The changes in absolute excretion of each ion were closely mirrored by changes in fractional excretion. CH2O became more negative at both levels of infusion. Small changes in GFR were measured at both rates of infusion. No changes in ERPF or renin secretion were observed. 3. ANF (99-126) infusion at 50 micrograms/h for 1 h increased the excretion of Li, such that more than 70% of the change in Na excretion was associated with the changes in Li clearance. Changes in GFR accounted for less than 10% of change in Na excretion. 4. Following either long-term (50 micrograms/h for 6 h) or repeated short-term (20 micrograms/h for 30 min) infusions of ANF (99-126), the response of Na excretion was not sustained. The mechanisms of the tachyphylaxis remains undetermined. 5. ANF (99-126) is a powerful stimulus to the absolute and fractional excretion of Na, K, Ca, Cl and HCO3. The mechanism of action is not known, but appears to be related to changes in tubular function and/or a change in glomerulotubular balance.
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PMID:Renal effects of atrial natriuretic factor (99-126) in conscious sodium-replete sheep. 297 47


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