scholarly journals Nocturia: a blinded, randomized, parallel placebo-controlled self-study of the effect of 5 different sedatives and analgesics

2008 ◽  
Vol 2 (6) ◽  
pp. 597 ◽  
Author(s):  
Michael Kaye
Keyword(s):  
Urine Volume ◽  
Sodium Reabsorption ◽  
Electrolyte Excretion ◽  
Self Study ◽  
Sleep Adequacy ◽  
Electrolyte Change ◽  
Water Salt ◽  
Sodium Loss ◽  
Renal Tubular ◽  
First Time

Background: In a previous study I noted that, when taken occasionally as a nighttime sedative, the benzodiazepine (BZD) oxazepam decreased nocturia. The objective of the present study was, using placebo and other sedatives and analgesics, to assess whether oxazepam decreases nocturia and, if so, how?Methods: I conducted a prospective, randomized, placebo-controlled self-study over a period of 10 months using oxazepam, zopiclone and trazodone as sedatives, and naproxen and oxycodone as analgesics. I assessed each medication 10 times, for a total of 60 tests. Each test included assessment of sleep adequacy, number and volume of overnight voidings and chemistries. Every test was a “first-time” or “naive” event.Results: All medications differed in several parameters from placebo, but nocturia only showed a significant reduction with naproxen and oxazepam. Nocturia occurred a mean (standard deviation [SD]) of 1.6 (0.84) times nightly with placebo and fell to 0.6 (0.5) with oxazepam, which was a 63% decrease without any change in urine volume. Naproxen reduced nocturia to a mean (SD) of 0.7 (0.8) times nightly by reducing water, salt and potassium excretion. Compared with placebo, all medications had less urine sodium loss and decreased fractional sodium excretion (FENa), suggesting increased renal tubular sodium reabsorption. This effect was most marked with naproxen. Neither improved sleep quality with zopiclone nor pain relief with oxycodone resulted in reduced nocturia.Conclusion: The effect of naproxen was probably a direct one on the kidney. The reduction of electrolyte excretion produced by the other medications is possibly a central effect on sympathetic activity, and the effect was too small to change urine volume. The effect of oxazepam was to make the bladder less irritable and could not be attributed to a decrease in urine volume, electrolyte change, sedation or analgesia. A central γ-aminobutyric acid–mediated effect in the cord or brain could explain the results observed with oxazepam.

Relationship between renal fluid and Mg secretion in a glomerular marine teleost

1980 ◽  
Vol 238 (2) ◽  
pp. F92-F98 ◽  
Author(s):  
J. L. Renfro
Keyword(s):  
Blood Flow ◽  
Urine Volume ◽  
Portal Blood Flow ◽  
Fluid Secretion ◽  
Urine Flow ◽  
Winter Flounder ◽  
Sodium Reabsorption ◽  
Pseudopleuronectes Americanus ◽  
Calculated Concentration ◽  
Renal Tubular

Renal tubular fluid secretion has been studied in seawater-acclimated winter flounder, Pseudopleuronectes americanus. Although this animal has a filtration kidney and a relatively high glomerular filtration rate (GFR = 1.35 ml . kg-1 . h-1), apparently more than half of the final urine volume was secreted fluid, and net fluid secretion was frequently observed. The dominant divalent ion excreted in the urine was Mg, of which 98% was secreted. A strong correlation (r = 0.98) was seen between secreted Mg and the rate of tubular fluid secretion. The calculated concentration of Mg in secreted fluid was 169 mM, a figure that was substantiated by values obtained for urine Mg concentration when urine flow was due almost entirely to tubular fluid secretion. Alterations in urine flow rate reflected changes in the rate of Mg secretion; however, no correlation was seen between GFR and secreted Mg, which may indicate independence of renal portal blood flow and glomerular blood flow. No relationship between Mg secretion and sodium reabsorption was apparent. These observations support the hypothesis that Mg secretion together with accompanying anions (Cl and SO4) accounts entirely for tubular fluid secretion in the winter flounder.

Chloride concentration gradient in newborn dogs in the presence of distal nephron blockade

1980 ◽  
Vol 239 (4) ◽  
pp. F328-F335
Author(s):  
Aviad Haramati ◽  
Leonard I. Kleinman
Keyword(s):  
Proximal Tubule ◽  
Ethacrynic Acid ◽  
Chloride Concentration ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Electrolyte Excretion ◽  
Newborn Animal ◽  
Plasma Chloride ◽  
Renal Tubular ◽  
Inner Cortex

Renal tubular Na+, Cl-, and H2O reabsorption was determined in 14 newborn dogs, 3–29 days of age, and in three adult dogs. In all animals NaCl reabsorption beyond the proximal tubule was blocked with ethacrynic acid (2 mg/kg) and amiloride (2.4 mg/kg). During distal blockade, fractional reabsorption of NaCl and water in both newborns and adults was approximately 70%, and there was a urine-to-plasma chloride gradient equal to 1.34 ± 0.01, indicating that the proximal tubules of the newborn as well as those of the adult can generate a transtubular Cl- gradient. Upon administration of acetazolamide (50 mg/kg), there was a dramatic increase in excretion of Na+, Cl-, HCO3-, and water, and a decrease in the transtubular chloride gradient. After acetazolamide, the degree of inhibition of HCO3- reabsorption was well correlated with that of Na+ (r = 0.77) or Cl- (r = 0.74), and Na+ or Cl- inhibition exceeded that of HCO3- In the newborn animal, the ratio of inner-to-outer cortical nephron function is high at birth and declines rapidly during the first few weeks of life. However, there was no correlation between age and changes in either electrolyte excretion or in the transtubular chloride gradient. Therefore, the newborn dog possesses Cl- permselective tubules in the inner cortex that, in the presence of intact HCO3- reabsorption, are capable of establishing a functional transtubular Cl- gradient contributing to NaCl reabsorption. bicarbonate reabsorption; sodium reabsorption; ethacrynic acid; amiloride; acetazolamide; proximal tubule Submitted on October 29, 1979 Accepted on April 18, 1980

Sodium and Water Excretion in Nephrotic Patients: Effects of Changes in Renal Haemodynamics

1990 ◽  
Vol 79 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Michael Allon ◽  
Charles B. Pasque ◽  
Mariano Rodriguez
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Sodium Reabsorption ◽  
Plasma Volume Expansion ◽  
Water Excretion ◽  
Significant Change

1. Eight nephrotic patients were studied in order to evaluate the effects of acute changes in renal plasma flow and glomerular filtration rate on renal solute and water handling, in the absence of plasma volume expansion. 2. The subjects were studied first after the administration of captopril, a manoeuvre that increased renal plasma flow without a significant change in glomerular filtration rate, and a second time after receiving combined therapy with captopril and ibuprofen, a manoeuvre that decreased glomerular filtration rate without a significant change in renal plasma flow. 3. After captopril therapy, despite the increase in renal plasma flow, there was no significant change in proximal sodium reabsorption (as estimated from fractional lithium reabsorption), urine volume or urine osmolality. 4. The decrease in glomerular filtration rate observed after the administration of captopril plus ibuprofen was associated with decreases in fractional excretion of sodium and urine volume, and an increase in urine osmolality. The changes in these parameters of tubular function were proportionate to the changes in glomerular filtration rate. Fractional proximal sodium reabsorption increased substantially. 5. These observations suggest that, in the absence of plasma volume expansion, an increase in renal plasma flow does not increase sodium or water excretion by the nephrotic kidney. Moreover, during acute decreases in glomerular filtration rate, glomerulotubular balance appears to be disrupted, resulting in disproportionately high rates of proximal tubule sodium reabsorption.

scholarly journals Localization of the novel angiotensin peptide, angiotensin-(1-12), in heart and kidney of hypertensive and normotensive rats

2008 ◽  
Vol 294 (6) ◽  
pp. H2614-H2618 ◽  
Author(s):  
Jewell A. Jessup ◽  
Aaron J. Trask ◽  
Mark C. Chappell ◽  
Sayaka Nagata ◽  
Johji Kato ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Renal Tubules ◽  
Uptake Mechanism ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Angiotensin Peptide ◽  
Wistar Kyoto ◽  
Renal Tubular ◽  
Alternate Substrate ◽  
First Time

A low expression of angiotensinogen in the heart has been construed as indicating a circulating uptake mechanism to explain the local effects of angiotensin II on tissues. The recent identification of angiotensin-(1-12) in an array of rat organs suggests this propeptide may be an alternate substrate for local angiotensin production. To test this hypothesis, tissues from 11-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats ( n = 14) were stained with purified antibodies directed to the COOH terminus of angiotensin-(1-12). Robust angiotensin-(1-12) staining was predominantly found in ventricular myocytes with less staining found in the medial layer of intracoronary arteries and vascular endothelium. In addition, angiotensin-(1-12) immunoreactivity was present in the proximal, distal, and collecting renal tubules within the deep cortical and outer medullary zones in both strains. Preadsorption of the antibody with angiotensin-(1-12) abolished staining in both tissues. Corresponding tissue measurements by radioimmunoassay showed 47% higher levels of angiotensin-(1-12) in the heart of SHR compared with WKY rats ( P < 0.05). In contrast, renal angiotensin-(1-12) levels were 16.5% lower in SHR compared with the WKY rats ( P < 0.05). This study shows for first time the localization of angiotensin-(1-12) in both cardiac myocytes and renal tubular components of WKY and SHR. In addition, we show that increased cardiac angiotensin-(1-12) concentrations in SHR is associated with a small, but statistically significant, reduction in renal angiotensin-(1-12) levels.

scholarly journals Proximal and Distal Nephron-specific Adaptation to Furosemide

2021 ◽  
Author(s):  
Aram J. Krauson ◽  
Steven Schaffert ◽  
Elisabeth M. Walczak ◽  
Jonathan M. Nizar ◽  
Gwen M. Holdgate ◽  
...  
Keyword(s):  
Cell Number ◽  
Differentially Expressed ◽  
Sodium Reabsorption ◽  
Thick Ascending Limb ◽  
Distal Nephron ◽  
Transcriptional Responses ◽  
Cell Hyperplasia ◽  
Diuretic Resistance ◽  
Nephron Segments ◽  
Renal Tubular

ABSTRACTFurosemide, a widely prescribed diuretic for edema-forming states, inhibits sodium reabsorption in the thick ascending limb of the nephron. Tubular adaptation to diuretics has been observed, but the range of mechanisms along the nephron has not been fully explored. Using morphometry, we show that furosemide induces renal tubular epithelial hyperplasia selectively in distal nephron segments. By comparison, we find progressive cellular hypertrophy in proximal and distal nephron segments. We next utilize single cell RNA sequencing of vehicle- and furosemide-treated mice to define potential mechanisms of diuretic resistance. Consistent with distal tubular cell hyperplasia, we detect a net increase in DCT cell number and Birc5, an anti-apoptotic and pro-growth gene, in a subset of DCT cells, as the most prominently up-regulated gene across the nephron. We also map a gradient of cell-specific transcriptional changes congruent with enhanced distal sodium transport. Furosemide stimulates expression of the mitogen IGF-1. Thus, we developed a mouse model of inducible deletion of renal tubular IGF-1 receptor and show reduced kidney growth and proximal, but not distal, tubular hypertrophy by furosemide. Moreover, genes that promote enhanced bioavailability of IGF-1 including Igfbp1 and Igfbp5 are significantly and differentially expressed in proximal tubular segments and correspond to IGF-1R-dependent hypertrophy. In contrast, downstream PI3-kinase signaling genes including Pdk1, Akt1, Foxo3, FKBP4, Eif2BP4, and Spp1 are significantly and differentially expressed in distal nephron segments and correspond to IGF-1R-independent hypertrophy. These findings highlight novel mechanisms of tubular remodeling and diuretic resistance, provide a repository of transcriptional responses to a common drug, and expand the implications of long-term loop diuretic use for human disease.

Mechanism of increased renal tubular sodium reabsorption in cirrhosis

1972 ◽  
Vol 52 (2) ◽  
pp. 198-202 ◽  
Author(s):  
C. Chaimovitz ◽  
P. Szylman ◽  
G. Alroy ◽  
O.S. Better
Keyword(s):  
Sodium Reabsorption ◽  
Tubular Sodium Reabsorption ◽  
Renal Tubular

Primary aldosteronism and other steroid-related causes of endocrine hypertension

2011 ◽  
pp. 810-824
Author(s):  
John M.C. Connell ◽  
E. Marie Freel
Keyword(s):  
Primary Aldosteronism ◽  
Sodium Content ◽  
Sodium Reabsorption ◽  
Plasma Volume Expansion ◽  
Inborn Errors ◽  
Adrenal Steroid ◽  
Reduced Body ◽  
Metabolism Syndrome ◽  
Apparent Mineralocorticoid Excess ◽  
Renal Tubular

Mineralocorticoid hypertension is characterized by increased distal renal tubular sodium reabsorption, raised body sodium content, plasma volume expansion, markedly reduced body potassium content, with a metabolic alkalosis and suppression of renin production by the juxtaglomerular cells of the kidney (and correspondingly low levels of angiotensin II). Primary aldosteronism is the most common cause of mineralocorticoid hypertension (1); less frequent causes include the rare inborn errors of adrenal steroid synthesis (11β‎-hydroxylase and 17α‎-hydroxylase deficiency), alterations in corticosteroid metabolism (syndrome of apparent mineralocorticoid excess), and constitutive activation of the epithelial sodium channel (Liddle’s syndrome).

Effect of acute unilateral renal denervation on tubular sodium reabsorption in the dog

1977 ◽  
Vol 232 (1) ◽  
pp. F16-F19
Author(s):  
G. Nomura ◽  
T. Takabatake ◽  
S. Arai ◽  
D. Uno ◽  
M. Shimao ◽  
...  
Keyword(s):  
Renal Denervation ◽  
Renal Plasma Flow ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Water Diuresis ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Tubular Sodium Reabsorption ◽  
Renal Tubular

The effects of acute denervation of the kidney on renal tubular sodium and water excretion were studied in anesthetized, hypophysectomized, and cortisone-treated mongrel dogs during stable water diuresis produced by the infusion of 2.5% dextrose. In all experiments, denervation natriuresis, and diuresis were observed without significant change in glomerular filtration rate (GRF) and renal plasma flow (RPF). Fractional sodium delivery to the distal nephron (CNa + CH2O/100 ml GFR) and fractional free water clearance (CH23/100 ml GFR) was significantly greater in the denervated kidney compared with the innervated kidney (9.6+/-1.2 vs. 6.7+/-0.9% and 8.8+/-1.2 vs. 6.5+/-0.8%, respectively). Distal tubular sodium reabsorption (CH2O/(CNa + CH2O)) was not significantly different. We conclude that renal denervation primarily affects the proximal tubule as manifested by a decrease in the reabsorption of sodium and water. A small effect of denervation on the distal nephron is not completely ruled out.

Differing renal effects of activated and nonactivated isoelectric peaks of human prorenin in rats

1991 ◽  
Vol 261 (6) ◽  
pp. F975-F981
Author(s):  
J. K. McKenzie ◽  
D. R. Jones ◽  
I. M. McKenzie ◽  
D. D. Smyth
Keyword(s):  
Physiological Function ◽  
Urine Volume ◽  
Sprague Dawley ◽  
Urine Sodium ◽  
Sodium Potassium ◽  
Renal Effects ◽  
Sprague Dawley Rats ◽  
Isoelectric Points ◽  
First Time ◽  
Ovarian Follicular Fluid

Isoelectric species of renin are physically heterogeneous. Recent evidence suggests that they may differ functionally, with some species producing natriuresis and diuresis, whereas others have no effect. A physiological function of secreted prorenin has not been documented in any species. The present study was designed to confirm and describe for the first time the renal effects of certain isoelectric species of prorenin. Anesthetized Sprague-Dawley rats were injected (0.1 ml) with trypsin-activated or nonactivated prorenin obtained from human ovarian follicular fluid. The dose chosen was calculated as sufficient to produce 2,300 ng angiotensin I.h-1.100 g rat body wt-1 in the presence of excess sheep substrate. Blood pressure, creatinine clearance, urine flow rate, and urine sodium, potassium, and osmolar excretion were measured. Activated prorenin from isoelectric peaks at isoelectric points (pI) 5.1, 5.2, 5.4, and 5.6 produced marked increases in urine volume (sixfold) and sodium excretion (7- to 10-fold) compared with the group receiving the vehicle (1% albumin in 0.9% saline). Activated prorenin from peaks at pI 4.9 and 5.8 produced no significant increase over the vehicle-only experiments. Captopril pretreatment (1 mg/kg iv) completely blocked the effects of peaks at pI 5.4 and 5.6. Interestingly, injection of nonactivated prorenin from peaks at pI 5.4 and 5.6 produced effects similar to the injection of activated prorenin from these peaks. Similarly, this effect was blocked by pretreatment with captopril. In summary, only certain isoelectric peaks of human prorenin whether activated, to active renin, or nonactivated produced a marked natriuresis and diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal and pressor action of angiotensin in the normal dog

1965 ◽  
Vol 208 (6) ◽  
pp. 1093-1099 ◽  
Author(s):  
John K. Healy ◽  
Carlos Barcena ◽  
J. M. Brian O'Connell ◽  
George E. Schreiner
Keyword(s):  
Filtration Rate ◽  
Pressor Response ◽  
Urine Flow ◽  
Sodium Reabsorption ◽  
Potassium Excretion ◽  
Control Blood Pressure ◽  
Electrolyte Excretion ◽  
Initial Depression ◽  
High Doses ◽  
Higher Doses

The renal and pressor actions of angiotensin in relation to dose were studied in unanesthetized dogs. Low doses caused depression of urine flow, electrolyte excretion, glomerular filtration rate (GFR), and Cpah. With higher doses, the initial depression of urine flow, GFR, and Cpah was greater, but subsequently these functions rose toward control values. In fact, diuresis occurred, accompanied by natriuresis, chloruresis, and kaliuresis. The natriuresis occurred at a time when GFR was significantly depressed. In longer experiments at high doses it was found that the natriuresis declined after 50 min despite continued angiotensin infusion; however, potassium excretion gradually increased throughout. These results help clarify the confusing literature regarding the effects of angiotensin on renal function in dogs and also support the hypothesis that angiotensin can block tubular sodium reabsorption. The pressor response was found to be proportional to the logarithm of the dose of angiotensin. It was also inversely related to the control blood pressure of the dog.

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