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PubMed1986

Pulmonary absorption of drugs in the dog: comparison with other species.

To investigate the pulmonary absorption rate of drugs in the anesthetized beagle dog, 5 ml of drug solution was administered into the lungs by rapid injection through a tracheal cannula. After various times, lungs were removed and assayed for unabsorbed drug. The dog absorbed lipid-insoluble drugs such as p-aminohippuric acid, mannitol, and procainamide ethobromide at the same rate as the rat, two times more rapidly than the rabbit, and approximately 2-3 times more slowly than the mouse and guinea pig. In contrast, the dog absorbed a lipid-soluble drug like procainamide at the same rate as the other four species. The results suggest that pulmonary absorption rates measured in small laboratory animals can be used to predict absorption rates in large animals.

Absorption↗

PubMed1994

Progression of glomerular sclerosis in experimental uremic rats by administration of indole, a precursor of indoxyl sulfate.

In uremia there is a marked elevation of serum levels of indoxyl sulfate due to its decreased renal clearance. Indoxyl sulfate is synthesized in the liver from indole which is produced by bacteria in the intestines. To determine the role of indoxyl sulfate in the progression of chronic renal failure, we administered indole, the precursor of indoxyl sulfate, to subtotally nephrectomized uremic rats. The oral administration of indole increased the serum levels of creatinine and blood urea nitrogen and decreased creatinine, inulin, and p-aminohippuric acid clearances. The glomerular sclerosis index in the indole-treated rats was higher than in the control uremic rats. After oral administration, indole could not be detected in the urine, but large amounts of its metabolite, indoxyl sulfate. Thus, indole administration stimulated glomerular sclerosis in a uremic model through the production of indoxyl sulfate.

Animals↗

PubMed1987

Renal and renin effects of sodium thiopental in rabbits.

Unilateral renal arterial infusion of sodium thiopental on renal function and renin secretion were investigated in unanesthetized rabbits. Sodium thiopental infusion in doses of less than 0.3 mg/kg/min into unilateral renal artery caused dose-dependent increases in urine flow, urinary excretion of electrolytes, fractional excretion of sodium and free water clearance with no changes in systemic blood pressure and clearance of p-aminohippuric acid (renal blood flow). An anesthetic dose of sodium thiopental administered intravenously caused decreases in systemic blood pressure, renal hemodynamics, urine flow and free water clearance during the early period of anesthesia followed by increases in urinary excretion of sodium and fractional excretion of sodium. Unilateral renal arterial infusion of sodium thiopental decreased the renin secretion rate and plasma norepinephrine concentration in renal vein, whereas an anesthetic dose of sodium thiopental administered intravenously increased the renin secretion rate. These observations suggest that the diuretic, natriuretic and renin suppressive effects of sodium thiopental may be due to an inhibition of intrarenal sympathetic nervous system or due to a direct tubular action.

Animals↗

PubMed1991

Influence of ciclosporin A on renal tubular function after kidney transplantation.

There are typical morphological indicators of tubular defects during the administration of ciclosporin A (CSA). Distal tubular function remains unclear although hyperkalemia is a common clinical feature in these patients. We performed renal function studies 3 months after renal transplantation on 35 patients (group 1) treated with CSA. The results were compared to those of a control group consisting of 15 patients transplanted earlier and treated with azathioprine (group 2). Only patients with stable renal function (creatinine less than or equal to 2.0 mg/dl) entered the investigation consisting of: inulin (In) clearance; p-aminohippuric acid (PAH) clearance; ammonium chloride loading; sodium sulfate loading, and sodium bicarbonate loading. Plasma renin activity and aldosterone were measured basally and after stimulation with 40 mg i.v. furosemide. Clearances of In and PAH were significantly impaired during the administration of CSA. Group 1: CIn 73.3 +/- 8.7 ml/min/1.73 m2 (p less than 0.01), CPAH 263 +/- 58.3 ml/min/1.73 m2 (p less than 0.01); group 2: CIn 89.6 +/- 19.1 ml/min/1.73 m2, CPAH 338.7 +/- 63.5 ml/min/1.73 m2. Incomplete distal tubular acidosis could be demonstrated in 8 patients from group 1 but none of group 2. Hyporeninemic hypoaldosteronism could be demonstrated in 4 patients during the administration of CSA. CSA in therapeutic doses significantly impairs renal perfusion, glomerular filtration, distal acidification and the renin-aldosterone axis.

Adult↗

PubMed1988

Renal effects of d-tubocurarine and pancuronium in the newborn rabbit.

The acute renal effects of d-tubocurarine and pancuronium were assessed in 14 anesthetized newborn rabbits. Glomerular filtration rate (GFR) and renal blood flow (RBF) were calculated from the inulin and p-aminohippuric acid clearances, respectively. Each animal acted as its own control. At doses used in human neonates, d-tubocurarine administration (0.80 mg/kg) produced a marked increase in renal vascular resistance (+123 +/- 62%) with a concomitant significant decrease in GFR (-35.4 +/- 12%) and RBF (-39 +/- 13%). Pancuronium administration (0.25 mg/kg) was associated with a nonsignificant decrease in GFR (-19 +/- 17%) and RBF (-20 +/- 12%) and an increase in renal vascular resistance (+66 +/- 52%). These results stress the need for careful monitoring of renal function in neonates receiving nondepolarizing muscle-relaxant agents.

Animals↗

PubMed1991

Hyperoxemia does not affect renal hemodynamics and function in newborn rabbits.

Renal hemodynamics and function were assessed in 10 anesthetized newborn rabbits undergoing acute hyperoxemia for 1 h. The hyperoxemic period either followed (group 1: n = 5) or preceded (group 2: n = 5) a normoxemic control period. Renal blood flow (RBF) and glomerular filtration rate (GFR) were assessed by the clearance of p-aminohippuric acid and inulin, respectively. Urine flow rate, GFR, RBF, renal vascular resistance, filtration fraction and sodium fractional excretion remained unchanged throughout the study whatever the order of the normoxemic and hyperoxemic periods. It is concluded that hyperoxemia up to PaO2 of 170 mm Hg does not alter renal function.

Animals↗

PubMed1995

Does endothelin-1 mediate the hypoxemia-induced renal dysfunction in newborn rabbits?

In the newborn rabbit, acute normocapnic hypoxemia increases the renal vascular resistance, leading to renal hypoperfusion and decreased glomerular filtration rate. Endothelin is a potent vasoconstrictor peptide, produced by vascular endothelial cells, which could play a role as a mediator of the hypoxemia-induced renal dysfunction. To test this hypothesis, experiments were performed in 24 anesthetized and mechanically ventilated newborn rabbits. Renal blood flow and glomerular filtration rate were determined by the clearance of p-aminohippuric acid and inulin, respectively. Each animal acted as its own control. In 8 newborn rabbits (group 1), a bolus injection of 5 nmol.kg-1 of endothelin caused a marked increase in mean blood pressure and renal vascular resistance leading to a significant fall in glomerular filtration rate (-12 +/- 4%) and renal blood flow (-16 +/- 3%). A second group of animals (n = 8) confirmed the neutralizing activity of the endothelin-1 antiserum in vivo. In spite of pretreatment with endothelin-1 antiserum, hypoxemia induced an increase in renal vascular resistance (+40 +/- 18%; p < 0.05) associated with a significant fall in glomerular filtration rate (-18 +/- 7%) and renal blood flow (-29 +/- 6%) in 8 newborn rabbits (group 3). The present results suggest that endothelin-1 does not mediate the hypoxemia-induced renal changes.

Animals↗

PubMed1996

Nitric oxide modulates glomerular filtration and renal blood flow of the newborn rabbit.

The current study was performed in 17 anesthetized and mechanically ventilated newborn rabbits to investigate the role of nitric oxide (NO) in the regulation of basal renal function of the immature kidney. Renal blood flow and glomerular filtration rate were determined by the clearance of p-aminohippuric acid and inulin, respectively. In 9 newborn rabbits (group 1), L-NAME, a NO synthesis inhibitor, significantly increased the renal vascular resistance by 31 +/- 9% and decreased the renal blood flow by 20 +/- 6%. The fraction of filtration significantly increased by 8 +/- 5% despite a delayed decline in glomerular filtration rate by 13 +/- 5%. Mean arterial pressure and heart rate were not altered. In 8 additional newborn rabbits (group 2), L-arginine, the physiological precursor of NO synthesis, partially reversed the renal hemodynamic changes induced by L-NAME. The present results demonstrate that the decrease in NO production induced by L-NAME (1) significantly affects the renal microcirculation of the immature newborn rabbit kidney and (2) predominantly increases the postglomerular renal vascular resistance. Endogenous NO thus appears to play a major role in maintaining the basal perfusion of the immature kidney.

Animals↗

PubMed1984

Urinary kallikrein excretion in patients with primary aldosteronism: differentiation of adrenal adenoma from idiopathic adrenal hyperplasia.

Following 7 days on a low sodium diet, a regular sodium diet or a high sodium diet each, urine samples were collected from 37 subjects in the final days of each sodium treatment. Urinary kallikrein excretion was determined in 9 patients with primary aldosteronism, 15 normal subjects and 13 patients with essential hypertension. Urinary aldosterone excretion, plasma renin activity (PRA), urinary sodium excretion, urinary potassium excretion and p-aminohippuric acid clearance were also determined on the same days. Levels of urinary kallikrein excretion in patients with primary aldosteronism due to aldosterone-producing adenoma (APA) were greater (p less than 0.05 to p less than 0.001) than those in patients with primary aldosteronism due to idiopathic adrenal hyperplasia (IHA) under any sodium diet. Other examined variables were of limited value in differentiating patients with APA from those with IHA. Urinary kallikrein excretion, urinary excretion of electrolyte, urinary aldosterone excretion, PRA and PAH clearance were similar in normal subjects and patients with essential hypertension. It appears reasonable to conclude from these data that urinary kallikrein does not play an important role in the pathogenesis of essential hypertension, and elevated urinary kallikrein excretion in patients with primary aldosteronism due to APA can be used for biochemical differentiation from those with IHA.

Adenoma↗

PubMed1977

The kidney in obstructive uropathy.

Explore the source record for details and available documents.

Acids↗

PubMed2006

Rapid nongenomic effects of aldosterone on the renal vasculature in humans.

There is increasing evidence for the importance of rapid nongenomic effects of aldosterone on the human vasculature. In vitro animal experiments in renal arterioles also suggest the presence of such effects on the renal vasculature. We conducted a clinical study to explore these effects in vivo in humans. Thirteen healthy male volunteers were examined. Aldosterone (500 microg) or placebo was injected intravenously with or without coinfusion of N(G) monomethyl-L-arginine (L-NMMA) in a randomized, double-blinded 4-fold crossover design. Renal plasma flow and glomerular filtration rate were measured by constant infusion clearance technique using inulin and para-aminohippuric acid. Injection of aldosterone without concomitant infusion of L-NMMA changed the renal plasma flow and glomerular filtration rate not statistically significant compared with placebo. Coinfusion of L-NMMA unmasked the effect of aldosterone: aldosterone with L-NMMA decreased the glomerular filtration rate slightly (-1.4+/-6.2 mL/min), whereas infusion of L-NMMA alone increased the glomerular filtration rate (8.3+/-9.8 mL/min; P=0.004). L-NMMA alone decreased renal plasma flow by 58.2+/-97.5 mL/min, and aldosterone with L-NMMA decreased renal plasma flow by 190.0+/-213.7 mL/min (P=0.074). Accordingly, Aldosterone with L-NMMA increased renal vascular resistance much more than L-NMMA alone (1588+/-237 versus 614+/-240 dynxsxcm(-5); P=0.014). These data indicate that aldosterone acts via rapid nongenomic effects in vivo in humans at the renal vasculature. Antagonizing the endothelial NO synthase unmasks these effects. Therefore, rapid nongenomic aldosterone effects increase renal vascular resistance and thereby mediate arterial hypertension if endothelial dysfunction is present.

Adult↗

PubMed1988

Abnormal renal responses to calcium entry blockade in normotensive offspring of hypertensive parents.

In nine young normotensive subjects with no family history of hypertension and nine age-matched normotensive subjects with one parent with essential hypertension, effective renal plasma flow (p-aminohippuric acid clearance), glomerular filtration rate (inulin clearance), and excretion of sodium and exogenously administered lithium were measured for 90 minutes before and after administration of a single 20-mg oral dose of the calcium entry blocker nifedipine. Segmental tubular handling of fluid and sodium was estimated using lithium clearance as a marker of proximal tubular reabsorption. Nifedipine did not cause any change in subjects with no family history of hypertension, but in those with one hypertensive parent there was a marked increase in effective renal plasma flow (from 644 +/- 39 to 847 +/- 42 [SEM] ml/min x 1.73 m2; p less than 0.001) and a decrease in filtration fraction (from 17.6 +/- 1.0 to 12.6 +/- 0.4%; p less than 0.001), while the glomerular filtration rate was unchanged, thus suggesting a prevailing efferent vasodilation. Sodium excretion rate (p less than 0.02) and fractional sodium excretion (p less than 0.025) increased slightly but significantly in subjects with one hypertensive parent, but not in normotensive subjects with no family history of hypertension. Lithium clearance also rose (from 29.0 +/- 2.0 to 32.8 +/- 1.9 ml/min, p less than 0.001), and the derived value of fractional proximal reabsorption diminished (from 75.8 +/- 1.0 to 71.3 +/- 1.2%, p less than 0.001). Estimated distal delivery of sodium and absolute distal sodium reabsorption both increased significantly (p less than 0.005), while fractional distal sodium reabsorption was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Accelerated decline in renal perfusion with aging in essential hypertension.

The present cross-sectional study was designed to assess the effect of the severity of hypertensive cardiovascular disease and age on renal hemodynamics. In a homogeneous population of 157 white men (aged 15 to 87 years), we assessed renal and systemic hemodynamics by measuring mean arterial pressure invasively, renal blood flow by 131I-para-aminohippuric acid clearance, and cardiac output by the indocyanine dye dilution technique. Stepwise multiple regression analysis revealed the following independent determinants of renal blood flow: age (beta = -.42, P < .001), height (beta = +.14, P < .03), mean arterial pressure (beta = -.15, P < .02), and cardiac output (beta = +.19, P < .008). Renal blood flow corrected for height correlated inversely with age in all three groups. However, the renal fraction of cardiac output did not correlate with age in borderline hypertension (r = .17, P = NS) and in normotension (r = .12, P = NS), suggesting a parallel decline in renal blood flow and cardiac output with aging. In contrast, in established hypertension, the renal fraction of cardiac output was closely linked to age (r = .52, P < .001) and significantly steeper (P < .01) than in normotension or borderline hypertension. We conclude that unlike in normotensive subjects or patients with borderline hypertension, patients with established hypertension have an accelerated decline in renal perfusion with aging, reflecting selective functional or structural changes or both in the renal vascular bed.

Adolescent↗

PubMed1986

Thromboxane synthesis and blood pressure in spontaneously hypertensive rats.

The present study examines effects of administration of OKY 046, an inhibitor of thromboxane synthesis, for 100 days on systemic blood pressure and renal function in spontaneously hypertensive rats and in normotensive control rats. Untreated spontaneously hypertensive rats had higher values for thromboxane excretion in the urine and higher values for blood pressure than did normotensive control rats. Administration of OKY 046 decreased systolic and mean arterial blood pressure and urinary excretion of thromboxane and protein in spontaneously hypertensive rats. Administration of OKY 046 decreased thromboxane excretion in the urine of normotensive control rats but had no effect on blood pressure or protein excretion. Renal function, as assessed by the clearances of inulin and p-aminohippuric acid, was greater in spontaneously hypertensive rats treated with OKY 046 than in those receiving vehicle alone. In normotensive control rats, OKY 046 administration did not affect renal function. These results suggest that increased renal synthesis of thromboxane may play a role in the pathogenesis of the elevated blood pressure of spontaneously hypertensive rats.

Acrylates↗

PubMed1982

Role of renal nerves, angiotensin II, and prostaglandins in the antinatriuretic response to acute hypercapnic acidosis in the dog.

Although clinical studies suggest that chronic hypercapnic acidosis may be associated with renal sodium retention, little information is available on the effect of acute hypercapnic acidosis on renal sodium excretion. We, therefore, increased PCO2 from 23 to 74 mm Hg in anesthetized dogs and observed a marked antinatriuresis as absolute sodium excretion (235 to 60 muEq/min, P less than 0.001) and fractional excretion of sodium (4.0 to 1.2 %, P less than 0.02) decreased significantly. This decrease in sodium excretion occurred independent of consistent changes in renal perfusion pressure, PO2, glomerular filtration rate, renal blood flow, extraction of P-aminohippuric acid, and filtration fraction. The antinatriuretic response to acute hypercapnic acidosis could be attenuated significantly by surgical renal denervation, intrarenal phenoxybenzamine, and by intrarenal infusion of 1-sarcosine,8-glycine angiotensin II. Administration of 10 mg/kg indomethacin enhanced the antinatriuretic response to hypercapnic acidosis in denervated kidneys. These results suggest that renal alpha-adrenergic nerves and the renal angiotensin system result in an antinatriuretic effect during acute hypercapnic acidosis. Renal prostaglandins or related substances may serve to attenuate this antinatriuretic response.

Acidosis↗

PubMed1971

Quantitative studies of the metabolism of chylomicron triglycerides and cholesterol by liver and extrahepatic tissues of sheep and dogs.

Unanesthetized sheep and dogs, previously fitted with indwelling catheters in the aorta, lower vena cava, mesenteric, portal, left hepatic and jugular veins, were given constant intravenous infusions of lymph in which the chylomicron lipids were variously labeled with (3)H or (14)C. Para-aminohippuric acid was infused into the mesenteric venous catheter for measurement of portal and hepatic venous blood flow. In some animals, alternately labeled free fatty acids bound to albumin were mixed with the lymph to be infused. In both species, chylomicron triglyceride fatty acids were taken up in the region drained by the lower vena cava and portal vein and free fatty acids derived from hydrolysis of these triglycerides were extensively recycled in the blood. Direct uptake of triglyceride fatty acids also occurred in liver and accounted for about 10% of the total triglyceride fatty acids removed from the blood in sheep and 22% in dogs. In sheep, 10% and, in dogs, about 40% of these triglyceride-fatty acids were released into the blood as free fatty acids. The free fatty acids recycled from various regions accounted for a substantial fraction of the chylomicron fat eventually deposited in each tissue. Uptake of chylomicron cholesterol from the blood of sheep occurred primarily in liver and to a small extent in certain tissues drained by the portal vein. The results obtained, together with other available data, demonstrate that chylomicron triglycerides are removed primarily in extrahepatic tissues of both species, while the liver removes cholesterol contained in chylomicron "skeletons" from which most of the triglycerides have been removed. The quantitative differences between transport of chylomicron lipid in sheep and dogs may be related to known differences in the structure of their hepatic sinusoids.

Animals↗

PubMed1975

Structural and functional studies of ligandin, a major renal organic anion-binding protein.

Sephadex gel filtration of the 1000,000 g supernate of homogenates of rat kidney revealed binding of various organic anions (penicillin, Bromsulphalein [BSP], bilirubin, phenolsulfonphthalein [PSP], phlorizin, glutathione [GSH], p-amino hippurate (PAH), probenecid, conjugated bilirubin, and BSP-GSH) to a nonalbumin-containing protein fraction (Y), which precipated on addition of monospecific anti-rat liver ligandin (Y protein)-IgG, but not control IgG. Quantitatively similar organic anion binding was observed in vivo after injection of BSP, BSP-GSH, phlorizin, probenecid, conjugated bilirubin, PAH, or penicillin. The binding protein was purified to apparent homogeneity and is a basic protein (pI 8.9) of 44,000 daltons with two apparently identical subunits of 22,000 daltons. Monospecific antibody was produced against the renal protein. The results of binding studies in vivo and in vitro and phsicochemical, immunologic, structural, and binding site investigations indicate that the renal protein is identical to hepatic ligandin. Immunofluorescent studies utilizing anti-ligandin IgG previously localized ligandin in the kidney to all proximal tubular cells. By quantitative radial immunodiffusion, the concentration of renal ligandin was 31.2 plus or minus 2.2 mug/mg supernatant protein and was increased 160% above basal values by pretreatment of rats with tetrachloro-dibenzo-p-dioxin. Pretreatment with phenobarbital, DDT, or pregnene-16alpha-carbonitrile did not increase renal ligandin concentration but doubled hepatic ligandin concentration. Circular dichroism studies of renal ligandin revealed percent helical structure similar to hepatic ligandin and primary association contrasts were derived for BSP (10-6 M-1) and PAH, probenecid, and penicillin (10-3 M-1). Administration of BSP or probenecid simultaneously with [C14] penicillin resulted in increased plasma retention and reduced kidney and urinary bladder content of [14C] penicillin and a correlation coefficient of -0.8 between total kidney/plasma radioactivity and percent of protein-bound radioactivity bound to ligandin in the kidney. These studies indicate that renal and hepatic ligandin are identical. Their response to drugs and chemicals varies. Competitive binding between several organic anions for ligandin correlated with their renal uptake from plasma, which suggests that ligandin may function in the proximal tubular cell as a component of the renal organic anion transport system.

Amino Acids↗

PubMed1987

Renal effects of theophylline and caffeine in newborn rabbits.

Renal hemodynamics and functions were assessed in four groups of anaesthetized newborn rabbits receiving a single intravenous dose of methylxanthines, i.e.: aminophylline: 3 mg/kg (A1) or 6 mg/kg (A2); sodium benzoate caffeine: 5 mg/kg (C1) or 10 mg/kg (C2). Each animal acted as its own control. The mean PAH extraction ratio was not modified by the methylxanthines. Renal blood flow and glomerular filtration rate were determined by clearances of para-aminohippuric acid and inulin, respectively. No changes in renal hemodynamics or renal functions were observed in group C1. In group C2, renal blood flow and filtration fraction did not vary significantly but renal vascular resistance showed a delayed increase. Systemic infusion of the two aminophylline regimens induced a delayed increase in renal vascular resistance with a concomitant fall in renal blood flow and an increase of filtration fraction in group A2. Glomerular filtration rate was either reduced (3 mg/kg aminophylline) or increased (6 mg/kg aminophylline and 10 mg/kg caffeine). Moreover, diuresis increased and tubular water reabsorption declined in groups A1, A2, and C2. High dose caffeine enhanced sodium fractional excretion. The acute renal effects of methylxanthines appeared dose- and time-related in immature animals and caffeine proved safer than aminophylline at doses used in human neonates.

Animals↗