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PubMed1993

Effects of endothelin on renal function in newborn rabbits.

The renal effects of endothelin-1 were investigated in 16 anesthetized and mechanically ventilated newborn rabbits. Renal blood flow and glomerular filtration rate were determined by the clearance of para-aminohippuric acid and inulin, respectively. Each animal acted as its own control. In eight newborn rabbits, a bolus injection of 5 nmol.kg-1 of endothelin-1 caused an initial fall in mean arterial blood pressure followed by a gradual, significant increase in mean arterial blood pressure that lasted for 45 min. The dramatic increase in renal vascular resistance (+28 +/- 4%) induced by endothelin led to a fall in glomerular filtration rate (-12 +/- 4%) and renal blood flow (-16 +/- 3%). In spite of the reduction of glomerular filtration rate and renal blood flow, urine flow and sodium excretion rates increased significantly (+20 +/- 5% and +49 +/- 9%, respectively). In eight additional newborn rabbits, a bolus injection of 1 nmol.kg-1 of endothelin--a dose that usually induces marked renal and systemic vasoconstriction in adult models--did not affect systemic or renal hemodynamics. In conclusion, endothelin induces renal and systemic vasoconstriction and affects water and sodium homeostasis during the neonatal period. These effects occur under higher doses than those used in adult animals. This age difference in systemic and renal responsiveness is probably mediated by receptor immaturity and/or interference of high levels of counteracting hormones present during the neonatal period.

Animals↗

PubMed1977

Renal extraction of endogenous gastrin in patients with normal renal function.

Renal extraction of gastrin in patients with normal clearance of inulin and p-aminohippuric acid was assessed by gastrin radioimmunoassay. In 23 fasting patients there was no significant difference in arterial gastrin (37.7 pg/ml serum +/- 25.1 S.D.) and the renal vein gastrin (35.9 +/- 24.6), resulting in a renal extraction ratio for gastrin not significantly different from zero (p greater than 0.5). The results in three patients indicated no extraction of gastrin for two consecutive periods after a protein-rich meal.

Brachial Artery↗

PubMed1996

Role of nitric oxide in the hypoxemia-induced renal dysfunction of the newborn rabbit.

The current study was performed in 30 anesthetized and mechanically ventilated newborn rabbits to investigate the role of the endothelium-derived relaxing factor nitric oxide (NO) in the renal vasoconstriction observed during hypoxemia. Renal blood flow (RBF) and GFR were determined by the clearance of p-aminohippuric acid and inulin, respectively. In nine newborn rabbits (group 1), acute hypoxemia induced a significant decrease in RBF (-17 +/- 7%) and GFR (-11 +/- 6%). A second group of nine animals was used to determine the role of NO in regulating renal hemodynamics of the immature kidney in physiologic conditions. N omega-Nitro-L-arginine methyl ester (L-NAME), a NO synthesis inhibitor, significantly increased the renal vascular resistance by 31 +/- 9% and decreased RBF and GFR (-20 +/- 6% and -13 +/- 5%, respectively). Acute hypoxemia was induced in 12 additional newborn rabbits during L-NAME infusion (group 3) to define the role of NO in the renal vasoconstriction observed during hypoxemia. The changes in renal hemodynamics were greater in this group than in those induced by hypoxemia alone. The present results suggest that: 1) endogenous NO has a crucial role in maintaining basal renal perfusion, 2) the activity of NO synthase is maintained during acute hypoxemia, and 3) NO could blunt the effects of acute hypoxemia in the immature newborn rabbit kidney.

Animals↗

PubMed1999

Protective effect of perindoprilat in the hypoxemia-induced renal dysfunction in the newborn rabbit.

The renal effects of acute hypoxemia and the ability of perindoprilat, a potent angiotensin-converting enzyme inhibitor, to prevent these effects were assessed in 31 anesthetized and mechanically ventilated newborn (5 to 8 d of age) rabbits. Renal blood flow (RBF) and GFR were determined by the clearances of para-aminohippuric acid and inulin, respectively. Each animal acted as its own control. In eight normoxemic rabbits (group 1), the i.v. infusion of saline did not change renal and hemodynamic functions. In eight additional rabbits, acute hypoxemia (PaO2= 40 mm Hg) induced a significant decrease in mean blood pressure (-8+/-2%), RBF (-36+/-3%), and GFR (-31+/-3%) and an increase in renal vascular resistance (+50+/-12%). A third group of newborn animals (n=7) was used to determine the renal effects of perindoprilat administration (20 microg/kg) under normoxemic conditions. RBF significantly increased (+15+/-2%) and renal vascular resistance significantly decreased (-15+/-3%), whereas GFR, mean blood pressure, and filtration fraction did not change significantly. In group 4 (n=7), perindoprilat infusion completely prevented the hypoxemia-induced alterations in GFR and renal vascular resistance and partially prevented the fall in RBF. These results demonstrate that angiotensin II modulates the renal immature microcirculation and that inhibition of its formation effectively prevents the hypoxemia-induced decrease in GFR.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2002

The effects of losartan on renal function in the newborn rabbit.

The low GFR of newborns is maintained by various factors including the renin-angiotensin system. We previously established the importance of angiotensin II in the newborn kidney, using the angiotensin-converting enzyme inhibitor perindoprilat. The present study was designed to complement these observations by evaluating the role of angiotensin-type 1 (AT(1)) receptors, using losartan, a specific AT(1)-receptor blocker. Increasing doses of losartan were infused into anesthetized, ventilated, newborn rabbits. Renal function and hemodynamic variables were assessed using inulin and para-aminohippuric acid clearances as markers of GFR and renal plasma flow, respectively. Losartan 0.1 mg/kg slightly decreased mean blood pressure (-11%) and increased diuresis (+22%). These changes can be explained by inhibition of the AT(1)-mediated vasoconstrictive and antidiuretic effects of angiotensin, and activation of vasodilating and diuretic AT(2) receptors widely expressed in the neonatal period. GFR and renal blood flow were not modified. Losartan 0.3 mg/kg decreased mean blood pressure significantly (-15%), probably by inhibiting systemic AT(1) receptors. GFR significantly decreased (-25%), whereas renal blood flow remained stable. The decrease in filtration fraction (-21%) indicates predominant efferent vasodilation. At 3 mg/kg, the systemic hypotensive effect of losartan was marked (mean blood pressure, -28%), with decreased GFR and renal blood flow (-57% and -51%, respectively), a stable filtration fraction, and an increase in renal vascular resistance by 124%. The renal response to this dose can be considered as reflex vasoconstriction of afferent and efferent arterioles, rather than specific receptor antagonism. We conclude that under physiologic conditions, the renin-angiotensin is critically involved in the maintenance of GFR in the immature kidney.

Angiotensin Receptor Antagonists↗

PubMed2003

Nimesulide, a cyclooxygenase-2 preferential inhibitor, impairs renal function in the newborn rabbit.

Tocolysis with nonsteroidal anti-inflammatory drugs (NSAIDs) has been widely accepted for several years. Recently, the use of the cyclooxygenase-2 (COX2) preferential NSAID nimesulide has been proposed. However, data reporting neonatal acute renal failure or irreversible end-stage renal failure after maternal ingestion of nimesulide question the safety of this drug for the fetus and the neonate. Therefore, this study was designed to define the renal effects of nimesulide in newborn rabbits. Experiments were performed in 28 newborn rabbits. Renal function and hemodynamic parameters were measured using inulin and para-aminohippuric acid clearances as markers of GFR and renal blood flow, respectively. After a control period, nimesulide 2, 20, or 200 microg/kg was given as an i.v. bolus, followed by a 0.05, 0.5, or 5 microg.kg(-1).min(-1) infusion. Nimesulide administration induced a significant dose-dependent increase in renal vascular resistance (29, 37, and 92%, respectively), with a concomitant decrease in diuresis (-5, -23, and -44%), GFR (-12, -23, and -47%), and renal blood flow (-23, -23, and -48%). These results are in contrast with recent reports claiming that selective COX2 inhibition could be safer for the kidney than nonselective NSAIDs. These experiments confirm that prostaglandins, by maintaining renal vasodilation, play a key role in the delicate balance regulating neonatal GFR. We conclude that COX2-selective/preferential inhibitors thus should be prescribed with the same caution as nonselective NSAIDs during pregnancy and in the neonatal period.

Animals↗

PubMed2004

Thyroid function and blood pressure homeostasis in euthyroid subjects.

Overt and subclinical hypothyroidism are associated with increased systemic vascular resistance and hypertension. We examined the relationship between thyroid function and blood pressure homeostasis in euthyroid individuals. A total of 284 subjects (68% hypertensive) consumed high- (200 mmol) and low- (10 mmol) sodium diets, and their blood pressure responses were assessed as percentage change in the mean arterial pressure (MAP). p-Aminohippuric acid clearance was used to estimate effective renal plasma flow. Renal vascular resistance (RVR) was calculated as MAP divided by effective renal plasma flow. Serum free T(4) index (FTI) was lower (P < 0.0001) and TSH was higher (P = 0.046) in hypertensive compared with normotensive subjects independent of other baseline characteristics. FTI (beta = -1.51, P < 0.0001), baseline MAP, and race independently predicted MAP salt sensitivity. The FTI relationship with salt sensitivity adjusted for baseline MAP and race was similar among normotensive (beta = -1.42, P = 0.008) and hypertensive subjects (beta = -1.66, P = 0.0001). FTI correlated negatively with high- (P = 0.0001) and low- (P = 0.008) salt RVR, whereas TSH correlated positively with high- (P = 0.016) and low- (P = 0.012) salt RVR independent of age, gender, race, and body mass index. We have found that FTI is lower and TSH is higher in hypertensive compared with normotensive euthyroid subjects and that FTI independently predicts blood pressure salt sensitivity. These data show that the influence of thyroid function on blood pressure homeostasis extends into euthyroid range and likely reflects the action of thyroid hormone on peripheral vasculature.

Adult↗

PubMed1994

Contrasting effects of vecuronium and succinylcholine on the renal microcirculation in rodents.

We assessed the effects of succinylcholine and vecuronium on renal function and on the renal microcirculation in a rodent model. Vecuronium (0.02 mg/kg followed by 0.2 mg.kg-1 x h-1) caused a significant decrease of 16.1% +/- 3.87% in inulin clearance from 0.92 +/- 0.07 to 0.71 +/- 0.05 mL.min-1 x gKW-1 (gram of kidney weight), and a decrease in para-aminohippuric acid clearance by 21.6% +/- 4.69% from 1.58 +/- 0.26 to 1.31 +/- 0.20 mL.min-1 x gKW-1 (P < 0.05), whereas succinylcholine (0.45 mg/kg followed by 2 mg.kg-1 x h-1) altered neither. The effect of these muscle relaxants was also determined on the renal microcirculation in separate experiments using videomicroscopy. Succinylcholine (n = 10; 10(-10) to 10(-6) M) and its parent compound, acetylcholine (n = 10, 10(-10) to 10(-6) M) used as a control, caused a significant vasodilation from baseline diameter in the interlobular, afferent, and efferent arterioles. The vasodilation caused by succinylcholine was significantly less than that observed with acetylcholine. Atropine blocked the response to succinylcholine, indicating the latter has a muscarinic effect. In contrast, vecuronium caused a significant, selective vasoconstriction from baseline diameter in the preglomerular vessels, but not in the postglomerular vessels. The vasoconstriction caused by vecuronium was significantly different than the vasodilation caused by succinylcholine. The preglomerular vasoconstriction observed with vecuronium may contribute to the decrease in renal plasma flow and glomerular filtration rate observed experimentally. The choice of a neuromuscular blocking drug can therefore have the potential to influence renal function by altering the renal microcirculation.

Animals↗

PubMed2005

Specificity of the fluorescein transport process in Malpighian tubules of the cricket Acheta domesticus.

We demonstrate the presence of an efficient, multispecific transport system for excretion of organic anions in the Malpighian tubules of the cricket Acheta domesticus using fluorescein (FL) as a model substrate. Malpighian tubules rapidly accumulated FL via a high affinity process (Km = 7.75 micromol l(-1)); uptake was completely eliminated by the prototypical organic anion transport inhibitor probenecid (1 mmol l(-1)), but not by p-aminohippuric acid (3 mmol l(-1)). FL uptake was inhibited by monocarboxylic acids at a high concentration (3 mmol l(-1)), and inhibition was more effective with an increase in the carbon chain of the monocarboxylic acid (37% inhibition by 5-carbon valeric acid, and 89% inhibition by 7-carbon caprylic acid). Likewise, tests using a series of aliphatic glutathione conjugates indicated that only the compound with the longest side-chain (decyl-glutathione) significantly inhibited FL uptake (81% inhibition). FL uptake was inhibited by a number of xenobiotics, including a plant alkaloid (quinine), herbicides (2,4-dichlorophenoxyacetic acid and 4-(2,4-dichlorophenoxy)-butyric acid), and the insecticide metabolites malathion monocarboxylic acid (MMA) and 3-phenoxybenzoic acid (PBA), suggesting that this transport system plays an active role in excretion of xenobiotics from Acheta by Malpighian tubules. HPLC quantification of MMA and PBA accumulation into Malpighian tubules verified that MMA accumulation was via a mediated transport process, but suggested that PBA accumulation was by nonspecific binding. The presence of a transport system in Malpighian tubules that handles at least one pesticide metabolite (MMA) suggests that transport processes could be a mechanism conferring resistance to xenobiotic exposure in insects.

Animals↗

PubMed1989

The effects of dietary phosphorus and parathyroid hormone (PTH) infusion rates on the avian phosphaturic response to PTH.

Experiments were performed to evaluate the effects of dietary available phosphorus (aP) and PTH infusion rates on avian urinary inorganic phosphate (Pi) excretion. In experiment I, female domestic fowl were fed diets containing low (0.45%) or high (0.83%) aP for 2-4 weeks prior to renal function studies. Pi excretion was significantly higher for birds fed the high-aP diet than for birds fed the low-aP diet. PTH was infused (60-240 units kg body mass-1 h-1) unilaterally into the renal portal system. Para-aminohippuric acid (PAH), included in the unilateral infusate as a marker for effective renal portal perfusion, indicated that PTH must have been delivered to the peritubular surfaces of the infused kidney. However, bilateral but not unilateral phosphaturia occurred, and there were no significant differences in the phosphaturic responses to PTH when low- and high-aP diet treatment groups were compared. In experiment II, PTH was infused at rates of 1-5 units h-1. Infusing PTH at 5 units h-1 caused a unilateral increase in urine flow but the phosphaturic response was still bilateral. It appears unlikely that unilateral renal portal PTH infusions can be used to trigger unilateral phosphaturia in domestic fowl.

Animals↗

PubMed1999

Fluid secretion by isolated Malpighian tubules of Drosophila melanogaster Meig.: effects of organic anions, quinacrine and a diuretic factor found in the secreted fluid.

Para-aminohippuric acid (PAH, 0.2 and 1 mmol l(-)(1)) had no effect on the basal fluid secretion rate (FSR) of isolated Malpighian tubules of Drosophila melanogaster Meig. and did not affect stimulation of the FSR induced by adenosine 3',5'-monophosphate (cAMP). Phenol Red (phenolsulphonphthalein, PSP; 0.5 and 1 mmol l(-)(1)) slowed the FSR and abolished stimulation of the FSR by cAMP. Diodrast (1 mmol l(-)(1)) slightly, but significantly, reduced the FSR and greatly reduced the stimulation of the FSR normally provoked by cAMP and by the 3',5'-monophosphates of guanosine (cGMP), inosine (cIMP) and uridine (cUMP). However, stimulation of the FSR by the 3', 5'-monophosphate of cytidine (cCMP) was little affected by diodrast. Probenecid (0.2 or 1 mmol l(-)(1)) consistently stimulated the FSR, on average by approximately 25 %, but did not markedly inhibit the subsequent stimulation of the FSR by cAMP, cGMP or cIMP. However, the FSR of tubules stimulated by cGMP was temporarily lowered by probenecid. Quinacrine (0.1 mmol l(-)(1)) slowed basal FSR by an average of approximately 30 %, but subsequent stimulation of the FSR by cAMP was not noticeably affected. Both 0.1 mmol l(-)(1) cAMP and 1 mmol l(-)(1) probenecid stimulated adenylate cyclase activity in extracts of Malpighian tubules, but cIMP, cGMP, cUMP and diodrast were without effect in this regard. Uptake of radioactivity from a solution containing 500 nmol l(-)(1) [(3)H]cAMP and 9.5 micromol l(-)(1) cAMP was reduced by more than 90 % by 1 mmol l(-)(1) PSP, by approximately 40 % by 0.2 mmol l(-)(1) probenecid, by 36 % by 1 mmol l(-)(1) diodrast and by 30 % by 1 mmol l(-)(1) PAH. Neither 0.01 mmol l(-)(1) ouabain nor 0.1 mmol l(-)(1) quinacrine affected the uptake of [(3)H]cAMP by the Malpighian tubules. Fluid secreted by isolated Malpighian tubules of Drosophila melanogaster contains a factor that stimulated the FSR on average by approximately 50 %. The presence in the secreted fluid of cGMP at a concentration of 8.3 micromol l(-)(1) did not explain the stimulatory effect on FSR. These results support the existence of a carrier-mediated uptake of cyclic nucleotides into the Malpighian tubules of Drosophila melanogaster, possibly involving a multispecific transporter.

Adenylyl Cyclases↗

PubMed1990

Effect of N-benzyl-D-glucamine dithiocarbamate on renal toxicity of inorganic mercury in rats.

The effect of N-benzyl-D-glucamine dithiocarbamate (BGD) on the renal toxicity of inorganic mercury in rats was studied. Rats were injected i.v. with saline or HgCl2 (300 micrograms Hg/kg) and 30 min later they were injected i.p. with saline or BGD (2778 mumol/kg, a quarter of an LD50). Urinary excretion of gamma-glutamyl-transpeptidase (gamma-GTP), which is a brush border enzyme, in rats after mercury treatment significantly increased compared to that of the control in the 12-24 h urine specimen and reached a maximum value within 24 h after the treatment. Urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG), which is a lysosomal enzyme, also significantly increased after mercury treatment compared to that of the control in the 12-24 h urine specimen and reached a maximum value within 48 h after the treatment. A change in urinary aspartate aminotransferase (AST) activity after mercury treatment followed a pattern similar to that observed with the urinary NAG. BGD treatment did not increase the urinary excretions of gamma-GTP, NAG, and AST. The uptake of p-aminohippuric acid (PAH) by renal cortical slices significantly decreased 24 h after mercury treatment. BGD injection after mercury treatment did not decrease the uptake of PAH by cortical slices. In addition, the microscopic examination of renal tissue from mercury-treated rats revealed necrosis of the proximal tubular cells. However, a photomicrograph of rat renal cortex after BGD treatment showed little abnormality. These results indicated that the mercury-induced renal damage was protected by the injection of BGD 30 min after mercury treatment.

Animals↗

PubMed1994

Effects of benidipine on renal function in anesthetized spontaneously hypertensive rats.

Effects of benidipine on urine volume, excretion of electrolytes and renal hemodynamics were investigated in anesthetized spontaneously hypertensive rats (SHR). Benidipine at 3 and 10 micrograms/kg (i.v.) significantly increased urine volume, sodium (Na) and potassium (K) excretion with no change of creatinine clearance (CCRE). The increase in K excretion was relatively slight when compared with that in Na excretion. In another series of experiments, the tubular sites of action of benidipine were determined by the lithium clearance (CLi) technique and the stop-flow method. Benidipine at 3 micrograms/kg (i.v.) increased CLi, decreased creatinine concentration and increased Na concentration in the stop-flow urine from the distal nephron. These results suggest that benidipine produces diuresis and natriuresis by the inhibition of water and Na reabsorption at both the proximal tubule and the distal nephron. Benidipine increased p-aminohippuric acid clearance, but not CCRE, at doses of 3 and 10 micrograms/kg (i.v.), suggesting that benidipine dilates the glomerular efferent arteriole as well as the afferent arteriole. It is, therefore, expected that benidipine does not cause intraglomerular hypertension and has a beneficial effect in progressive renal disease.

Anesthesia↗

PubMed1999

The contribution of nitric oxide to diuretic and natriuretic effects of renal kinins in normotensive rats.

We have reported that diuresis and natriuresis due to increase in renal kinins induced by the neutral endopeptidase 24.11 (NEP) inhibitor were attenuated by nitric oxide (NO) synthase inhibitor. To further clarify the water-sodium excretory mechanism of renal kinins, we estimated NO2+NO3 (NOx) and cGMP in plasma and urine with and without a specific NEP inhibitor, thiorphan. P-aminohippuric acid (PAH) and inulin were injected into male Sprague-Dawley rats. Vehicle (n = 8) or thiorphan (30 mg/kg, n = 10) was injected after the control period. Mean blood pressure (MBP), plasma and urinary PAH, inulin, NOx and cGMP, urinary volume (UV) and urinary sodium excretion (UNaV) were measured before and after injection of the reagents. MBP, renal plasma flow and glomerular filtration rate were not affected by thiorphan. Plasma NOx and cGMP with thiorphan did not differ from the vehicle, while urinary NOx and cGMP increased. None of the variables were affected by vehicle. UV and UNaV were higher with thiorphan than with vehicle. Positive correlation was found between urinary deltaNOx and deltacGMP. Each urinary deltaNOx and deltacGMP was significantly correlated to both deltaUV and deltaUNaV. Urinary NOx and cGMP were increased while maintaining correlations to UV and UNaV, but plasma NOx and cGMP were not affected by thiorphan. This implies that the mechanism of water-sodium excretion induced by NEP inhibitor is mediated by renal NO. Therefore, renal NO may contribute to the diuretic and natriuretic effects of renal kinins.

Animals↗

PubMed1987

Dopamine affects angiotensin II-induced steroidogenesis by altering clearance of the peptide in man.

Infusion of dopamine is reported to reduce the response of aldosterone to infused angiotensin II in sodium-deplete but not sodium-replete man. Six normal male subjects were infused with angiotensin II in graded doses (2, 4 and 8 ng/kg per min) with or without dopamine (1.0 microgram/kg per min) during both dietary sodium repletion and depletion. The responses of both aldosterone and 18-hydroxycorticosterone to infusion of angiotensin II appeared to be reduced by dopamine in sodium-deplete, but not sodium-replete, subjects. However, when the relationships between plasma concentrations of angiotensin II and corticosteroid were examined it was evident that plasma concentrations of angiotensin II were lower when dopamine was infused concurrently with the peptide (P less than 0.05). In a second study, six sodium-deplete males were infused with angiotensin II at a constant rate (6 ng/kg per min) while dopamine (or placebo) was given in graded doses (0.5, 1 and 5 micrograms/kg per min). Renal plasma flow was estimated from total body clearance of para-aminohippuric acid. Overall, angiotensin II concentrations were lower during dopamine infusion compared with those during infusion of placebo (63.2 +/- 9.7 (S.E.M.) vs 92.3 +/- 6.4 pmol/l; P less than 0.01) and this was associated with a 40% increase in effective renal plasma flow (627 +/- 68 vs 451 +/- 15 ml/min; P less than 0.05); there again appeared to be a reduced aldosterone response during combined angiotensin II/dopamine infusion compared with that during infusion of angiotensin II alone (1003 +/- 404 vs 1225 +/- 146 pmol/l; 0.05 less than P less than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)

18-Hydroxycorticosterone↗

PubMed1994

Net uptakes of oestradiol-17 beta and progesterone across the portal-drained viscera and the liver of ewes.

The objective of this study was to determine whether circulating concentrations or prior exposure to estradiol-17 beta (OE2) and progesterone affected their uptake by splanchnic tissues. Catheters were surgically placed in the portal vein, a branch of the hepatic vein, a mesenteric vein and the abdominal aorta of three multiparous ovariectomized Dorset ewes. Blood and plasma flow across the portal-drained viscera (PDV) and the liver, and net uptake of OE2 and O2 consumption in these same tissues were determined in ovariectomized ewes (control), during OE2 infusion into the jugular vein, 7 days after an OE2 implant had been given, and during OE2 infusion into the jugular vein 7 days after an OE2 implant. The above treatments were repeated for progesterone. Plasma flows across visceral organs were determined by marker dilution (para-aminohippuric acid), and OE2 and progesterone concentrations were determined by radioimmunoassay. During the infusion with OE2, OE2 arterial concentration (mean +/- S.D.) was 346 +/- 199 pg/ml, PDV net uptake was 9.7 +/- 5.6 micrograms OE2/h and hepatic net uptake was 15.5 +/- 9.5 micrograms OE2/h. Hepatic uptake was 82% of the jugular OE2 infusion rate. Blood flow and oxygen consumption by hepatic tissue increased when ewes were exposed to an OE2 implant for 7 days. During the infusion with progesterone, progesterone arterial concentration (mean +/- S.D.) was 8.8 +/- 3.4 ng/ml, PDV net uptake was 220 +/- 118 micrograms progesterone/h and hepatic net uptake was 238 +/- 52 micrograms progesterone/h. Hepatic net uptake was 23% of the progesterone jugular infusion rate.

Animals↗

PubMed1995

How should renal hemodynamic data be indexed in obesity?

Clearance data are customarily indexed to body surface area of 1.73 m2. This study examined whether this standard procedure gives correct values for renal perfusion in obese subjects. In 215 subjects who varied in age, gender, height, weight, obesity, and mean arterial blood pressure, RPF was determined by measuring the clearance of (131I)para-aminohippuric acid. Multiple regression analysis of the whole study group revealed that age (beta = -0.44, P < 0.001), height (beta = +0.25, P < 0.01), and arterial blood pressure (beta = -0.19, P < 0.01) were independent predictors of RPF, but that weight or body mass index was not. When related to body surface area, RPF appeared to decline with increasing obesity as follows: normal weight, 609 +/- 153 mL/min per 1.73 m2; overweight, 572 +/- 149 mL/min per 1.73 m2; severely overweight, 530 +/- 145 mL/min per 1.73 m2 (P < 0.012). In contrast, RPF related to height reflected a pattern concordant with the multiple regression analysis: normal weight, 3.76 +/- 0.9 mL/min per meter; overweight, 3.86 +/- 1.0 mL/min per meter; and severely overweight, 3.86 +/- 1.0 mL/min per meter (not significant). A separate repetition of the whole analysis for both normotensive (N = 55) and hypertensive subjects (N = 160) revealed a result similar to that found for the whole group. Thus, our results show that obesity was not a determinant of RPF, and when related to body surface area, inappropriately low values of RPF were calculated for obese patients. It was concluded that RPF values correlate with height and not with surface area in obese subjects.

Adolescent↗

PubMed1996

Renal findings in patients with short-term type 2 diabetes.

Under semiambulatory conditions, 85 consecutive patients with the diagnosis of Type 2 diabetes of short duration (excluding patients with islet cell antibodies or maturity onset diabetes of the young) were admitted to a self-control training program and were examined in this study. A comprehensive renal assessment was performed, including evaluation of albumin excretion rate (AER), renal hemodynamics, blood pressure (BP) profile, and indicators of genetic risk. AER > or = 30 mg/24 h was found in 13 (15%) of patients; in two of these patients, AER was > or = 300 mg/24 h. By logistic regression, high HbA1, current smoking, and BP parameters were significantly correlated with an increased risk of microalbuminuria (MA). In a multiple linear regression model, accounting for 57% of total variance, HbA1, ERPF, and current smoking were significantly correlated with AER. Median GFR (Cin(inulin clearance) 136 mL/min per 1.73m2; range, 94 to 194) and ERPF (Cpah(para-aminohippuric acid clearance) 733; range, 451 to 1328) were significantly higher in patients than in control subjects (upper 95th percentile, 131 and 706 mL/min per 1.73m2, respectively). In a multiple linear regression model, explaining 27% of total variance, age, AER, gender, and fasting blood glucose were significantly correlated to GFR. According to the criteria of average daytime BP > or = 135/85 mm Hg or 24-h BP > or = 130/80 mm Hg, 60% of patients were hypertensive (HT). Sixty-one percent of all patients (including 50% of the untreated normotensive patients) were "nondippers", i.e., < 15% nighttime decrease of mean arterial pressure. Either HT or nondipping was found in 79% of all patients, so that only 21% had a completely normal blood pressure profile. Ninety-four percent of untreated hypertensive patients had no MA. First-degree relatives of patients with MA compared with patients without MA had more frequent cardiovascular events (69% versus 31%). The risk of MA in diabetic patients with positive family history was amplified by poor glycemic control. MA, but not hypertension, was marginally related to K(m) of Na+/Li+ countertransport. It was concluded that (1) microalbuminuria is found in 15% of patients newly presenting with Type 2 diabetes; (2) a high proportion of patients exhibit hyperfiltration; (3) according to ambulatory BP only, 21% of patients have a completely normal circadian BP profile; (4) a family history of cardiovascular events interacts with glycemic control to increase the risk of MA.

Adult↗