Search PubMed⌕ Search

Biomedical subjects

R L Chevalier

Publications and source records attributed to R L Chevalier.

At least 73 records · Page 4Linked to original sources
PubMed1992

Distribution and content of renin and renin mRNA in remnant kidney of adult rat.

To determine whether kidney hypertrophy secondary to reduction of renal mass affects the intrarenal distribution and concentration of renin mRNA and its protein, adult male Sprague-Dawley rats were studied 4 wk after sham operation (Sham, n = 10), uninephrectomy (UNX, n = 14), or five-sixths nephrectomy (5/6 NX, n = 12). Left kidney weight-to-body weight ratio (x10(3)) was higher in 5/6 NX (6.6 +/- 0.2) than in UNX (4.5 +/- 0.2) or Sham (3.8 +/- 0.1) groups (P < 0.001). The percentage of juxtaglomerular apparatuses (%JGA) containing renin was lower in 5/6 NX (32 +/- 5) than in UNX (56 +/- 2, P < 0.001) or Sham (50 +/- 1, P < 0.05) groups. Renal renin mRNA concentrations (pg renin mRNA/microgram total RNA) detected by radiodensitometric renin mRNA dot-blot assay were lower in 5/6 NX (1.8 +/- 0.3) than in UNX (13.2 +/- 1) or Sham (14.2 +/- 1.1, P < 0.001). In situ hybridization histochemistry demonstrated that in all groups of rats renin mRNA was confined to the JGA. However, the hybridization signals (grains/JGA) were less intense in 5/6 NX (211 +/- 24) than in UNX (486 +/- 35) or Sham (541 +/- 40) groups (P < 0.001). Renal renin concentration (ng angiotensin I.mg protein-1.h-1) tended to be lower in 5/6 NX (20 +/- 15) than in UNX (44 +/- 7.8) or Sham (60.8 +/- 10) groups. In addition, plasma renin activity (ng.ml-1.h-1) was lower in 5/6 NX (3.8 +/- 0.6) than in UNX (8.8 +/- 1.8, P < 0.05) or Sham (14.3 +/- 2, P < 0.001) groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Inhibition of ANP clearance receptors and endopeptidase 24.11 in maturing rats.

Systemic clearance of atrial natriuretic peptide (ANP) decreases during postnatal development. To determine the relative contribution of ANP clearance (C) receptors and neutral endopeptidase 24.11 (NEP; EC 3.4.24.11) in regulation of plasma ANP concentration ([ANP]) during maturation, 18- to 60-day-old male Sprague-Dawley rats were anesthetized and infused with rat ANP (35 ng.kg-1.min-1). Infusion of the NEP inhibitor phosphoramidon increased [ANP] and urine guanosine 3',5'-cyclic monophosphate (cGMP) excretion in both weanling and adult rats. Infusion of C-ANP, an analogue that binds C receptors selectively, resulted in a greater rise in [ANP] in preweaned than in adult rats, suggesting a maturational decrease in function of C receptors. Despite the increase in [ANP], however, urine flow, cGMP, and sodium excretion failed to increase in preweaned compared with adult rats. Combined infusion of phosphoramidon and C-ANP resulted in a marked increase in [ANP] and cGMP excretion in weanling and adult rats. These results indicate that both C receptors and NEP modulate plasma [ANP] in the physiological range and that each pathway compensates when the other is inhibited. Age-related differences in the renal response to ANP clearance inhibitors may have important physiological implications in the regulation of sodium balance during development.

Animals↗
PubMed1991

Renal nerves modulate renin gene expression in the developing rat kidney with ureteral obstruction.

Chronic unilateral ureteral obstruction (UUO) in newborn rats activates renin gene expression in the obstructed kidney, and increases renin distribution along afferent glomerular arterioles in both kidneys. To investigate the role of the renal nerves in this response, 2-d-old Sprague-Dawley rats were subjected to UUO or sham operation. Chemical sympathectomy was performed by injection of guanethidine, whereas, control groups received saline vehicle. At 4-5 wk, renal renin distribution was determined by immunocytochemistry, and renin mRNA levels were determined by Northern blot hybridization. Compared to the saline-treated rats with UUO, renin remained localized to the juxtaglomerular region in both kidneys of rats with UUO receiving guanethidine (P less than 0.05). Moreover, renin mRNA levels were eightfold lower in obstructed kidneys of rats receiving guanethidine than in those receiving saline. Additional groups of rats with UUO were subjected to unilateral mechanical renal denervation: renin gene expression in the obstructed kidney was suppressed by ipsilateral but not by contralateral renal denervation. These findings indicate that either chemical or mechanical denervation suppressed the increase in renin gene expression of the neonatal kidney with ipsilateral UUO. We conclude that the renal sympathetic nerves modulate renin gene expression in the developing kidney with chronic UUO.

Animals↗
PubMed1991

Hepatic angiotensinogen gene regulation in the fetal and pregnant rat.

To determine whether expression of the hepatic angiotensinogen (Ao) gene is modulated by 1) ontogeny, 2) pregnancy, 3) glucocorticoids, or 4) triiodothyroxine (T3), time-dated pregnant Wistar-Kyoto rats were studied at different gestational ages (15, 17, and 20 d) without the influence of hormonal treatment or were given a daily intraperitoneal injection of dexamethasone (Dex) or T3 for 5 d (chronic Dex or T3) or a single injection of Dex (acute Dex). Maternal and fetal hepatic Ao mRNA levels were detected by dot and Northern blot analysis by using a full-length rat Ao cDNA. Fetal Ao mRNA levels were lower than in their maternal counterparts and lower than in adult rats of either sex. Maternal hepatic Ao mRNA levels were markedly diminished. mRNA levels were their lowest at 15 d of gestation and increased progressively as gestation advanced, reaching a peak at 20 d of gestation. Chronic Dex treatment resulted in a 190% increase in maternal and a 370% increase in the fetal hepatic Ao mRNA levels. Acute Dex treatment resulted in a 260% increase in maternal hepatic Ao mRNA levels with no change in the fetus. Hepatic Ao mRNA levels increased to the nonpregnant level with acute and chronic Dex treatment. Chronic T3 treatment resulted in a 20% increase in maternal hepatic Ao mRNA levels, without alteration of fetal Ao gene expression. We conclude that 1) the fetal and pregnant state results in a profound decrease in maternal and fetal hepatic Ao gene expression, 2) Ao gene expression is regulated by glucocorticoids in the term fetal and maternal liver, and 3) chronic T3 treatment results in a modest increase in maternal hepatic Ao gene expression.

Angiotensinogen↗
PubMed1990

Acute torsion of a renal transplant: cause of organ loss.

Acute torsion of a renal allograft has not been previously described as a cause of organ loss. We present a case of acute torsion of a transplanted kidney in a patient with prune-belly syndrome which led to renal necrosis, necessitating organ removal.

Humans↗
PubMed1990

Counterbalance in functional adaptation to ureteral obstruction during development.

Renal counterbalance, as described by Hinman in 1923, is the phenomenon of increased function of the intact kidney in proportion to the loss of function resulting from unilateral ureteral obstruction (UUO). In the neonatal guinea pig, chronic partial UUO results in severe vasoconstriction and growth arrest of the ipsilateral kidney. Angiotensin II appears to contribute significantly to the vasoconstriction, and the renin-angiotensin system is also involved in the hemodynamic response of the intact opposite kidney to UUO and to relief of UUO. Immunolocalization of renin following complete UUO in the neonatal rat revealed extension of renin-containing cells along the length of the afferent arteriole in both the obstructed and the intact opposite kidney. The proportion of juxtaglomerular apparatuses with detectable renin and renin messenger ribonucleic acid (mRNA) (identified by in situ hybridization), as well as renal renin content (a measure of active renin), were increased in the obstructed kidney compared with the intact opposite kidney. Chemical sympathectomy by chronic guanethidine administration reduced the total renin mRNA in the obstructed kidney (determined by Northern blot analysis) and prevented the increased renin immunostaining in both kidneys. Thus, renal counterbalance in the developing kidney subjected to UUO is mediated or modulated by the renal nerves and involves marked alterations in gene expression and cellular processing of renin.

Humans↗
PubMed1990

Interrelationship of atrial natriuretic peptide, atrial volume, and renal function in premature infants.

Infants experience dramatic changes in fluid balance during the first few days of life, which provides an opportunity to observe the interrelationships of changing atrial size, atrial natriuretic peptide (ANP) secretion, and renal function during a relatively short period. To study these relationships, we examined nine infant boys (mean birth weight 1180 gm and gestational age 30 weeks) at 20 to 28 hours of age and then at four 24-hour intervals. Measurements included plasma ANP concentration, two-dimensional echocardiographic estimations of left and right atrial volumes, Doppler determination of ductus arteriosus patency, creatinine clearance, urine flow rate, urinary sodium excretion, and cyclic guanosine monophosphate (cGMP) excretion. Plasma ANP concentration was found to decrease with age and to correlate with decreasing size of the right atrium, closure of the ductus arteriosus, urinary cGMP excretion, and sodium excretion. We speculate that elevated plasma ANP values in a preterm neonate reflect an expanded volume state. As volume contraction, reflected by decreasing atrial volume and body weight occurs, ANP levels decrease, which may diminish diuresis. These findings are compatible with a significant role for ANP in volume homeostasis of newborn infants.

Atrial Natriuretic Factor↗
PubMed1990

Special needs of the newborn infant in fluid therapy.

The preterm baby, although less able to tolerate high fluid and solute loads, has a remarkable ability to adapt to a rather broad range of environmental challenges, and thus renal function in the preterm infant should no longer be considered impaired. Lower rather than higher fluid administration is the current trend in neonatal care because it is safer and more physiologic. Although changes in body weight over time provide a good indicator of water balance, determination of plasma and urine electrolytes and tonicity are also essential in the monitoring of fluid therapy in preterm infants.

Body Water↗
PubMed1990

Expression of renin and its mRNA in the adult rat kidney with chronic ureteral obstruction.

Angiotensin II has been implicated in mediating renal vasoconstriction resulting from chronic unilateral ureteral obstruction (UUO) in both mature and developing animals. We have previously shown that chronic neonatal UUO results in increased distribution of renin and its mRNA in the obstructed kidney, as well as of immunoreactive renin in the intact opposite kidney. The present study was designed to evaluate the effects of 24 hours versus 4 weeks of UUO on the distribution of renin mRNA and its protein in the adult rat kidney. Renin was detected by immunocytochemistry using a polyclonal anti-rat renin antibody. Renin mRNA was localized by in situ hybridization to an oligonucleotide complementary to renin mRNA. UUO of 24 hours' or 4 weeks' duration did not alter the distribution of renin and its mRNA in the obstructed kidneys as compared with sham-operated kidneys, although kidneys obstructed for 4 weeks had a significant increase in the percent of renin-containing juxtaglomerular apparatuses (JCA) when compared with the intact opposite kidneys (P less than 0.05). Compensatory hypertrophy was not present in the intact opposite kidneys after 24 hours of UUO and distribution of renin gene expression was not altered at that time. However, 4 weeks following contralateral UUO, the intact kidneys were hypertrophied and showed a decrease in renin gene expression relative to the obstructed and sham-operated kidneys. We conclude that unlike UUO during early development, chronic UUO in the mature animal does not activate renin gene expression nor alter renin distribution in the obstructed kidneys. Renin gene expression is suppressed in the hypertrophied kidney with prolonged contralateral UUO.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Dopamine-1 and dopamine-2 mechanisms in the control of renal function.

Dopamine (DA), a catecholamine produced in the kidney, is a renal vasodilator and natriuretic substance, but its action at dopamine-1 (DA-1), dopamine-2 (DA-2) and alpha- and beta-adrenergic receptors limits its effectiveness as a heuristic tool and pharmacologic agent. We have studied the effects of highly selective DA-1 and DA-2 receptor agonists and antagonists in normal human subjects and experimental animals to determine the precise physiological role of renal dopamine at DA-1 and DA-2 receptors within the kidney. We studied fenoldopam, a selective DA-1 agonist, in normal human subjects in metabolic balances at high (300 mEq/day) and low (10 mEq/day) sodium (Na) intake. Selective DA-1 receptor stimulation during high Na intake resulted in renal vasodilation, natriuresis and diuresis in a sustained manner for 3 hours. The natriuresis was mediated by a reduction in Na reabsorption at both proximal and distal tubular sites. In contrast, during low Na intake, DA-1 receptor stimulation did not engender a natriuretic or diuretic response. Thus, sodium depletion may inhibit the function of renal tubular cells in response to DA-1 stimulation. DA-1 receptors are present in the medial layer of the renal vasculature, proximal tubule and cortical collecting duct; DA-2 receptors are localized to the glomerulus, the renal nerves surrounding renal blood vessels and possibly the renal vascular endothelium. We have performed studies in conscious dogs with indwelling renal arterial catheters to identify the physiological role of renal DA to DA-1 and DA-2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1990

Hematocrit modulates response of ANP to volume expansion in immature rats.

Compared with the adult, the immature kidney responds to acute volume expansion (VE) with reduced diuresis and natriuresis. The underlying mechanisms are poorly understood. Diuresis and natriuresis are blunted despite a lower hematocrit (Hct) in the immature rat, which should enhance the response to VE. The present study was designed to evaluate the role of atrial natriuretic peptide (ANP), its second messenger, guanosine 3',5'-cyclic monophosphate (cGMP), and Hct in the regulation of the renal response to acute saline VE (3% body wt) during postnatal development in rats. Anesthetized Sprague-Dawley rats were studied in the preweaning (group P) or postweaning period (group W). In additional groups, Hct was increased in preweaned rats (group PI) and decreased in postweaned rats (group WD) by isovolemic exchange transfusion before VE. Although control plasma ANP concentration [( ANP]) was not different among the four groups, the increased diuretic and natriuretic response to VE in group W was associated with a greater increase in [ANP] and urinary cGMP excretion (UcGMPV) than in group P (P less than 0.05). Experimental increases in Hct in group PI resulted in greater [ANP] after VE but a reduction in UcGMPV and diuresis (P less than 0.05), whereas decrease in Hct in group WD increased UcGMPV without a significant effect on [ANP], diuresis, or natriuresis. We conclude that ANP may contribute to the increasing renal response to VE with maturation and that Hct modulates ANP release, UcGMPV, and the renal response to VE in postnatal maturation.

Aging↗
PubMed1990

In situ localization of renin and its mRNA in neonatal ureteral obstruction.

Angiotensin II is an important mediator of renal vasoconstriction resulting from chronic unilateral ureteral obstruction (UUO). Distribution of renin mRNA and immunoreactive renin (IR) was examined in kidneys of 1-mo-old Sprague-Dawley rats subjected to either sham operation (n = 21), left complete UUO (n = 21), or right uninephrectomy (UNX, n = 16) at 2 days of age. There were no differences among the three groups in mean arterial pressure or plasma renin activity. Unlike sham kidneys, in which IR was detected in less than 55% of juxtaglomerular apparatuses (JGA) and was confined to a juxtaglomerular location, IR in both kidneys of animals with UUO appeared in greater than 75% of JGA and extended along most of the length of the afferent arteriole (P less than 0.01). In contrast, IR in kidneys of UNX rats was localized to the JGA as in sham-operated animals. Compared with sham-operated kidneys, renal renin content was increased in the obstructed kidneys (P less than 0.01) but decreased in the intact opposite kidneys of UUO rats and in the remaining kidneys of UNX rats (P less than 0.05). Renin mRNA, detected by in situ hybridization histochemistry, was localized to the JGA in kidneys of all groups. However, the fraction of JGA containing detectable renin mRNA was higher in obstructed kidneys than in intact opposite, UNX, or sham kidneys (P less than 0.05). In conclusion, UUO alters intrarenal renin independent of the systemic renin-angiotensin system. The greater distribution of IR, increased renin content, and renin gene expression of kidneys with ipsilateral UUO are consistent with a role for renin-angiotensin in mediating the vasoconstriction resulting from UUO.

Animals↗
PubMed1990

Recruitment of renin gene-expressing cells in adult rat kidneys.

To define whether angiotensin I-converting enzyme (ACE) inhibition affects the distribution of renin gene-expressing cells within the kidney, a control group of adult male Wistar-Kyoto rats (C, n = 7) was compared with a group of rats treated with enalapril (E, n = 6) for 5 days. Renin mRNA distribution was assessed using in situ hybridization to a 35S-labeled 28 mer oligonucleotide complementary to rat renin mRNA. Whereas in control rats renin mRNA was confined to a juxtaglomerular location, in enalapril-treated rats, renin mRNA extended proximally along the length of the afferent arteriole. The percent of visible afferent arteriolar length containing renin mRNA was higher in enalapril-treated (71.7 +/- 2.8%) than in control (49.6 +/- 2.1%) rats (P less than 0.0001). These findings were accompanied by an increase in the percent of juxtaglomerular apparatuses (JGAs) containing renin mRNA (71 +/- 2.2 vs. 49 +/- 2.9%; E vs. C, P less than 0.0001). Also, the intensity of the JGA hybridization signals was higher in enalapril-treated (757 +/- 59 grains/JGA) than in control (167 +/- 11 grains/JGA) rats (P less than 0.00001). We conclude that the increased kidney renin gene expression elicited by ACE inhibition is the result of an increase in renin mRNA content per JGA, an increase in the number of JGAs expressing the renin gene, and a recruitment of renin gene-expressing cells along the afferent arteriole.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Evidence that dopamine-2 mechanisms control renal function.

Dopamine is synthesized by the kidney, and dopamine-2 (DA2) receptors are present in the renal glomerulus. However, no role for DA2 receptors in the kidney has been defined. We investigated the possible role of DA2 receptors in control of renal function by intrarenal infusion of a highly specific DA2 antagonist YM-09151 (YM), in conscious uninephrectomized dogs (n = 5) in metabolic balance at Na intake 40 meq/day. YM infused at 0.01 pmol.kg-1.min-1 did not cause any changes in urinary flow rate or Na excretion. Administration of YM (infusions from 0.1 to 10.0 pmol.kg-1.min-1) caused a significant dose-dependent diuresis (F = 20.3; P less than 0.001) and natriuresis (F = 35.2; P less than 0.0001) and an increase in glomerular filtration rate (F = 45.4; P less than 0.0001), renal plasma flow (F = 209.3; P less than 0.0001), and filtration fraction (F = 11.2; P less than 0.0001). No significant changes in plasma renin activity, plasma aldosterone concentration, or mean arterial blood pressure occurred with any of the doses of YM infused into the renal artery. Coinfusion of LY-171555, a specific DA2 agonist, at a dose that itself did not affect renal function, completely abrogated the renal hemodynamic and excretory changes induced by YM. The data suggest that dopamine produced intrarenally may act at renal vascular and/or glomerular DA2 receptors to control renal function.

Animals↗