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Biomedical subjects

J E Robillard

Publications and source records attributed to J E Robillard.

At least 91 records · Page 5Linked to original sources
PubMed1988

Ontogeny of alpha-adrenoceptor responses in renal vascular bed of sheep.

The renal hemodynamic response to renal arterial infusions of guanabenz (alpha 2-adrenoceptor agonist) and phenylephrine (alpha 1-adrenoceptor agonist) were compared in conscious and chronically instrumented fetal (132-140 days gestation; term 145 days), newborn (6-15 days postnatal), and nonpregnant adult sheep. Phenylephrine produced similar dose-related decreases in renal blood flow velocity in all three groups at low concentrations (less than 1.8 X 10(-7) M) of drug in renal blood, whereas at the highest concentration adults demonstrated the most vasoconstriction and newborns the least (P less than 0.05 ANOVA). Responses to phenylephrine infusion during renal alpha 1-adrenoceptor blockade with prazosin were completely inhibited. Guanabenz produced greater renal vasoconstriction in adult sheep (P less than 0.05 ANOVA) at all concentrations (0.6 X 10(-6) to 8 X 10(-6) M) when compared with fetal and newborn sheep. Guanabenz-mediated vasoconstriction was not affected by alpha 1-adrenoceptor blockade with prazosin but was completely inhibited by the addition of an alpha 2-adrenoceptor antagonist idazoxan. Results of the present study demonstrate that renal vasoconstriction is mediated by both alpha 1- and alpha 2-adrenoceptors in fetal, newborn, and adult sheep. Moreover, these results suggest that renal alpha 1- and alpha 2-adrenoceptor-mediated vasoconstrictor responses mature at different rates.

Animals↗
PubMed1988

Ontogeny of the renal response to natriuretic peptide in sheep.

The ontogeny of the renal response to continuous systemic infusion of atrial natriuretic peptide (ANP) was studied in chronically instrumented fetal, newborn, and adult nonpregnant sheep. Plasma immunoreactive ANP (ANPir) concentrations during low (0.025 microgram.kg-1.min-1) and high rate (0.1 microgram.kg-1.min-1) ANP infusion were similar between each group of animals. Decrease in renal blood flow velocity (RBFV) and rise in renal vascular resistance (RVR) were observed in fetal and newborn lambs during ANP infusion. The percent changes in RBFV and RVR were of significantly (P less than 0.05) greater magnitude during high ANP infusion rate in fetuses (-28.5 +/- 8.5 and 93 +/- 6.4%) than in adult sheep (-6.6 +/- 3.2 and -4.4 +/- 4.9%). ANP produced no changes in urine flow (V) in fetuses but increased V significantly in newborn lambs and adult sheep. Glomerular filtration rate increased significantly during ANP infusion in adult sheep but not in fetal and newborn lambs. Percentage changes in urinary excretion rate of Na (UNaV) during high ANP infusion rate were significantly higher in adult sheep (3,520 +/- 2,414%) than in newborn (157 +/- 106%) and fetal lambs (198 +/- 84%). These results suggest that the cardiovascular, renal hemodynamic, and possibly renal function responses to continuous ANP infusion increase during maturation, the overall response being larger in adult animals.

Animals↗
PubMed1988

Neurohormonal regulation of renal function during development.

This review summarizes current understanding of fetal renal physiology and considers the role of the neuroadrenergic system and renin-angiotensin system in controlling renal hemodynamics and function during development. Recent evidence suggests that renal innervation appears early during fetal life but is not an important modulator of renal hemodynamics and function during resting conditions in immature animals. It has also been observed that the renal hemodynamic response to renal nerve stimulation (RNS) is less in fetal and newborn animals than in adults. But contrary to previous findings in adult animals, RNS during alpha-adrenoceptor antagonism produces renal vasodilation in fetal and newborn sheep, but not in adult ewes. The role of the renin-angiotensin system (RAS) in modulating renal hemodynamics and function during prenatal and postnatal maturation is discussed. It is suggested that the RAS plays an important role in regulating blood pressure early during fetal life, whereas its influence on renal hemodynamics and function appears later during development.

Aging↗
PubMed1988

Hormonal regulation of renal function during development.

The present review summarizes current and new knowledge concerning the major hormonal systems that directly or indirectly affect renal function during development. The role of the renin-angiotensin-aldosterone system in regulating renal function during fetal and postnatal life is reviewed. A summary of the role of this system during fetal and postnatal stresses is also provided. The physiological role of the renal kallikrein-kinin system in the control of renal blood flow, renin release and sodium excretion during development is examined. Possible influences of the prostaglandin system on regulation of renal function and renin secretion during fetal and postnatal maturation are explored. The effect of vasopressin on the ability of the fetal and postnatal kidney to concentrate urine and regulate body fluid homeostasis is reviewed in detail. The physiologic action of vasotocin on renal sodium and water homeostasis is described. New information regarding the role of the sympathetic system in the regulation of renal hemodynamics and in the control of renal function during development is presented. Finally, recent studies demonstrating the effect of atrial natriuretic factor and corticosteroids on the developing kidney are discussed.

Animals↗
PubMed1988

Renal hemodynamic responses to hypoxemia during development: relationships to circulating vasoactive substances.

Chronically catheterized fetal lambs (n = 11, gestational age 111-139 days) and neonatal lambs (n = 20, postnatal age 4-30 days) were studied to explore during development the relationship of renal hemodynamic responses during hypoxemia to plasma epinephrine concentration (E), plasma norepinephrine concentration (NE), plasma arginine vasopressin concentration (AVP), and plasma renin activity (PRA). A low oxygen gas mixture (11.1 +/- 0.1% O2) was administered for 30 min to the pregnant ewe or neonatal lamb to induce hypoxemia with maintenance of normal arterial pCO2 and pH. Arterial blood pressure was recorded continuously and renal blood flow (RBF) was determined by the radiolabeled microsphere technique. Moderate hypoxemia (pO2 16 +/- 2 torr and 33 +/- 6 torr in fetus and neonate, respectively) induced increases in E, NE (measured by radioenzymatic assay), and AVP (measured by radioimmunoassay) in both fetus and neonate. PRA (measured by radioimmunoassay) also increased in response to hypoxemia in neonatal lambs. The change in mean arterial pressure with hypoxemia (delta MAP) was significant in fetuses (delta MAP 8 +/- 14%, p less than 0.05) but not in lambs (delta MAP 1 +/- 10%, p greater than 0.5). Similarly, the change in renal blood flow with hypoxemia (delta RBF) was significant (delta RBF -51 +/- 24%, p less than 0.001) in fetuses but not in neonatal lambs (delta RBF -9 +/- 38%, p greater than 0.1). These results reflected a change in renal vascular resistance with hypoxemia (delta RVR) that was significant in fetal lambs (delta RVR 169 +/- 168%, p less than 0.01) but not in neonatal lambs (delta RVR 51 +/- 180%, p greater than 0.2).(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1988

Effects of epinephrine on the renal vascular bed of fetal, newborn, and adult sheep.

The renal hemodynamic response to renal artery infusions of epinephrine were compared in conscious and chronically instrumented fetal (125-139 days gestation; term 145 days), newborn (5-13 days postnatal), and nonpregnant adult sheep. Epinephrine produced similar dose related decreases in renal blood flow velocity in all three groups. The mean estimated concentration of epinephrine in renal blood producing a 50% decrease in renal blood flow velocity, ED50, was 0.008 microgram/ml. Epinephrine infusions during renal alpha-adrenoceptor blockade with phentolamine produced increases in renal blood flow velocity that were of greater magnitude in fetal compared to newborn and adult sheep. The maximal increase in renal blood flow velocity observed were 57 +/- 11%, 22 +/- 3%, and 18 +/- 3% in fetal, newborn, and adult sheep, respectively (p less than 0.001). This vasodilation produced by epinephrine during alpha-adrenoceptor blockade was completely inhibited by ICI 118,551, a beta 2-adrenoceptor antagonist. Inhibition of renal vascular beta-adrenoceptors with propranolol in fetal sheep did not enhance alpha-adrenoceptor-mediated renal vasoconstriction with epinephrine infusions. Results of the present study demonstrate similar renal vasoconstrictor responses to renal artery infusion of epinephrine in fetal, newborn, and adult sheep. In contrast, the renal vasodilator responses observed with epinephrine infusions during renal alpha-adrenoceptor blockade were greater in fetal compared to newborn and adult sheep. However, epinephrine-mediated renal vasoconstriction was not enhanced by blockade of beta-adrenoceptors in fetal sheep.

Aging↗
PubMed1988

Plasma and urinary clearance rates of atrial natriuretic factor during ontogeny in sheep.

The present study was designed to determine the plasma clearance rate of atrial natriuretic factor (ANF) during development in chronically-instrumented fetal, newborn and adult non-pregnant sheep. To determine the contribution of the kidney in the metabolism of ANF, urinary clearance of ANF was also measured. Intravenous infusion of ANF (0.025 and 0.1 microgram.min-1.kg-1) produced a significant decrease in mean arterial blood pressure in newborn lambs and in adult non-pregnant sheep. Estimated plasma ANF clearance rate for the 0.025 and 0.1 microgram.min-1.kg-1 ANF infusion rate were respectively 177 +/- 55 and 155 +/- 34 ml.min-1.kg-1 in fetuses, 138 +/- 26 and 97 +/- 13 ml.min-1.kg-1 in newborn lambs and, 148 +/- 33 and 103 +/- 25 ml.min-1.kg-1 in adult nonpregnant ewes. Fetal, newborn and adult ANF plasma clearance rates during high ANF infusion rate (0.1 microgram.min-1.kg-1) were not significantly different. Low or high ANF infusion rate was not associated with significant changes in urinary ANF concentration or urinary ANF excretion rate. Taken together, the present study demonstrates that ANF plasma clearance rate is similar in fetal, newborn and adult non-pregnant sheep and that the excretory function of the kidney contributes only minimally to ANF plasma clearance rate.

Animals↗
PubMed1988

Ontogeny of renal hemodynamic response to terbutaline and forskolin in sheep.

The renal hemodynamic response to renal arterial infusions of terbutaline and forskolin were compared in chronically instrumented fetal (129-139 days gestation; term 145 days), newborn (7-14 days old) and nonpregnant adult sheep. Infusions of terbutaline produced renal vasodilation in all age groups with maximal increases being higher in fetal (47 +/- 7%) than in newborn (30 +/- 8%) or adult sheep (24 +/- 5%). Terbutaline-mediated renal vasodilation was inhibited by the selective beta 2 adrenoceptor antagonist, ICI 118,551, whereas infusion of selective beta 1 adrenoceptor antagonist, ICI 89,406, had no effect. Moreover, terbutaline effects were unchanged after phentolamine infusion to inhibit potential antagonistic effects of neuronal norepinephrine release by presynaptic beta 2 adrenoceptor stimulation. Renal arterial infusion of forskolin produced renal vasodilation of similar magnitude in all age groups, with maximal increases of 46 +/- 5, 38 +/- 3 and 38 +/- 5% in fetal, newborn and adult sheep, respectively. Taken together, these results suggest that renal vasodilatory mechanisms stimulated by selective activation of beta 2 adrenoceptors (terbutaline) are greater during fetal life. However, direct activation of adenylate cyclase with forskolin produces essentially similar renal vasodilatory responses during development in sheep. Thus, reasons to explain age-dependent differences in renal vasodilation observed previously with endogenous catecholamines may be at the receptor-hormone level.

Animals↗
PubMed1987

Renal hemodynamics and natriuresis induced by the dopamine-1 agonist, SKF 82526.

The intrarenal infusion of dopamine (DA) during alpha- and beta-adrenergic blockade has been reported to increase renal blood flow (RBF) and sodium excretion by occupation of DA-1 receptors. In addition, DA may potentially influence renal function by occupation of DA-2 receptor subtypes. This study was designed to examine the hemodynamic and/or tubular mechanisms of the natriuretic effect of DA-1 in dogs anesthetized with pentobarbital. The intrarenal infusion of the DA-1 agonist, SKF 82526 (10(-9), 10(-8), 10(-7) M), resulted in dose related increases in RBF and absolute and fractional sodium excretion. These changes were not associated with alterations in urinary prostaglandin E2, F2 alpha, or kallikrein excretion. To determine the role of RBF in the natriuresis due to SKF 82526 infusion (10(-7) M), the renal artery was constricted to return RBF to control levels during continued SKF 82526 infusion. Although absolute and fractional sodium excretion decreased during this maneuver, they remained higher than control. These studies support both a hemodynamic and a tubular mechanism for the natriuretic effect of the DA-1 agonist, SKF 82526. These effects do not appear to be mediated by the renal prostaglandin or kallikrein systems.

Animals↗
PubMed1987

Effects of dopamine in the renal vascular bed of fetal, newborn, and adult sheep.

The renal hemodynamic response to renal arterial dopamine infusions was compared in unanesthetized fetal (129-137 days gestation, full term 145 days), newborn, and adult sheep. Mean arterial blood pressure and heart rate remained unchanged during intrarenal dopamine infusions. Dopamine produced dose-related decreases in mean renal blood flow velocity in all three groups. When compared with adult sheep fetal sheep were slightly more sensitive to the vasoconstrictive effects of dopamine ED50 (mean effective dose ratio: fetus/ED50 adult = 0.368 +/- 0.047, P less than 0.05). Increases in mean renal blood flow velocity were not seen at any dose given (1-16 micrograms/kg body wt in fetuses, 2-32 micrograms/kg body wt in newborns and adults) until dopamine was infused during alpha- and beta-adrenoceptor blockade. The largest mean increase in renal flow velocity was 13 +/- 3, 16 +/- 3, and 17 +/- 4% in fetal, newborn, and adult sheep, respectively. cis-Flupentixol inhibited the vasodilation. This study demonstrates the presence of renal vasodilation following renal arterial dopamine infusions in fetal, newborn, and adult sheep when renal alpha- and beta-adrenoceptors are blocked. Vasodilator responses are similar in all three groups, and increases in renal blood flow velocity are small compared with that of other experimental models.

Adrenergic beta-Antagonists↗
PubMed1987

Ontogeny of renal hemodynamic response to renal nerve stimulation in sheep.

The renal hemodynamic response to direct electrical stimulation of renal nerves was studied in conscious and chronically instrumented fetal (130-142 days gestation; term 145 days), newborn (7-12 days postnatal), and adult nonpregnant sheep. Renal nerve stimulation (RNS) produced a significant decrease in renal blood flow (RBF) velocity and a significant increase in renal vascular resistance (RVR) in all three groups of animals. The overall decline in RBF velocity and the overall rise in RVR was less pronounced in fetal than in adult sheep (P less than 0.05). Changes in RBF velocity and RVR using an RNS frequency of 16 Hz were -35 +/- 4 and 81 +/- 19% in fetal sheep, -61 +/- 10 and 374 +/- 128% in newborn lambs, and -84 +/- 12 and 540 +/- 94% in adult sheep, respectively. RNS during intrarenal infusion of the alpha-adrenoceptor antagonist phentolamine was associated with a significant increase in RBF velocity and decrease in RVR in both fetal sheep and newborn lambs, but not in adult sheep. Moreover, it was found that the rise in RBF velocity and the decrease in RVR associated with RNS during alpha-adrenoceptor antagonism were completely inhibited by intrarenal infusion of ICI 118,551, a beta 2-adrenoceptor antagonist and unaffected by either cholinergic or dopaminergic antagonists. Taken together, these results suggest that the overall renal vasoconstrictor response to RNS is age dependent. Furthermore, the present results demonstrate that, contrary to observations made in adult animals, RNS can produce renal vasodilation in immature animals that is mediated by beta 2-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1987

Renal hemodynamics and functional changes during the transition from fetal to newborn life in sheep.

The effects of delivery on renal function and renal hemodynamics were studied in conscious and chronically instrumented fetal sheep. Each fetus was studied 1 h before delivery and 1, 4, and 24 h following delivery by cesarean section. Delivery was not associated with significant changes in plasma renin activity, plasma angiotensin II, plasma aldosterone, and plasma arginine vasopressin concentrations when determined 1 h after birth. On the other hand, the transition from fetal to newborn life was accompanied by significant increases in plasma epinephrine and norepinephrine concentrations. No significant changes in renal blood flow velocity or in renal vascular resistance were observed during the transition from fetal to newborn life; percent changes in renal blood flow velocity and renal vascular resistance values were respectively 15.4 +/- 11 and -2.4 +/- 1.0% at 1 h, 4.0 +/- 8.0 and 5.8 +/- 9.1% at 4 h, and 3.2 +/- 8.0 and 9.7 +/- 13% at 24 h. No significant changes in urinary flow rate, urine osmolality, free water clearance, and osmolar clearance were observed in the first 24 h following delivery. On the other hand, glomerular filtration rate increased 3-fold from 3.3 +/- 0.4 ml/min in fetuses to 10.1 +/- 1.2 ml/min in newborn lambs at 24 h of age. This rise in glomerular filtration rate was associated with significant decreases in urinary sodium excretion (UNaV) (from 36 +/- 7 to 13 +/- 3 microEq/min) and fractional excretion of sodium (FENa) (from 7.6 +/- 0.9 to 1.1 +/- 0.3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Severe chloride deficiency in the neonate: the canine puppy as an animal model.

Studies were designed to develop an animal model for the syndrome of hypochloremic, hypokalemic metabolic alkalosis (HMA), and failure to thrive in infants due to intake of chloride-deficient formula. Littermate canine puppies, 2 wk old, were fed soy formula containing normal chloride, 20 mEq/liter (NC, n = 5), or low chloride, 1 mEq/liter (LC, n = 5) for 4 wk, first by gavage and ad libitum thereafter. After 1 wk of LC formula, HMA developed in LC puppies although both NC and LC puppies had similar fluid and caloric intake and gain in weight and forelimb length. Two wk of LC formula also resulted in a higher serum creatinine and calcium but lower phosphate level in LC than NC puppies. After 4 wk of LC, weight and forelimb length were much less in LC than NC puppies. Plasma renin activity decreased with age in NC but remained elevated in LC. In a separate group of puppies (n = 6) with HMA, chloride supplementation of LC formula as NaCl to NC levels corrected HMA despite continued citrate intake. We conclude that the canine puppy is an appropriate model to study HMA due to decreased chloride intake. Low chloride intake independent of citrate caused the HMA.

Alkalosis↗
PubMed1987

Ontogeny of renal beta-adrenoceptor-mediated vasodilation in sheep: comparison between endogenous catecholamines.

The renal hemodynamic response to renal arterial infusions of norepinephrine was compared to epinephrine infusions during renal alpha-adrenoceptor blockade in chronically instrumented and unanesthetized fetal (127-141 days gestation; term 145 days), newborn (6-10 days old), and nonpregnant adult sheep. Infusions of either catecholamines produced renal vasodilation which was of greater magnitude in fetal compared to newborn and adult sheep. Maximal increases in renal blood flow velocity during norepinephrine infusion were 64 +/- 5% in fetal, 23 +/- 4% in newborn, and 24 +/- 7% in adult sheep (p less than 0.001). Similar age-dependent increases in renal blood flow velocity were observed during epinephrine infusion, with maximal changes being 74 +/- 10% in fetal, 23 +/- 4% in newborn, and 19 +/- 4% in adult sheep (p less than 0.001). Increases in renal blood flow velocity produced by both norepinephrine and epinephrine infusions were completely inhibited by intrarenal infusion of ICI 118,551, a beta 2-adrenoceptor antagonist. Taken together, these results suggest that the renal vascular beta 2-adrenergic receptor that mediates vasodilation may be stimulated by both norepinephrine and epinephrine with equal potency. In addition, results of this study demonstrate that enhanced beta 2-adrenoceptor mediated renal vasodilatory capacity is observed during fetal life.

Animals↗
PubMed1987

Changes in arterial blood gases following cardiac asystole during fetal life.

A case of suspected fetal cardiac asystole with normal umbilical cord blood gas values is reported. Possible explanations of this apparent discrepancy were examined by measuring sequential changes in fetal arterial acid-base and blood gas values after induced cardiac asystole in chronically instrumented fetal lambs at 132-141 days' gestation. Arterial pH values did not decrease from baseline for at least ten minutes. Elevation of pCO2 values were observed at 30 minutes. Arterial pO2 and HCO3 values remained unchanged for at least 30 minutes. Therefore, we conclude that sudden fetal cardiac asystole occurring within ten minutes of delivery may be one reason why umbilical cord acid-base and blood gas values do not correlate with Apgar scores.

Acid-Base Equilibrium↗
PubMed1987

Effect of metabolic acidosis on fetal renal haemodynamics.

The effects of metabolic acidosis on renal haemodynamics and intrarenal blood flow distribution was studied in two groups of chronically-catheterized fetal sheep between 122 and 130 days of gestation. One group (experimental group) was studied before and during infusion of 1.1 M lactic acid, whereas the second group received on infusion of dextrose 5% (w/v) in water and served as a time-control group. Infusion of lactic acid for 2 h decreased fetal arterial pH from 7.37 +/- 0.01 to 6.95 +/- 0.02, did not change arterial blood pressure, but produced a significant decrease in renal blood flow (41 +/- 3 to 33 +/- 7 ml/min, P less than 0.05) and a significant increase in renal vascular resistance (1.42 +/- 0.13 to 1.86 +/- 0.18 mmHg/ml/min, P less than 0.05). Moreover, a significant decline in cortical blood flow was also observed in the outer portion of the renal cortex during lactic acidosis. Taken together, these results suggest that metabolic acidosis produces significant changes in fetal renal haemodynamics not associated with changes in arterial blood pressure.

Acidosis↗
PubMed1986

Effects of renal denervation on renal responses to hypoxemia in fetal lambs.

The role of renal nerves in mediating renal hemodynamics and renal function during normal physiological conditions and following moderate hypoxemia was studied in chronically catheterized fetal lambs (125-141 days of gestation) following unilateral renal denervation. Base-line values for renal blood flow (RBF), renal vascular resistance (RVR), glomerular filtration rate (GFR), urinary flow rate (UFR), urinary electrolyte (Na+, K+, and Cl-) excretion rate, and urine osmolality (Uosm) were similar in both intact and denervated kidneys. Hypoxemia was associated with a significant rise in mean arterial blood pressure and a significant decrease in heart rate. Hypoxemia produced a similar decrease in GFR and similar increases in urinary Na+ and Cl- excretion rates in both intact and denervated kidneys. However, the effect of hypoxemia on renal hemodynamics differed between intact and denervated kidneys. Hypoxemia produced a continuous and progressive decrease in RBF and increase in RVR in the intact kidney. On the other hand, renal denervation was associated with an early renal vasodilation and attenuated the reduction in RBF and the rise in RVR during hypoxemia; this early renal vasodilation was blunted following prostaglandin synthesis inhibition. Taken together, these results suggest that fetal renal denervation is not associated with significant changes in renal hemodynamics or renal function during normal physiological conditions but that renal denervation partially inhibited the renal vasoconstriction associated with fetal hypoxemia. Finally, it was found that endogenous prostaglandins counteract the renal vasoconstriction associated with fetal hypoxemia.

Animals↗