The Effects of Antidiuretic Hormone on Urine Flow and Composition in the Chronically‐cannulated Ovine Fetus

Lingwood, Barbara E.; Hardy, Kenneth J.; Horacek, I.; M, McPhee; Scoggins, Bruce A.; Wintour, E. M.

doi:10.1113/expphysiol.1978.sp002445

Cited by 59 publications

(37 citation statements)

References 22 publications

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“…Arginine vasopressin is known to contribute to water reabsorption and amniotic fluid volume in the fetal kidney via action on type-2 receptors on the collecting tubules (see Robillard, Porter & Jose, 1994), promoting the reabsorption of water and thereby reducing UO. Arginine vasopressin infusion into the fetus increases urine osmolarity and decreases urine flow rate (Lingwood, Hardy, Horacek, McPhee, Scoggins & Wintour, 1978), and fetal dehydration is associated with raised fetal AVP and decreased UO (Herin, Kim, Schrier, Meschia & Battaglia, 1988). Furthermore, while oliguria resulting from prostaglandin blockade is associated with a rise in circulating AVP (Walker, Moore, Cheung & Brace, 1992), similar treatment is not associated with altered RBF (Arnold-Aldea, Auslender & Parer, 1991) …”

Section: Blood Gases and Phmentioning

confidence: 99%

The role of carotid chemoreceptors in the effects of hypoxia on renal blood flow in the late gestation sheep fetus

Green

Robson²,

Hanson³

1997

Experimental Physiology

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SUMMARYPrevious studies of the effect of hypoxia on fetal renal haemodynamics have demonstrated a fall, a rise or no change in renal blood flow (RBF). The underlying mechanisms are not understood but involve a balance between neural vasoconstrictor and opposing vasodilator mechanisms. Since carotid chemoreflex mechanisms contribute to vasoconstriction in other fetal vascular beds and in the adult renal vasculature, we examined their effects on RBF during 1 h of acute hypoxia in late gestation fetal sheep (n = 12). Renal blood flow was measured continuously and urine collected at 15 min intervals. Seven fetuses underwent bilateral section of the carotid sinus nerves (CSD fetuses). During hypoxia CSD fetuses showed a transient initial rise in RBF (P < 0.05) and then a subsequent fall (P < 0.05) to levels comparable with that recorded in intact fetuses. There was no change in urine output in either intact or CSD fetuses during hypoxia. Thus the initial fall in RBF during hypoxia is a carotid chemoreflex but other mechanisms, e.g. vasoconstrictor hormones, contribute to the sustained response.

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Section: Blood Gases and Phmentioning

confidence: 99%

The role of carotid chemoreceptors in the effects of hypoxia on renal blood flow in the late gestation sheep fetus

Green

Robson²,

Hanson³

1997

Experimental Physiology

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“…1) is probably due to increased water reabsorption from the distal parts ofthe nephron consequent upon an increase in fetal vasopressin levels. The fetus can produce vasopressin (Rurak, 1979) and the fetal kidney responds to infusions of vasopressin (Robillard, Weitzman, Fisher & Smith, 1979;Lingwood, Hardy, Horacek, McPhee, Scoggins & Wintour, 1978). This increase in water reabsorption occurred only following i.v.…”

mentioning

confidence: 99%

Changes in fetal renal function in response to infusions of a hyperosmotic solution of mannitol to the ewe.

Lumbers¹,

Stevens²

1983

The Journal of Physiology

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SUMMARY1. In six pregnant ewes a reduction in transplacental water transfer was produced by increasing maternal osmolality (by infusion of 180 g of mannitol in 500 ml of 0-15 M-sodium chloride) and the fetal renal responses to this reduction in water transfer were studied. These responses were compared with the renal responses of five other chronically catheterized fetal lambs whose mothers received I.v. infusions of 500 ml of 0-15 M-sodium chloride.2. Intravenous infusion of 500 ml of 0-15 M-sodium chloride to the ewe produced no changes in fetal plasma sodium, potassium or plasma renin activity and had no effect on fetal renal function.3. After i.v. infusion of mannitol to the ewe, fetal urinary flow rate fell from control levels of 0-69 + 0-12 ml/min to 0-32 + 0 04 ml/min (S.E. of mean, P < 0 006). This fall in urinary flow rate was due to increased water reabsorption because there was no change in glomerular filtration rate and osmolar clearance.4. Fetal urinary sodium excretion increased from 16-2 + 2-0 /imol/min, to 34-2 + 6-,9 ,mol/min (S.E. of mean, P < 0 04). This increase in fetal urinary sodium excretion was due to a fall in the fractional reabsorption of sodium which was related to the rise in fetal plasma sodium levels that occurred following infusion of mannitol to the ewe. The increases in fetal plasma sodium levels were also associated with reductions in fetal plasma renin activity.5. It is concluded that the fetal lamb is capable of limiting renal water excretion and modifying renal sodium excretion in order to maintain the volume and composition of its body fluids.

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“…The chronically cannulated fetuses of cross-bred and low birth wt neonates with increases in plasma aldosterone Merino ewes of known mating dates were used for the present concentration, suggesting that renal insensitivity to aldosterone investigation. The procedure for fetal cannulation and the maintenance of cannulas has been described previously (15). Briefly, 7 surgery, while being maintained in individual metabolic cages with food and water ad libitum.…”

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confidence: 99%

Gestational Changes in Renal Responsiveness to Cortisol in the Ovine Fetus

1989

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ABSTRACT. The ontogenetic renal responsiveness to exogenous cortisol was examined in the chronically cannulated ovine fetus. The contribution of effects a t proximal and distal tubule of the kidney were studied also. Cortisol (81.5 pg/h) was infused into immature ovine fetuses (mean gestational age -113.9 days) on five occasions and increased blood cortisol from 0.8 f 0.5 to 21.3 + 6.2 nmol/ liter. This dose of cortisol produced a highly significant diuresis and natriuresis, in part due to an increase in GFR and in part due to a significant decrease in proximal tubular reabsorption of sodium. Cortisol (107.2 + 4.7 &h) was infused into mature fetuses (mean gestational age 133.4 days) and produced an increase in blood cortisol concentration from 11.4 + 5.6 to 33.7 2 6.8 nmol/liter. No natriuresis or diuresis was seen in the mature fetuses. Cortisol caused a significant depression of proximal tubular sodium reabsorption in mature fetuses, but this extra load was reabsorbed in the distal tubule in these fetuses. The inability of the premature or very low birth wt baby to maintain normal sodium balance on a standard salt intake may be due, at least in part, to a "fetal" renal response to the high plasma cortisol concentrations found in such babies. As the kidney matures it becomes capable of increasing distal tubular sodium reabsorption to compensate for any increased distal tubular fluid delivery. (Pediatr Res 26: 6-10, 1989) Abbreviations FRN,, fractional reabsorption of sodium FR,,i, fractional reabsorption of lithium uN,,v, uKV, UclV, Uc.V, renal excretion rate of sodium/ potassium/chloride/calcium may be responsible for neonatal hyponatremia. However, subsequent investigations have shown that a characteristic of this defect is decreased proximal tubule reabsorption of sodium (2) implying that renal insensitivity to aldosterone may be only partially responsible. The relative immaturity of renal function in very low birth wt and premature neonates seems to be important in the pathogenesis of hyponatremia. Premature neonates exhibit a greater natriuresis and a lower GFR in response to oral salt loading when compared to full-term neonates (5, 6). This is consistent with histopathologic studies that show that glomerular formation in the human infant is not complete until late in gestation (7), whereas tubular development is not complete until 1 y after birth (8).In mature mammals the presence of adrenal steroids is essential for normal renal function. A characteristic of adrenalectomized or hypophysectomized animals and patients with adrenal or pituitary insufficiency is a delayed diuresis following oral or parenteral water loading, accompanied by impaired sodium conservation and reduced GFR and renal blood flow. Administration of deoxycortisone acetate or aldosterone in the presence of normal sodium balance and extra-cellular volume has no effect on the delayed diuresis, whereas cortisol-like steroids correct this diuresis (9-1 1).Clinical investigations have reported that premature neonates have higher plasma co...

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The Effects of Antidiuretic Hormone on Urine Flow and Composition in the Chronically‐cannulated Ovine Fetus

Cited by 59 publications

References 22 publications

The role of carotid chemoreceptors in the effects of hypoxia on renal blood flow in the late gestation sheep fetus

The role of carotid chemoreceptors in the effects of hypoxia on renal blood flow in the late gestation sheep fetus

Changes in fetal renal function in response to infusions of a hyperosmotic solution of mannitol to the ewe.

Gestational Changes in Renal Responsiveness to Cortisol in the Ovine Fetus

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