Intraruminal rehydration of ovine fetuses

1991 ◽  
Vol 261 (6) ◽  
pp. R1381-R1387
Author(s):  
M. G. Ross ◽  
D. J. Sherman ◽  
M. G. Ervin ◽  
L. Day
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Distilled Water ◽  
Intravascular Volume ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Arterial Po2

During oral rehydration of adult mammals, oropharyngeal stimulation, the act of swallowing, and/or gastric factors contribute to a rapid decrease in plasma arginine vasopressin (AVP) that precedes plasma osmolality changes. To determine whether similar mechanisms are present in the developing fetus, six chronically prepared ovine fetuses were rehydrated with intraruminal (IR) distilled water infusions (1 ml.kg-1.min-1 for 60 min) after 43 +/- 3 h of maternal water deprivation. In response to maternal dehydration, significant increases were noted in maternal and fetal mean plasma osmolalities, sodium and AVP concentrations, and fetal urine osmolality. As estimated by hematocrit, fetal intravascular volume decreased by 11%. Fetal rehydration via IR distilled water infusion evoked a significant decrease in fetal plasma osmolality but no change in urine osmolality. Unexpectedly, fetal arterial blood pressure increased and arterial PO2 decreased while fetal hematocrit indicated a further 7% decrease in intravascular volume after the IR infusion. There was a nonsignificant trend toward increased fetal glomerular filtration rate, urine volume, and plasma AVP concentrations. Identical IR water infusions to five euhydrated fetuses resulted in significant decreases in fetal plasma osmolality and increases in glomerular filtration rate, urine flow, and osmolar excretion. The euhydrated fetuses also exhibited significant increases in mean arterial blood pressure and hematocrit and decreased fetal arterial PO2. These results indicate that IR water does not suppress AVP secretion in the dehydrated ovine fetus. Rather, both euhydrated and dehydrated fetuses exhibit an idiosyncratic vasoconstrictive response to IR water.

Maternal dehydration-rehydration: fetal plasma and urinary responses

1988 ◽  
Vol 255 (5) ◽  
pp. E674-E679 ◽  
Author(s):  
M. G. Ross ◽  
D. J. Sherman ◽  
M. G. Ervin ◽  
R. Castro ◽  
J. Humme
Keyword(s):  
Glomerular Filtration Rate ◽  
Arginine Vasopressin ◽  
Filtration Rate ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Fetal Plasma ◽  
Urine Production ◽  
The Impact ◽  
Observation Period

Pregnant women may be exposed to exercise, thermal, or gastrointestinal (hyperemesis) water loss, all of which commonly induce a greater than 10 mosmol increase in plasma osmolality. Although fetal osmolality is dependent on maternal osmolality, the impact of maternal dehydration and subsequent maternal rehydration on the fetus has not been explored. Five pregnant ewes with singleton fetuses (136 +/- 1 day) were water deprived for 36 h resulting in a significant increase in plasma osmolality (298 +/- 3.4 to 313 +/- 5.0 mosmol). In response to maternal dehydration, fetal plasma osmolality (297.0 +/- 4.1 to 309.3 +/- 4.1 mosmol), arginine vasopressin (AVP) levels (1.5 +/- 0.2 to 7.9 +/- 1.0 pg/ml), hematocrit (35.1 to 38.6%), and urine osmolality (161.3 +/- 10.7 to 348.9 +/- 21.9 mosmol) significantly increased. Subsequently, ewes were rehydrated over 4 h with intravenously infused 0.45% saline (20 ml.kg-1.h-1). In response to maternal rehydration, maternal and fetal plasma osmolality decreased to basal values (298.9 +/- 3.2 and 300.1 +/- 3.8 mosmol, respectively) and fetal glomerular filtration rate (1.72 +/- 0.30 to 3.08 +/- 0.66 ml/min) and urine volume significantly increased (0.33 +/- 0.02 to 0.71 +/- 0.13 ml/min). However, fetal hematocrit (37.4%), plasma AVP (3.1 +/- 0.9 pg/ml), and urine osmolality (255.4 +/- 28.8 mosmol) did not return to basal levels during the observation period. These results demonstrate fetal hyperosmolality, blood volume contraction, AVP secretion, and altered urine production in response to maternal dehydration. Despite maternal rehydration and normalization of maternal and fetal plasma osmolality, fetal endocrine and fluid responses are prolonged.(ABSTRACT TRUNCATED AT 250 WORDS)

Meclofenamate and urine concentration with and without exposure of the renal papilla

1981 ◽  
Vol 240 (5) ◽  
pp. F423-F429 ◽  
Author(s):  
R. J. Roman ◽  
C. Lechene
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Urine Osmolality ◽  
Urine Concentration ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Renal Papilla ◽  
Arterial Blood ◽  
Pelvic Urine

The recent finding that inhibitors of prostaglandin synthesis prevent the fall in urine concentration produced by papillary exposure challenges the hypothesis that contact between the pelvic urine and papilla is essential to the renal concentrating process. The present study examines the change in urine osmolality produced by exposure of the renal papilla in rats given meclofenamate. In control animals urine osmolality(Uosmol) decreased 57% after 2 h of exposure of the renal papilla. In rats given meclofenamate 4 mg/kg urine osmolality increased 16%, urine flow decreased 30%, and glomerular filtration rate was unchanged in the nonexposed kidney. Meclofenamate, however, did not alter the decrease in Uosmol seen in the kidney with the exposed papilla. Meclofenamate 10 mg/kg was also ineffective in preventing the fall in urine osmolality produced by papillary exposure, although this higher dose decreased glomerular filtration rate and arterial blood pressure. These results are consistent with the finding that pelvic urine urea is important to the urinary concentrating process and with the hypothesis that urine osmolality falls after papillary exposure because contact between pelvic urine and papilla is interrupted.

Ovine fetal adaptations to chronically reduced urine flow: preservation of amniotic fluid volume

1996 ◽  
Vol 81 (6) ◽  
pp. 2588-2594 ◽  
Author(s):  
Stephanie E. Mann ◽  
Mark J. M. Nijland ◽  
Michael G. Ross
Keyword(s):  
Amniotic Fluid ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Fluid Volume ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Amniotic Fluid Volume ◽  
Fetal Urine ◽  
Ovine Fetal

Mann, Stephanie E., Mark J. M. Nijland, and Michael G. Ross.Ovine fetal adaptations to chronically reduced urine flow: preservation of amniotic fluid volume. J. Appl. Physiol. 81(6): 2588–2594, 1996.—Adequate amniotic fluid (AF) volume is maintained by a balance of fetal fluid production (lung liquid and urine) and resorption (swallowing and intramembranous flow). Because fetal urine is the principle source of AF, alterations in urine flow and composition directly impact AF dynamics. Intra-amniotic 1-desamino-8-d-arginine vasopressin (DDAVP) is rapidly absorbed into fetal plasma and induces a marked fetal urinary antidiuresis. To examine the effect of intra-amniotic- DDAVP-induced fetal urinary responses on AF volume and composition, six chronically prepared ewes with singleton fetuses (gestation 128 ± 2 days) were studied for 72 h after a single intra-amniotic DDAVP (50-μg) injection. After DDAVP, fetal urine osmolality significantly increased at 2 h (157 ± 13 to 253 ± 21 mosmol/kg) and remained elevated at 72 h (400 ± 13 mosmol/kg). Urinary sodium (33.0 ± 4.5 to 117.2 ± 9.7 meq/l) and chloride (26.0 ± 2.8 to 92.4 ± 8.1 meq/l) concentrations similarly increased. AF osmolality increased (285 ± 3 to 299 ± 4 mosmol/kgH2O), although there was no change in fetal plasma osmolality (294 ± 2 mosmol/kg). Despite a 50% reduction in fetal urine flow (0.12 ± 0.03 to 0.05 ± 0.02 ml ⋅ kg−1 ⋅ min−1at 2 h and 0.06 ± 0.01 ml ⋅ kg−1 ⋅ min−1after 72 h), AF volume did not change (693 ± 226 to 679 ± 214 ml). There were no changes in fetal arterial blood pressures, pH,[Formula: see text], or[Formula: see text] after DDAVP. We conclude the following. 1) Intra-amniotic DDAVP injection induces a prolonged decrease in fetal urine flow and increases in urine and AF osmolalities. 2) Despite decreased urine flow, AF volume does not change. We speculate that, in response to DDAVP-induced fetal oliguria, reversed intramembranous flow (from isotonic fetal plasma to hypertonic AF) preserves AF volume.

The giraffe kidney tolerates high arterial blood pressure by high renal interstitial pressure and low glomerular filtration rate

2015 ◽  
Vol 214 (4) ◽  
pp. 497-510 ◽  
Author(s):  
M. Damkjaer ◽  
T. Wang ◽  
E. Brøndum ◽  
K. H. Østergaard ◽  
U. Baandrup ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Arterial Blood Pressure ◽  
Filtration Rate ◽  
Interstitial Pressure ◽  
Arterial Blood

Endothelin-induced natriuresis and diuresis are pressure-dependent events in the rat

1993 ◽  
Vol 265 (1) ◽  
pp. R90-R96 ◽  
Author(s):  
K. Uzuner ◽  
R. O. Banks
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Arterial Pressure ◽  
Filtration Rate ◽  
Urine Flow ◽  
Female Rats ◽  
Arterial Blood ◽  
Site Of Action ◽  
Baseline Values ◽  
The Right

The goal of the current study was to determine the mechanism by which doses of endothelin (ET) that do not markedly affect the glomerular filtration rate (GFR) cause a natriuresis and diuresis. ET was infused into pentobarbital-anesthetized female rats at 50 ng.kg-1.min-1 iv for 30 min. In controls (n = 6 rats; n = 5 in all other groups), ET increased mean arterial blood pressure (MAP) from 95 +/- 2 to 131 +/- 2 (SE) mmHg, Na excretion (UNa V) from 0.34 +/- 0.07 to 1.83 +/- 0.2 meq/min, and urine flow rate (V) from 13 +/- 1 to 24 +/- 3 ml/min (all P < 0.01 vs. baseline). At 15 min during infusion of ET, the GFR was not affected (2.1 +/- 0.1 to 2.2 +/- 0.1 ml/min) but modestly decreased to 1.8 +/- 0.1 ml/min at 30 min (P < 0.05 vs. baseline). Either removing the capsule from both kidneys during surgery or maintaining renal arterial pressure at baseline values with an adjustable clamp on the aorta above the right renal artery abolished the ET-induced increase in UNa V and V. Meclofenamate also did not alter the ET-induced increase in MAP, V, or UNa V. To determine the intrarenal site of action of ET, experiments were conducted with ET plus amiloride or with a combination of amiloride plus furosemide; there was a larger ET-induced diuresis and natriuresis in amiloride-treated rats and an even larger response with amiloride plus furosemide compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Localization of alpha 2-adrenoceptor-mediated increase in renal Na+, K+, and water excretion

1987 ◽  
Vol 252 (6) ◽  
pp. F1016-F1021 ◽  
Author(s):  
B. Stanton ◽  
E. Puglisi ◽  
M. Gellai
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Water Transport ◽  
Filtration Rate ◽  
Distal Tubule ◽  
Fractional Excretion ◽  
Urine Osmolality ◽  
Water Excretion ◽  
Arterial Blood ◽  
Adrenoceptor Agonist

Free-flow micropuncture and clearance studies were conducted in male Sprague-Dawley rats to investigate the effects of alpha 2-adrenoceptor stimulation on Na+, K+, and water transport along the nephron. Intravenous infusion of the selective alpha 2-adrenoceptor agonist B-HT 933 at 1 mg X kg-1 X h-1 increased urinary flow rate from 16.2 +/- 3.6 to 84.8 +/- 11.9 microliter/min, fractional excretion of Na+ from 1.36 +/- 0.31 to 3.57 +/- 0.52%, and fractional excretion of K+ from 26.9 +/- 3.0 to 42.3 +/- 2.2%, The diuresis, saluresis, and kaliuresis were not the result of increases in glomerular filtration rate or mean arterial blood pressure. Urine osmolality decreased from 1,126 +/- 177 to 325 +/- 33 mosmol/kg water and in 8 of the 11 animals studied B-HT 933 decreased urine osmolality to hyposmotic levels, suggesting a possible interaction between the alpha 2-adrenoceptor agonist and vasopressin. The alpha 2-adrenoceptor antagonist yohimbine (0.25/mg bolus, iv) inhibited the diuresis, saliuresis, and kaliuresis. In micropuncture studies, B-HT 933 was without effect on single-nephron glomerular filtration rate or on Na+, K+, and water transport along the superficial proximal tubule, loop of Henle, or distal tubule. Thus stimulation of alpha 2-adrenoceptors increases Na+, K+, and water excretion by inhibiting tubule reabsorption of these substances at nephron sites beyond the superficial distal tubule, most likely by the collecting tubule.

Abstract 386: A Novel Aquaretic and Glomerular Filtration Rate Enhancing Peptide Without Vascular Vasodilatory Actions in Experimental CHF.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Horng H Chen ◽  
ShuChong Pan ◽  
John C Burnett ◽  
Robert D Simari
Keyword(s):  
Blood Pressure ◽  
Amino Acids ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Water Excretion ◽  
Arterial Blood ◽  
Change In Mean

BACKGROUND: BNP is a cardiac peptide with vasodilatory, natriuretic and diuretic properties. Recent studies have suggested that its vasodilatory hypotensive properties may limit the renal actions of BNP, especially in patients with borderline low blood pressure. We have recently identified an alternatively spliced transcript for BNP (ASBNP) that includes a unique and distinct longer carboxyl-terminus consisting of 34 amino acids. Based upon preliminary studies, we generated a truncated form (ASBNP2.1) that contains the first 16 amino acids of the C-terminal of ASBNP. METHODS: We determined the cardiorenal and humoral actions of intravenous infusion of ASBNP2.1 at 2 pmol/Kg/min, 10 pmol/Kg/min and 100 pmol/Kg /min in 10 dogs with rapid ventricular pacing induced overt CHF (240 bpm for 10 days). * p<0.05 RESULTS: IV infusion of ASBNP 2.1 increased aquaresis (from 0.19±0.04 to 0.32±0.07, 0.46±0.11 and 0.39±0.09 ml/min*) without a significant change in urinary sodium excretion. Importantly, ASBNP 2.1 enhanced glomerular filtration rate (GFR), from 31±4 to 47±8, 69±10 and 56±9 ml/min*. These renal actions were associated with increases in urinary BNP*, ANP* and cGMP* excretion. BNP 2.1 did not have any systemic vasodilatory action resulting in no change in mean arterial blood pressure or cardiac-filling pressures even at the highest dose. There was not change in serum sodium concentration. CONCLUSION: We report for the first time that this novel peptide based upon ASBNP has potent aquaretic and GFR enhancing actions without the vasodilatory hypotensive properties in an experimental model of overt CHF. The lack of vasodilatation but with renal actions also suggest that the C-terminus plays a key role in the vascular actions of this peptide offering new insights into vascular-renal structure function of BNP and related peptides. This renal specific peptide may have potential therapeutic benefit in states of renal dysfunction with volume overload to enhance GFR and water excretion without the detrimental side effect of hypotension.

Effect of inhibition of MAO and COMT on intrarenal dopamine and serotonin and on renal function

2001 ◽  
Vol 280 (1) ◽  
pp. R248-R254 ◽  
Author(s):  
Yongqing Wang ◽  
Theresa J. Berndt ◽  
Jennifer M. Gross ◽  
Michael A. Peterson ◽  
Mathew J. So ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Monoamine Oxidase ◽  
Filtration Rate ◽  
Interstitial Fluid ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Arterial Blood ◽  
Fractional Excretion Of Sodium

The purpose of the present investigation was to study the effects of inhibition of monoamine oxidase (MAO) and/or catechol- O-methyltransferase (COMT), enzymes involved in the degradation of dopamine (DA) and serotonin (5-HT), on intrarenal DA and 5-HT, as reflected in the renal interstitial fluid (RIF) microdialysate and urine, and on renal function. Inhibition of MAO selectively increased RIF 5-HT from 3.16 ± 0.38 to 8.03 ± 1.83 pg/min ( n = 7, P < 0.05), concomitant with decreases in mean arterial blood pressure and glomerular filtration rate (2.09 ± 0.18 to 1.57 ± 0.22 ml/min, n = 7, P < 0.05). Inhibition of COMT significantly increased RIF DA (3.47 ± 0.70 to 8.68 ± 1.96 pg/min, n = 9, P < 0.05), urinary DA (2.00 ± 0.16 to 2.76 ± 0.26 ng/min, n = 9, P < 0.05), and absolute excretion of sodium (6.42 ± 2.00 to 9.82 ± 1.62 μmol/min, n = 10, P < 0.05). Combined inhibition of MAO and COMT significantly increased RIF DA, urinary DA, and urinary 5-HT, which was accompanied with increases in urine flow rate, and absolute (3.03 ± 0.59 to 8.40 ± 1.61 μmol/min, n = 9, P < 0.01) and fractional excretion of sodium. We conclude that inhibition of MAO selectively increases RIF 5-HT. COMT appears to be more important than MAO in the metabolism of intrarenal DA. Physiological increases in intrarenal DA/5-HT induced by inhibition of their degrading enzymes are accompanied with significant alterations of renal function.

Angiotensin-(1–7) in the ovine fetus

2001 ◽  
Vol 280 (2) ◽  
pp. R404-R409 ◽  
Author(s):  
Karen M. Moritz ◽  
Duncan J. Campbell ◽  
E. Marelyn Wintour
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Flow Rate ◽  
Filtration Rate ◽  
Plasma Concentrations ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Ang Ii ◽  
Arterial Blood

In the adult animal, ANG-(1–7) may counterbalance some effects of ANG II. Its effects in the fetus are unknown. Basal ANG-(1–7), ANG I, ANG II, and renin concentrations were measured in plasma from ovine fetuses and their mothers ( n = 10) at 111 days of gestation. In the fetus, concentrations of ANG I, ANG-(1–7), and ANG II were 86 ± 21, 13 ± 2, and 14 ± 2 fmol/ml, respectively. In the ewe, concentrations of ANG I were significantly lower (20 ± 4 fmol/ml, P < 0.05) as were concentrations of ANG-(1–7) (2.9 ± 0.6 fmol/ml), whereas ANG II concentrations were not different (10 ± 1 fmol/ml). Plasma renin concentrations were higher in the fetus (4.8 ± 1.1 pmol ANG I · ml−1 · h−1) than in the ewe (0.9 ± 0.2 pmol · ml−1 · h−1, P < 0.05). Infusion of ANG-(1–7) (∼9 μg/h) for a 3-day period caused a significant increase in plasma concentrations of ANG-(1–7) reaching a maximum of 448 ± 146 fmol/ml on day 3 of infusion. Plasma levels of ANG I and II as well as renin were unchanged by the infusion. Urine flow rate, glomerular filtration rate, and fetal arterial blood pressure did not change and were not different than values in fetuses receiving a saline infusion for 3 days ( n = 5). However, the osmolality of amniotic and allantoic fluid was significantly higher in fetuses that received ANG-(1–7). Also, compared with the saline-infused animals, mRNA expression levels of renin, the AT1 receptor, and AT2 receptor were elevated in kidneys of fetuses that received infusions of ANG-(1–7). Infusion of an ANG-(1–7) antagonist {[d-Ala7]-ANG-(1–7), 20 μg/h} for 3 days had no effect on fetal blood pressure or renal function. In conclusion, although infusion of ANG-(1–7) did not affect fetal urine flow rate, glomerular filtration rate, or blood pressure, changes in fetal fluids and gene expression indicate that ANG-(1–7) may play a role in the fetal kidney.

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