Comparison of the effects of parathyroid hormone (PTH) and recombinant PTH-related protein on bicarbonate excretion by the isolated perfused rat kidney

1990 ◽  
Vol 126 (3) ◽  
pp. 403-408 ◽  
Author(s):  
A. G. Ellis ◽  
W. R. Adam ◽  
T. J. Martin
Keyword(s):  
Parathyroid Hormone ◽  
Rat Kidney ◽  
Urine Volume ◽  
Clinical Manifestations ◽  
Fractional Excretion ◽  
Bicarbonate Concentration ◽  
Isolated Perfused Rat Kidney ◽  
Amino Terminal ◽  
Fractional Excretion Of Sodium ◽  
Perfused Rat Kidney

ABSTRACT The isolated perfused rat kidney was used to study the effects of amino-terminal fragments of human parathyroid hormone, hPTH(1–34), bovine parathyroid hormone, bPTH(1–84) and of PTH-related proteins, PTHrP(1–34), PTHrP(1–84), PTHrP(1–108) and PTHrP(1–141) on urinary bicarbonate excretion. PTHrP(1–34) (7 nmol/l), bPTH(1–84) (5·5 nmol/l) and hPTH(1–34) (7 nmol/l) had similar effects in increasing bicarbonate excretion with respect to the control. At lower concentrations (0·7 nmol/l) all PTHrP components, but not hPTH(1–34) or bPTH(1–84) increased bicarbonate excretion significantly. Infusions of PTHrP(1–108) and PTHrP(1–141) at 0·7 nmol/l, while associated with a rise in urinary bicarbonate concentration and excretion during the early stages of perfusion, produced a sharp decline in bicarbonate concentration and excretion in the latter part of perfusion. The different peptides produced no significant differences in glomerular filtration rate, fractional excretion of sodium or urine volume. The absence of substantial differences between the effects of hPTH(1–34) and PTHrP(1–34) are as noted in previous studies. The differences between PTHrP(1–108)/PTHrP(1–141) and PTHrP(1–34) demonstrated here are consistent with (1) the clinical manifestations of acidosis in hyperparathyroidism and alkalosis in humoral hypercalcaemia of malignancy, and (2) an independent action of a component of PTHrP beyond amino acids 1–34. Journal of Endocrinology (1990) 126, 403–408

Effect of vasoactive intestinal peptide on isolated perfused rat kidney

1985 ◽  
Vol 249 (5) ◽  
pp. E494-E497 ◽  
Author(s):  
R. M. Rosa ◽  
P. Silva ◽  
J. S. Stoff ◽  
F. H. Epstein
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Rat Kidney ◽  
Urine Volume ◽  
Fractional Excretion ◽  
Rectal Gland ◽  
Renal Nerves ◽  
Isolated Perfused Rat Kidney ◽  
Fractional Excretion Of Sodium ◽  
Perfused Rat Kidney ◽  
Renal Tubular

Vasoactive intestinal peptide, a polypeptide neurotransmitter, stimulates salt secretion by the mammalian intestine and the rectal gland of the dogfish shark. Because of the recent identification of vasoactive intestinal peptide in renal nerves, the present study was undertaken to investigate its effects on the isolated perfused rat kidney. The addition of vasoactive intestinal peptide to the recirculating perfusate produced a significant increase in urine volume, fractional excretion of sodium, chloride, and potassium, as well as osmolar clearance when compared with control kidneys. These changes associated with addition of vasoactive intestinal peptide occurred without any significant changes in perfusion flow, renal vascular resistance, or inulin clearance. These experiments strongly suggest an action of vasoactive intestinal peptide on renal tubular reabsorption.

Effect of epinephrine on renal potassium excretion in the isolated perfused rat kidney

1984 ◽  
Vol 247 (2) ◽  
pp. F331-F338
Author(s):  
L. D. Katz ◽  
J. D'Avella ◽  
R. A. DeFronzo
Keyword(s):  
Rat Kidney ◽  
Fractional Excretion ◽  
Beta Agonist ◽  
Potassium Excretion ◽  
Isolated Perfused Rat Kidney ◽  
Beta Agonists ◽  
Beta Adrenergic Agonists ◽  
Urinary Potassium ◽  
Perfused Rat Kidney ◽  
Renal Potassium Excretion

The effects of beta-agonists (epinephrine, isoproterenol, and ITP) and beta-antagonists (propranolol, metoprolol, and butoxamine) on renal potassium excretion were examined using the isolated perfused rat kidney preparation. Following 30 min of control perfusion, one of the above beta-adrenergic agonists or antagonists was added to the perfusion medium. Following epinephrine, a combined beta 1- and beta 2-agonist, urinary potassium excretion (UKV; 0.55 +/- 0.55 vs. 0.36 +/- 0.04 mueq/min, P less than 0.001) and fractional excretion of potassium (FEK; 24.6 +/- 2.4 vs. 18.2 +/- 2.0%, P less than 0.001) both decreased. When isoproterenol, a nonspecific beta-agonist, was added to the perfusate, UKV (0.49 +/- 0.10 vs. 0.27 +/- 0.04 mueq/min, P less than 0.02) and FEK (29.0 +/- 5.2 vs. 16.3 +/- 2.9%, P less than 0.01) again decreased. ITP, a specific beta 1-agonist also caused a decrease in UKV (0.60 +/- 0.13 vs. 0.39 +/- 0.04 mueq/min, P less than 0.02) and FEK (30.2 +/- 5.1 vs. 17.8 +/- 2.8%, P less than 0.02). In contrast, when propranolol, a nonspecific beta-antagonist, was added to the perfusate, the opposite effects on renal potassium handling were observed. UKV (0.45 +/- 0.05 vs. 0.70 +/- 0.07 mueq/min, P less than 0.001) and FEK (23.0 +/- 2.1 vs. 42.5 +/- 3.1%, P less than 0.001) both increased. Metoprolol (50 ng/ml), a specific beta 1-antagonist, increased UKV (0.56 +/- 0.10 vs. 0.68 +/- 0.15 mueq/min, P less than 0.02) and FEK (31.0 +/- 3.8 vs. 48.0 +/- 7.1%, P less than 0.02). A similar effect was observed when a higher dose of metoprolol (200 ng/ml) was employed.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of atrial natriuretic peptides on metabolism of arginine vasopressin by isolated perfused rat kidney

1992 ◽  
Vol 263 (2) ◽  
pp. R273-R278
Author(s):  
M. R. Lebowitz ◽  
A. M. Moses ◽  
S. J. Scheinman
Keyword(s):  
Arginine Vasopressin ◽  
Rat Kidney ◽  
Fractional Excretion ◽  
Metabolic Clearance ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney ◽  
Clearance Receptor ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) antagonizes the release and action of arginine vasopressin (AVP) both in vivo and in vitro. We have reported that ANP increases the urinary and metabolic clearances of AVP in normal subjects (A. M. Moses et al. J. Clin. Endocrinol. Metab. 70: 222-229, 1990). To clarify this effect, we perfused isolated rat kidneys in vitro and measured the clearances of AVP for 30 min after the addition of rat ANP [rANP-(1-28), 10(-7) M]. In the perfused kidney, rANP increased the urinary clearance of AVP (UCAVP) from 321 +/- 19 to 417 +/- 20 microliters/min (P less than 0.01) and increased the glomerular filtration rate (GFR) from 558 +/- 28 to 696 +/- 28 microliters/min (P less than 0.01). Fractional excretion of AVP was unchanged. Rates of AVP reabsorption were directly related to filtered AVP, and this relationship was not altered by ANP. ANP did not affect the total organ clearance or the renal metabolic clearance of AVP. The increase in GFR was associated with increases in renal vascular resistance (P less than 0.05), filtration fraction (P less than 0.01), and sodium excretion (P less than 0.001). UCAVP also increased when GFR was raised without ANP by perfusing at higher pressures. The rat ANP clearance receptor agonist [cANP- (4-23), 10(-7) M] did not change GFR or UCAVP. ANP increases UCAVP in the isolated perfused rat kidney. This appears to be a hemodynamic effect of ANP, acting through its biological receptor and not the clearance receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Low concentrations of ANP cause pressure-dependent natriuresis in the isolated kidney

1988 ◽  
Vol 255 (3) ◽  
pp. F391-F396 ◽  
Author(s):  
J. D. Firth ◽  
A. E. Raine ◽  
J. G. Ledingham
Keyword(s):  
Filtration Rate ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Fractional Excretion ◽  
Renal Perfusion ◽  
Isolated Kidney ◽  
Renal Perfusion Pressure ◽  
Low Concentrations ◽  
Fractional Excretion Of Sodium ◽  
Perfused Rat Kidney

The effect of alteration in renal perfusion pressure on the response of the isolated perfused rat kidney to concentrations of alpha-human atrial natriuretic peptide (ANP) within the pathophysiological range has been examined. At a perfusion pressure of 90 mmHg ANP concentrations of 50, 200, and 1,000 pmol/l were without effect on any parameter tested. At a perfusion pressure of 130 mmHg 50 pmol/l ANP produced an increase of 3.13 +/- 0.68 mumol/min in sodium excretion (UNa V), compared with a fall of 0.33 +/- 1.04 mumol/min in controls (P less than 0.02); fractional excretion of sodium (FENa) rose by 1.45 +/- 0.36% vs. -0.12 +/- 0.47% (P less than 0.05); glomerular filtration rate (GFR) was unchanged. At 200 and 1,000 pmol/l larger changes in UNa V and FENa were seen; only at 1,000 pmol/l was a significant effect on GFR observed. In contrast, frusemide (furosemide) at concentrations of 10 and 100 mumol/l was natriuretic at both 90 and 130 mmHg, with lesser absolute but greater proportional changes being seen at the lower pressure. It was concluded 1) the response of the isolated kidney to ANP is critically dependent on perfusion pressure, 2) at elevated levels of perfusion pressure the isolated kidney can respond to levels of ANP within the upper physiological and pathophysiological range.

scholarly journals Renin stimulating properties of parathyroid hormone-related peptide in the isolated perfused rat kidney

1993 ◽  
Vol 44 (4) ◽  
pp. 764-773 ◽  
Author(s):  
Christian Saussine ◽  
Thierry Massfelder ◽  
Frederique Parnin ◽  
Clement Judes ◽  
Umberto Simeoni ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Rat Kidney ◽  
Isolated Perfused Rat Kidney ◽  
Related Peptide ◽  
Perfused Rat Kidney ◽  
Parathyroid Hormone Related Peptide

Lactate increases potassium secretion by perfused rat kidney

1986 ◽  
Vol 251 (5) ◽  
pp. F873-F878
Author(s):  
M. Brezis ◽  
K. Spokes ◽  
P. Silva ◽  
F. H. Epstein
Keyword(s):  
Rat Kidney ◽  
Distal Tubule ◽  
Fractional Excretion ◽  
Metabolic Inhibitors ◽  
Metabolic Substrates ◽  
Fractional Excretion Of Sodium ◽  
Renal Oxygen Consumption ◽  
Perfused Rat Kidney ◽  
K Secretion

The effect of exogenous metabolic substrates on K+ secretion was evaluated in the isolated perfused rat kidney in the presence of 2-deoxyglucose and 2-tetradecylglycidic acid to inhibit utilization of glucose and fatty acids from endogenous sources. L-Lactate (15 mM) added to the perfusion medium enhanced renal oxygen consumption (4.0 +/- 1.1 mumol X min-1 X g-1 vs. 2.0 +/- 1.0 without lactate) while decreasing fractional excretion of sodium (19.3 +/- 2.4% vs. 47.3 +/- 1.8). L-Lactate markedly increased the fractional excretion of K+ to 181 +/- 29% compared with 68 +/- 12% without lactate (P less than 0.001). The poorly metabolized isomer D-lactate did not alter these parameters. The addition of alpha-ketoglutarate only slightly increased K+ excretion. In the absence of metabolic inhibitors and in the presence of glucose (5 mM), L-lactate also increased K+ excretion significantly more than did D-lactate (108 +/- 19% vs. 69 +/- 11, P less than 0.02). At the end of 90 min of perfusion with L-lactate medium, K+ concentration in the perfusate dropped from 4.7 +/- 0.05 to 3.2 +/- 0.2 meq/liter (vs. 3.8 +/- 0.1 meq/liter with D-lactate, P less than 0.005) without differences in glomerular filtration rate or sodium excretion. L-Lactate appears to increase K+ secretion by preferential metabolic stimulation of the distal tubule, a process that may help in vivo to prevent hyperkalemia in lactic acidosis.

Aldosterone metabolism in isolated perfused rat kidney.

1978 ◽  
Vol 234 (5) ◽  
pp. E472
Author(s):  
H Nakane ◽  
Y Nakane ◽  
G Reach ◽  
P Corvol ◽  
J Menard
Keyword(s):  
Urinary Excretion ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Urine Volume ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Renal Metabolism ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney ◽  
Acid Labile

The renal metabolism and handling of [1,2-3H]aldosterone ([3H]A) was studied using isolated perfused rat kidney under different perfusion conditions. The metabolite production rate (MPR) and the urinary excretion of [3H]A together with its radiometabolites (UV/P3H) were studied. Among the formed metabolites, no acid-labile conjugate of aldosterone (ALC) was detected. The MPR was not altered in studies using nonfiltering kidney, a result that suggests that the majority of metabolites were formed without requirement of the process of glomerular filtration and tubular uptake of the hormone. High perfusion pressure (high PP) resulted in a striking increase in whole metabolic clearance rate of aldosterone (MCR[3H]A) due mostly to an enhanced urinary excretion of intact aldosterone and, to a lesser degree, to a significant increase in MPR. Factors determining the excretion rate of [3H]A and its metabolites were than investigated under administration of diuretics. Mannitol (44 mM) induced a marked increase in urine volume (UV) accompanied by a significant UV/P3H increase. Meanwhile, 0.1 mM furosemide resulted in an increase only in UV, but not in UV/P3H. These results revealed the UV dependence of aldosterone excretion in certain diuretic conditions.

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