Effects of dopamine blockade on renal sodium excretion

1983 ◽  
Vol 245 (2) ◽  
pp. F247-F253 ◽  
Author(s):  
J. C. Pelayo ◽  
R. D. Fildes ◽  
G. M. Eisner ◽  
P. A. Jose
Keyword(s):  
Sodium Excretion ◽  
Dopamine Antagonist ◽  
Single Nephron ◽  
Proximal Tubular ◽  
In Trans ◽  
Series Of Experiments ◽  
Tubular Flow ◽  
Excretion Rates ◽  
A Site ◽  
Renal Responses

The renal responses to a specific dopamine antagonist (cis-flupentixol) and its stereoisomer (trans-flupentixol), a weak dopamine antagonist, were examined during hydropenia and Ringer loading in anesthetized rats. During hydropenia glomerular filtration (GFR), absolute (UNaV), and fractional (FENa) sodium excretion rates were similar as were single-nephron filtration (SNGFR) and proximal tubular flow rate (VTF). After Ringer loading GFR, UNaV, and FENa increased in all groups, but the increments were less in the cis-flupentixol than in the control or trans-flupentixol group. SNGFR and VTF increased similarly in all groups. In another series of experiments Ringer loading was performed prior to drug administration. Perfusion pressure (PP) was decreased in trans-flupentixol rats by aortic constriction to control for cis-flupentixol-induced reduction in PP. UNAV and FENa were lower in the cis-flupentixol- than trans-flupentixol-treated rats at comparable PP and GFR. In conclusion, dopamine blockade attenuated the natriuresis of Ringer loading; the mechanism is uncertain but may be related to a tubular effect at a site beyond the proximal convoluted tubule and/or in deeper nephrons.

Feedback pressure-flow responses in normal and angiotensin-prostaglandin-blocked rats

1984 ◽  
Vol 247 (6) ◽  
pp. F925-F931 ◽  
Author(s):  
A. E. Persson ◽  
L. C. Gushwa ◽  
R. C. Blantz
Keyword(s):  
Flow Rate ◽  
Enzyme Inhibitor ◽  
Tubuloglomerular Feedback ◽  
Maximal Response ◽  
Ang Ii ◽  
Single Nephron ◽  
Proximal Tubular ◽  
Flow Pressure ◽  
Tubular Flow ◽  
Stop Flow

We have examined the response of directly and indirectly (stop-flow) measured glomerular capillary hydrostatic pressure (PGC) and single nephron glomerular filtration rate (SNGFR) to increases in late proximal tubular flow rate in hydropenic rats and rats in which angiotensin II (ANG II) and prostaglandin generation was reduced by 3- to 5-day pretreatment with converting enzyme inhibitor (MK-421) and meclofenamate. In control rats, PGC (48 +/- 2 mmHg) decreased 9 +/- 1 mmHg when 25 nl/min was added to late proximal flow in unobstructed tubules, and PGC decreased 9 +/- 1 mmHg when late proximal perfusion rate was increased from 0 to 40 nl/min, incrementally, in wax-blocked tubules. The turning point or half-maximal response for PGC was at perfusion rates of 23 +/- 2 nl/min. Stop-flow estimated PGC (47 +/- 1 mmHg = control) responses were nearly identical. SNGFR decreased from 30 +/- 1 to 21 +/- 1 nl/min with increased perfusion in control rats. In ANG II-prostaglandin-blocked rats, PGC and stop-flow pressure responses were completely eliminated, yet SNGFR response persisted (36.2 to 28.0 nl/min) but to a somewhat lesser extent. Both direct and indirect PGC decrease with increases in late proximal flow rate in untreated rats. Studies in ANG II-prostaglandin-blocked rats suggest that tubuloglomerular feedback SNGFR responses can occur without changes in PGC, possibly via parallel changes in afferent and efferent arteriolar resistances.

Stimulation by antidiuretic hormone of electrolyte tubular reabsorption in rat kidney

1983 ◽  
Vol 244 (2) ◽  
pp. F156-F164 ◽  
Author(s):  
C. de Rouffignac ◽  
B. Corman ◽  
N. Roinel
Keyword(s):  
Rat Kidney ◽  
Phosphate Transport ◽  
Urinary Flow ◽  
Thick Ascending Limb ◽  
Loop Of Henle ◽  
Proximal Tubular ◽  
Tubular Flow ◽  
Excretion Rates ◽  
In Vivo Administration

The effects of 1-desamino-8-D-arginine vasopressin (dDAVP) on renal excretion and tubular transport of water and electrolytes were investigated in homozygous DI Brattleboro rats. To ascertain these effects on the loop of Henle, circulating glucagon, parathyroid hormone, and thyrocalcitonin were reduced before the experiments, as these hormones are believed to stimulate the same cells of the thick ascending limb as ADH. dDAVP did not alter either glomerular or proximal tubular functions. In the loop, it consistently raised reabsorption of Mg, Ca, K, and, to a lesser extent, Na and Cl, but phosphate transport was not affected. dDAVP lowered the urinary excretion rates for Mg, Ca, K, Cl, and total solutes. For Mg, this reduction was independent of the drop in the urinary flow rate following dDAVP administration but was significantly correlated to this drop in the case of Ca, K, Cl, and total solutes. Na and P excretions were not altered by dDAVP. It is concluded that, in vivo, administration of ADH 1) stimulates reabsorption of Na, Cl, Mg, Ca, and K by the thick ascending limb, 2) consistently enhances Mg reabsorption by the whole kidney by enhancing reabsorption in the loop of Henle, and 3) at maximal antidiuresis, raises Ca, K, Cl, and total solute reabsorption, probably because of the drop in tubular flow rates in the distal parts of the nephron consequent to the hormone administration.

Renal Responses to Vena Caval and Portal Venous Infusions of Sodium Chloride in Unanaesthetized Dogs

1970 ◽  
Vol 39 (1) ◽  
pp. 13-20 ◽  
Author(s):  
S. Potkay ◽  
J. P. Gilmore
Keyword(s):  
Sodium Chloride ◽  
Sodium Excretion ◽  
Sodium Concentration ◽  
Urine Flow ◽  
Routes Of Administration ◽  
Renal Tubular Reabsorption ◽  
Venous Infusion ◽  
Renal Tubular ◽  
Excretion Rates ◽  
Renal Responses

1. Recent investigation has shown that sodium excretion is greater following portal venous infusion of 5% sodium chloride (w/v) than after systemic infusion in anaesthetized dogs. It was suggested that a factor of hepatic origin which is capable of depressing renal tubular reabsorption may be involved in this response. The present experiments were undertaken to determine the renal responses of conscious, unanaesthetized dogs to infusions of 5% NaCl administered systemically and by the portal venous routes. 2. No differences were observed in urine flow or sodium excretion rates in normal dogs when responses to the two routes of NaCl infusion were compared; potassium excretion was elevated following systemic as compared to portal NaCl infusion (P < 0·05). Urine flow was significantly greater (P < 0·05) in vasopressin and mineralocorticoid treated dogs following portal infusion of 5% NaCl, but no differences in electrolyte excretion were observed between routes of administration. 3. These findings are not compatible with the concept that a natriuretic factor is released from the liver consequent to elevation of portal venous sodium concentration in the conscious dog.

scholarly journals R-STIPPLED MAIZE AS A TRANSPOSABLE ELEMENT SYSTEM

Genetics ◽  
1984 ◽  
Vol 107 (3) ◽  
pp. 477-488
Author(s):  
W M Williams ◽  
K V Satyanarayana ◽  
J L Kermicle
Keyword(s):  
Transposable Element ◽  
Pollen Grains ◽  
Linkage Phase ◽  
Element System ◽  
In Trans ◽  
A Site

ABSTRACT The I-R element at the R locus destabilizes kernel pigmentation giving the variegated pattern known as stippled (R-st). In trans linkage phase with R-st the element was shown to act as a modifier of stippled, intensifying seed spotting in parallel with effects of the dominant linked modifier M-st. Presence of I-R in the genome was, therefore, shown to be detectable as a modifier of R-st. When this test was used, new modifiers resembling M-st were often detected following mutations of R-st to the stable allele R-sc. Such mutations evidently occurred by transposition of I-R away from the R locus to a site where it was identifiable as a modifier. M-st may be such a transposed I-R. Analysis of mutations to R-sc during the second (sperm-forming) mitosis in pollen grains showed that some of the transposed I-R elements were linked with R, whereas others assorted independently. Their strengths varied from barely discernible to a level equal to M-st. Overreplication frequently accompanied transposition at the sperm-forming mitosis, leading to transposed I-R elements in both the mutant and nonmutant sperm.

Renal blood flow, early distal sodium, and plasma renin concentrations during osmotic diuresis

2000 ◽  
Vol 279 (4) ◽  
pp. R1268-R1276 ◽  
Author(s):  
Paul P. Leyssac ◽  
Niels-Henrik Holstein-Rathlou ◽  
Ole Skøtt
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Urine Flow ◽  
Sodium Reabsorption ◽  
Osmotic Diuresis ◽  
Nacl Concentration ◽  
Proximal Tubular ◽  
Distal Tubules

Inconsistencies in previous reports regarding changes in early distal NaCl concentration (EDNaCl) and renin secretion during osmotic diuresis motivated our reinvestigation. After intravenous infusion of 10% mannitol, EDNaCl fell from 42.6 to 34.2 mM. Proximal tubular pressure increased by 12.6 mmHg. Urine flow increased 10-fold, and sodium excretion increased by 177%. Plasma renin concentration (PRC) increased by 58%. Renal blood flow and glomerular filtration rate decreased, however end-proximal flow remained unchanged. After a similar volume of hypotonic glucose (152 mM), EDNaClincreased by 3.6 mM, ( P < 0.01) without changes in renal hemodynamics, urine flow, sodium excretion rate, or PRC. Infusion of 300 μmol NaCl in a smaller volume caused EDNaCl to increase by 6.4 mM without significant changes in PRC. Urine flow and sodium excretion increased significantly. There was a significant inverse relationship between superficial nephron EDNaCl and PRC. We conclude that EDNa decreases during osmotic diuresis, suggesting that the increase in PRC was mediated by the macula densa. The results suggest that the natriuresis during osmotic diuresis is a result of impaired sodium reabsorption in distal tubules and collecting ducts.

ANAESTHESIA WITH PENTOBARBITONE BLOCKS THE PROGESTERONE-INDUCED LUTEINIZING HORMONE SURGE IN THE OVARIECTOMIZED RHESUS MONKEY

1982 ◽  
Vol 92 (3) ◽  
pp. 327-339 ◽  
Author(s):  
E. TERASAWA ◽  
J. NOONAN ◽  
W. E. BRIDSON
Keyword(s):  
Pituitary Gland ◽  
Peak Latency ◽  
Single Peak ◽  
First Response ◽  
Sequential Administration ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Series Of Experiments ◽  
Lh Releasing Hormone ◽  
A Site

Although the anterior pituitary gland has been shown to be a site of oestrogen feedback in the non-human primate, the role of the hypothalamus as a site of ovarian steroid feedback in facilitating gonadotrophin release has not been ruled out. In the present study, LH release in response to 2·5 mg progesterone with oestradiol benzoate (OB; 10 μg or 30 μg) 30 h earlier was observed in the ovariectomized monkey. Then pentobarbitone sodium was administered to block the progesterone-induced LH response. Serum levels of LH, oestradiol (OE2) and progesterone were measured by radioimmunoassay. In the first series of experiments a group of nine rhesus monkeys received subcutaneous implants of a small silicone elastomer capsule containing OE2. Two weeks later, either OB and oil, or OB and progesterone were injected sequentially. Oestradiol benzoate (10 μg) followed by oil 30 h later failed to cause any clear LH release, while 30 μg OB followed by oil induced a single peak of LH release with a peak latency of 16·5 ± 1·9 (s.e.m.) h after oil, and a duration of 69·8 ± 10·2 h. Regardless of the dose of OB, however, progesterone induced an LH release with two peaks in all animals. The peak latency (7·3 ±0·9 h) and the duration (19·3 ±1·3 h) of the first response with 30 μg OB + progesterone were virtually identical to those with 10 μg OB + progesterone (7·0 ±0·7 h, 18·0 ± 1·4 h respectively), whilst both components of the first response with 30 μg OB + progesterone were significantly shorter than those with 30 μg OB + oil (P < 0·001 for both). The peak latency of the second response with 30 μg OB + progesterone (42·7+ 4·8 h) was similar to that with 10 μg OB + progesterone (38·3 ±3·2 h), but the duration of the second response with 30 μg OB + progesterone (46·0 ± 1·7 h) was longer than that (35·7 ±3·2 h) with 10 μg OB + progesterone (P <0·02). In the second series of experiments the same nine animals received an OE2-capsule implantation and 10 μg OB (subthreshold) injections before pentobarbitone and progesterone. Pentobarbitone was first given 6 h before progesterone and additional injections were made to maintain the anaesthetized state for 21·6 ± 1·3 h. This period was to cover the progesterone-induced first LH response. Pentobarbitone completely blocked the expected first response of the progesterone-induced LH release in six animals. In the remaining three animals an enhanced LH surge occurred, but it consisted of a single peak with long latency 16·0 ± 2·0 h) and duration (66·0 ± 10·5 h) and was essentially the same as that observed in animals treated with a suprathreshold dose (30 μg) of OB alone. Anaesthesia did not, on the other hand, alter the response of the pituitary gland to LH releasing hormone. Therefore it was concluded that (1) sequential administration of oestrogen and progesterone induces an LH release with two phases in the ovariectomized monkey and (2) the facilitatory action of progesterone on the first phase of LH release requires the involvement of the brain.

scholarly journals Nitric oxide mediates anomalous tubuloglomerular feedback in rats fed high-NaCl diet after subtotal nephrectomy

2019 ◽  
Vol 316 (2) ◽  
pp. F223-F230 ◽  
Author(s):  
Scott C. Thomson
Keyword(s):  
Nitric Oxide ◽  
Tubuloglomerular Feedback ◽  
Cross Term ◽  
Nitric Oxide Signaling ◽  
Subtotal Nephrectomy ◽  
Single Nephron ◽  
Nos Inhibitor ◽  
Tubular Flow ◽  
Fluid Collections ◽  
Distal Delivery

Tubuloglomerular feedback (TGF) responses become anomalous in rats fed high-NaCl diet after subtotal nephrectomy (STN), such that stimulating TGF causes single nephron GFR (SNGFR) to increase rather than decrease. Micropuncture experiments were performed to determine whether this anomaly results from heightened nitric oxide response to distal delivery, which is a known mechanism for resetting TGF, or from connecting tubule TGF (cTGF), which is a novel amiloride-inhibitable system for offsetting TGF responses. Micropuncture was done in Wistar Froemter rats fed high-NaCl diet (HS) for 8–10 days after STN or sham nephrectomy. TGF was manipulated by orthograde microperfusion of Henle’s loop with artificial tubular fluid with or without NOS inhibitor, LNMMA, or the cell-impermeant amiloride analog, benzamil. SNGFR was measured by inulin clearance in tubular fluid collections from the late proximal tubule. TGF responses were quantified as the increase in SNGFR that occurred when the perfusion rate was reduced from 50 to 8 nl/min in STN or 40 to 8 nl/min in sham animals. The baseline TGF response was anomalous in STN HS (−4 ± 3 vs 14 ± 3 nl/min, P < 0.001). TGF response was normalized by perfusing STN nephron with LNMMA (14 ± 3 nl/min, P < 0.005 for ANOVA cross term) but not with benzamil (−3 ± 4 nl/min, P = 0.4 for ANOVA cross term). Anomalous TGF occurs in STN HS due to heightened effect of tubular flow on nitric oxide signaling, which increases to the point of overriding the normal TGF response. There is no role for cTGF in this phenomenon.

Mechanisms of angiotensin II natriuresis and antinatriuresis

1985 ◽  
Vol 249 (2) ◽  
pp. F299-F307 ◽  
Author(s):  
M. E. Olsen ◽  
J. E. Hall ◽  
J. P. Montani ◽  
A. C. Guyton ◽  
H. G. Langford ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Distal Tubule ◽  
Urinary Sodium Excretion ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Sodium Load ◽  
Proximal Tubular ◽  
Anesthetized Dogs

The aim of this study was to determine the role of changes in renal arterial pressure (RAP), renal hemodynamics, and tubular reabsorption in mediating the natriuretic and antinatriuretic actions of angiotensin II (ANG II). In seven anesthetized dogs, endogenous ANG II formation was blocked with captopril, and ANG II was infused intravenously at rates of 5-1,215 ng X kg-1 X min-1 while RAP was either servo-controlled at the preinfusion level or permitted to increase. When RAP was servo-controlled, ANG II infusion at all rates from 5-1,215 ng X kg-1 X min-1 decreased urinary sodium excretion (UNaV) and fractional sodium excretion (FENa) while increasing fractional reabsorption of lithium (FRLi) (an index of proximal tubular fractional sodium reabsorption) and causing no change in calculated distal tubule fractional sodium reabsorption (FRDNa). When RAP was permitted to increase, ANG II infusion rates up to 45 ng X kg-1. min-1 also decreased UNaV and FENa while increasing FRLi and causing no change in FRDNa. However, at 135 ng X kg-1 X min-1 and above, UNaV and FENa increased while FRLi and FRDNa decreased when RAP was allowed to rise, even though renal blood flow and filtration fraction were not substantially different from the values observed when RAP was servo-controlled. Filtered sodium load was slightly higher when RAP was permitted to increase during ANG II infusion compared with when RAP was servo-controlled, although the differences were not statistically significant. Thus, even very large doses of ANG II cause antinatriuresis when RAP is prevented from increasing.(ABSTRACT TRUNCATED AT 250 WORDS)

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