ISSN:1420-4096    

DOI:10.1159/000172918

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

We have tested a hypothesis proposed to explain glomerulotubular balance (GTB) as a consequence of variations in prostaglandin synthesis. Arachidonic acid (40 µg • kg-1 • min-1) infused into the renal artery of anesthetized dogs raised renal blood flow (RBF) by 41 + 5% in hydropenic and by 24 + 11% in volume-expanded dogs, but the absolute changes were similar. The infusion of arachidonic acid after the administration of indomethacin (10 mg·kg-1) had no effect on RBF. Arachidonic acid infusion increased the excretion of sodium and chloride in hydropenic dogs but not after the administration of ethacrynic acid in volume-expanded dogs. During continued infusion of ethacrynic acid, the glomerular filtration rate (GFR) was lowered by suprarenal aortic constriction and raised by carotid constriction. A linear relationship between electrolyte reabsorption and GFR (GTB) was observed when GFR was varied between 20 and 110% of control. GTB and tubular reabsorption at comparable GFR were not significantly altered during arachidonic acid infusion or after indomethacin administration. In all experimental settings, bicarbonate, chloride, and sodium reabsorption were altered in molar ratios of 1:2:3 during variations in GFR. We conclude that GTB is independent of variations in prostaglandin synt

ISSN:1420-4096    

DOI:10.1159/000172919

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Immediately after unilateral nephrectomy, the glomerular filtration rate (GFR) and urinary excretion rate increase in the remaining transplanted rat kidney. In a previous study, we found that GFR in a transplanted kidney was reduced through an activation of the tubuloglomerular feedback control. Excision of the rat’s own remnant kidney then reduced feedback sensitivity and thereby allowed GFR to rise. The present study aimed at investigating whether prostaglandins are involved in this functional adaptation. Clearance and micropuncture experiments were performed before and after administration of indomethacin and after subsequent unilateral nephrectomy. GFR and the urinary excretion rate of electrolytes and water were measured. From proximal tubular stop-flow pressure (PSF) measurements the feedback characteristics were determined as the maximal stop-flow pressure response (ΔPSF) to an increase in distal flow and the turning point (TP), i.e. the end proximal flow rate that caused 50% reduction of ΔPSF. The results showed that following nephrectomy the tubuloglomerular feedback sensitivity was decreased, with an increased TP and reduced ΔPSF. Pretreatment with indomethacin (2 mg/kg BW) prevented not only the change in feedback sensitivity at nephrectomy but also the rise in GFR. These results suggest that the prostaglandins play a possible role as one link in the chain of adaptive events occurring immediately after nephron

ISSN:1420-4096    

DOI:10.1159/000172920

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The present study was done to determine: (1) regional (cortex, red medulla and papilla) changes in ATP, ADP and AMP resulting from periods of ischemia of 30-300 s; (2) whether ischemic changes in adenine nucleotides or lactate were modified by hypertonic saline loading, and (3) whether adenylate kinase activity was present in each region. Ischemia led to changes in all three adenine nucleotides which were characteristic for each region. In cortex, there was a major decrease in ATP, increase in AMP and a small transient increase in ADP. In red medulla there were slower changes in ATP, ADP and AMP. In papilla, ATP decreased slightly and ADP, as opposed to AMP, accumulated. Hypertonic saline loading increased the rate of ATP decrease and AMP accumulation, most markedly in red medulla. Lactate concentration rose similarly in control and hypertonic saline studies. Adenylate kinase activity was found to be present in each region. In conclusion: (1) the rate of change of all three adenine nucleotides differs among the three renal areas studied; (2) increases in renal transport work, associated with hypertonic saline loading, are reflected in an increase in the rate of ATP decay during ischemia; (3) anaerobic metabolism, as indicated by tissue lactate concentration, is not altered by hypertonic saline loading, and (4) the failure of AMP to accumulate in papilla is not due to the absence of adenylate kinase.

ISSN:1420-4096    

DOI:10.1159/000172921

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The role of renal glutamine synthesis for the rapid decrease in renal ammonia-genesis occurring early in the recovery phase (24 h) of metabolic acidosis was studied in rats. L-Methionine-DL-sulfoximine (MSO), an irreversible inhibitor of glutamine synthetase, depressed the renal enzyme activity by 50% but did not impair the recovery from acidosis. Since extrarenal glutamine synthesis was decreased by this manoeuvre with lowering of blood glutamine, an intravenous load of L-glutamine sufficient to elevate blood concentration to 1 mM was superimposed on the MSO treatement. The glutamine load did not increase the ammoniuria. Infusion of glutamine alone to rats recovering from metabolic acidosis for 12–24 h did not change their ammoniuria. In contrast, glutamine administration together with HC1 produced a marked ammoniuric response in rats recovering from acidosis. Conversely, the administration of bicarbonate to chronically acidotic rats acutely depressed renal ammonia production. It is concluded that glutamine synthetase activity is probably not required for recovery from metabolic acidosis, and that the post-acidosis alkaline rebound occurring in the rat may play a direct role in suppressing the ammonia-genie pathway either by drastic reduction in mitochondrial permeability for glutamine or acute inhibition of intramitochondrial deamidation of this amino aci

ISSN:1420-4096    

DOI:10.1159/000172922

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Determinants of glomerular ultrafiltration were studied by micropuncture in clamped kidneys of one-kidney Goldblatt rats (n = 10, mean arterial pressure (MAP) = 183 + 18 (SD) mm Hg) and in control kidneys of unilateral nephrectomized rats (n = 14, MAP = 120 ± 14 mm Hg). Following saralasin infusion, no significant MAP change occurred in either group. Renal perfusion pressure of clamped kidneys (115 ± 13 mm Hg) was not different from MAP in controls. Hydrostatic pressure in glomerular capillaries in clamped kidneys was not different from that in controls (60.9 + 2.1 vs. 61.7 + 3.5 mm Hg). Early proximal flow rate, as a measure for single-nephron GFR, was decreased to 29.5 + 1.5 vs. 36.6 + 4.4 nl/min in controls (p < 0.01). Total renal resistance was increased by 102% in the hypertensive group, mainly due to the stenosis (75%) rather than the renal vasculature (27%). Due to a predominant increase of postglomerular vascular resistance, filtration fraction was increased in clamped kidneys (0.37 + 0.05 vs. 0.34 + 0.06, p < 0.001). Single nephron glomerular plasma flow was decreased to 158 + 23.5 vs. 209 + 45.1 nl/min in controls (p < 0.001). Efferent net ultrafiltration pressure did not differ significantly from zero in either group, i.e. filtration equilibrium was achieved. These results indicate an increased vascular resistance in clamped kidneys, which is caused by a preferential efferent vasocon-striction. This pattern of the vascular bed helps to prevent a further reduction of GFR despite a decrease of blood flo

ISSN:1420-4096    

DOI:10.1159/000172923

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Despite the absence of vasopressin, Brattleboro homozygous (DI) rats concentrate their urine to hypertonic levels when deprived of drinking water. Ultimately this rise in urine osmolality must follow from increased osmolality of the corticopapillary gradient and/or increased osmotic equilibration across the collecting ducts. In this study we examined the concentrations and contents of total solute, urea, and nonurea solute in tissue from cortex to papillary tip of DI rats before and after dehydration for 12, 24, and 48 h. The greatest increase in osmolality occurred during the first 12 h; both urea and nonurea solute concentrations increased, but urea preferentially. From 12 to 48 h there were only small further increases in these concentrations, largely as a result of decreased tissue water content. Osmotic equilibration (reflected by urine/papillary tip osmolality) increased dramatically during dehydration, presumably because of decreased flow rate, attaining full equilibration by 48 h. The rise in urine osmolality during the first 12 h of dehydration was due to increased osmotic equilibration and to the enhanced corticopapillary gradient; urine became more concentrated from 12 to 48 h largely as a result of increased osmotic equilibration.

ISSN:1420-4096    

DOI:10.1159/000172924

出版商:S. Karger AG    

年代:1984

数据来源: Karger