Effect of chronic cardiac denervation on renal response to saline infusion.
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Animals↗
Biomedical subjects
F G Knox
Publications and source records attributed to F G Knox.
Effects of osmotic diuresis on sodium reabsorption and oxygen consumption of kidney.
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Animals↗
Effect of phosphate deprivation on enzymes of the cyclic adenosine monophosphate metabolism in rat proximal convoluted and proximal straight tubules.
Phosphate deprivation causes a resistance to the phosphaturic effect of parathyroid hormone (PTH). The present study determined whether acute phosphate deprivation alters basal or stimulated activities of key enzymes of the cyclic adenosine monophosphate (cAMP) metabolism in microdissected proximal convoluted and proximal straight tubules, since blunted cAMP levels in these proximal subsegments might account for refractoriness to the effect of PTH on phosphate reabsorption in the proximal convoluted and proximal straight tubule segments. In the proximal convoluted tubules of rats fed a normal-phosphate diet (NPD), PTH increased the adenylate cyclase activity by tenfold. In the proximal convoluted tubule of rats fed a low-phosphate diet (LPD), PTH also increased the adenylate cyclase activity by tenfold. In addition, forskolin increased the adenylate cyclase activity to levels similar to PTH in the proximal convoluted tubule of rats fed NPD or LPD. In the proximal straight tubule of rats fed NPD, PTH resulted in an approximately fivefold increase in adenylate cyclase activity. In the proximal straight tubule of rats fed LPD, PTH resulted in a fourfold increase in adenylate cyclase activity. The forskolin-stimulated adenylate cyclase activity was markedly decreased (46%) in the proximal straight tubule of phosphate-deprived rats. The cAMP-phosphodiesterase activity in the proximal convoluted tubule was significantly increased by 26% in phosphate-deprived rats. The cAMP-phosphodiesterase activities in the proximal straight tubules from rats fed NPD or LPD were similar. We conclude that distinct differences in key enzymes of cAMP metabolism exist in the proximal convoluted and proximal straight tubule subsegments. Further, phosphate deprivation affects the cAMP-phosphodiesterase and adenylate cyclase activities differently in these nephron subsegments.(ABSTRACT TRUNCATED AT 250 WORDS)
3',5'-Cyclic-AMP Phosphodiesterases↗
Effect of renal decapsulation on lithium excretion in the presence and absence of volume expansion.
The relationship between fractional sodium excretion (FENa) and fractional lithium excretion (FELi) was determined in Munich-Wistar rats with intact capsules (control, n = 16), and in rats with acute bilateral renal decapsulation (n = 16) during hydropenia and acute saline volume expansion. In response to volume expansion, the glomerular filtration rate increased significantly in both decapsulated and intact groups, but was similar in the two groups of rats at the same period. The FENa and FELi increased significantly from 0.49 +/- 0.10 and 20.09 +/- 1.76% to 1.71 +/- 0.20 and 34.14 +/- 2.82% in control rats with volume expansion. In decapsulated rats, FENa and FELi were 0.17 +/- 0.03 and 11.64 +/- 1.39% during control and increased to 1.04 +/- 0.21 and 26.23 +/- 1.17% during volume expansion. The FELi and FENa were significantly greater in control rats compared with decapsulated rats during both control and volume expansion periods. The lower FELi in bilateral renal decapsulation suggests reduced delivery of sodium from the proximal tubule.
Absorption↗
Isoproterenol infusion increases the maximal tubular capacity of phosphate reabsorption.
Isoproterenol, a beta-adrenoreceptor agonist, decreases urinary phosphate (Pi) excretion; however, plasma phosphate concentration also decreases. The purpose of the present study was to determine the effect of isoproterenol infusion on phosphate reabsorption with concomitant phosphate infusions and in the presence and absence of parathyroid hormone (PTH). Clearance experiments were performed on male Sprague-Dawley rats which were acutely thyroparathyroidectomized (TPTX) and successive infusions of phosphate (1, 2, and 3 mumol/min) were used to determine the maximal tubular capacity of phosphate reabsorption (TmPi) factored for the glomerular filtration rate (GFR) in four groups of rats. In the saline-infused control group the TmPi/GFR was 2.87 +/- 0.19 mumol/ml (n = 8). When isoproterenol was infused intravenously at a rate of 0.005 mg/kg/min, urinary cAMP excretion was significantly increased and the TmPi/GFR was 3.53 +/- 0.17 mumol/ml (n = 10, p less than 0.05). In the PTH-infused group (33 U/kg bolus followed by a sustaining infusion of 1 U/kg/min) TmPi/GFR was 1.69 +/- 0.15 mumol/ml (n = 9). Coadministration of isoproterenol and PTH significantly increased the TmPi/GFR to 3.25 +/- 0.64 mumol/ml (n = 9). Basal cAMP excretion was similar in both groups. These results demonstrate that the stimulation of renal beta-adrenoreceptors by isoproterenol infusion markedly increases phosphate reabsorption and reverses the decrease in the maximal tubular capacity of phosphate reabsorption induced by PTH infusion.
Absorption↗
Effect of furosemide on renal function in the stenotic and contralateral kidneys of patients with renovascular hypertension.
In a group of six patients diagnosed as having unilateral renovascular hypertension due to fibromuscular dysplasia, inulin glomerular filtration rate, (GFR) and PAH renal plasma flow, (RPF) clearances, urine flow (V), urine sodium (UVNa), potassium (UVK), urinary excretion of prostaglandin E2 (UVPGE2), thromboxane B2 (UVTxB2), and 6-keto prostaglandin F1 alpha (UVPGF1 alpha) were measured in each kidney before and after the i.v. administration of furosemide (20 mg). The basal values of GFR, RPF, UVNa, UVPGE2, UVTxB2, and UV6-keto-PGF1 alpha were lower (p less than 0.01) in the stenotic kidney. Furosemide increased RPF 11% and 50%, GFR 25% and 62%, and V 142% and 280% in the contralateral and stenotic kidney respectively. The increase of UVNa was similar in the two kidneys. In the stenotic kidney, both UVPGE2 and UV6-keto-PGF1 alpha increased significantly (p less than 0.01) with furosemide while UVTxB2 remained unchanged. Furosemide did not alter the rate of excretion of the three prostaglandins measured in the contralateral kidney. We conclude that furosemide significantly improves renal circulatory and excretory function of the stenotic kidney. Since prostaglandin excretions also increased, the vasodilatation in the stenotic kidney may be prostaglandin mediated.
Adult↗