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T F Ferris

Publications and source records attributed to T F Ferris.

At least 55 records · Page 3Linked to original sources
PubMed1975

Potassium transport in the distal tubule and collecting duct of the rat.

Because of recent conflicting results, micropuncture studies were performed to clarify the respective role of the distal convoluted tubule and collecting duct in the regulation of urinary potassium excretion. Five groups of Sprague-Dawley rats were studied: group I, hydropenia (n = 10); group II, Ringer loading (n = 7); group III, acute KC1 loading (n = 6); group IV, mannitol diuresis (n = 6); group V, KC1 infusion during mannitol diuresis (n = 7). Early and late distal tubules were identified with intravenous injections of lissamine green. In each animal net secretion of potassium occurred along the distal convoluted tubule, and a direct relationship between distal tubular flow rate and potassium secretion was observed. The magnitude of potassium secretion at high distal tubular flow rates was dependent on the model studied. Potassium transport beyond the distal tubule was evaluated by comparing end distal potassium delivery and fractional potassium excretion. At low urinary flow rates net reabsorption was observed, whereas at higher flow rates no net transport occurred. Thus, flow rate along the collecting duct may be a major determinant of urinary potassium excretion.

Animals↗
PubMed1975

Renin and the kidney.

The factors involved in renin release have been extensively evaluated. The primary determinants are the transmural pressure at the afferent arteriole, sodium delivery to the macula densa, and the activity of the adrenergic nervous system. Other possible factors include circulating catecholamines, the serum and cerebrospinal fluid sodium concentration, serum potassium concentration, angiotensin II concentration, and antidiuretic hormone release. There is no convincing evidence that the renin-angiotensin system mediates renal autoregulation. Plasma renin activity is altered in a number of clinical settings. This parameter is elevated in most patients with cirrhosis and the nephrotic syndrome as well as in individuals with severe congestive heart failure. Despite inappropriately large weight gains, plasma renin suppresses normally with increased salt intake in edematous patients who have a normal glomerular filtration rate. The mechanisms of the alteration in the renin-angiotensin system in Bartter's syndrome is still not clear.

Angiotensin II↗
PubMed1975

Role of the collecting duct in the regulation of sodium balance.

A large body of evidence has accumulated which demonstrates that sodium transport in some distal nephron segment is altered in response to changes in extracellular fluid volume. Sodium reabsorption in the loop of Henle and distal tubule is directly related to delivery rate and is not inhibited by volume expansion. In contrast, recent studies have shown that Ringer loading causes a greater natriuretic response than hyperoncotic albumin because of diminished collecting duct sodium transport in the former model. Additional studies in animals with different basal extracellular fluid volumes and in DOCA-escape rats indicate further that the collecting duct is an important regulator of sodium balance. Although the factors that modulate sodium transport in the collecting duct are not clear, it is postulated that the local release of prostaglandins may be of major importance.

Albumins↗
PubMed1975

Uterine prostaglandin E secretion and uterine blood flow in the pregnant rabbit.

Studies were performed in pregnant rabbits to assess the effect of inhibition of prostaglandin synthesis on uterine blood flow. Cardiac output and uteroplacental blood flow (UPBF) were measured using radiolabeled microspheres. Prostaglandin E (PGE) concentration was measured by radioimmunoassay in the uterine vein and peripheral artery of the pregnant nephrectomized rabbit. Either meclofenamate or indomethacin 2 mg/kg were utilized to inhibit prostaglandin synthesis. Systemic arterial pressure increased from 86 mm Hg to 98 mm Hg (P less than0.0001) after prostaglandin inhibition. Cardiac output was unchanged after the inhibition of prostaglandin synthesis, 326 ml/min to 7.8 ml/min. Uterine vein PGE concentration was extremely high, 172.4 ng/ml, with concomitant peripheral arterial PGE 2.1 NG/ML. Intravenous administration of either meclofenamate or indomethacin reduced uterine vein PGE to 23 ng/ml (P less than 0.01) and arterial PGE to 1.0 ng/ml (P less than 0.05). Male and nonpregnant female rabbits had lower arterial PGE, 0.37 ng/ml (P less 0.05). Studies in non-nephrectomized pregnant animals demonstrated that uteroplacental secretion of PGE was greater than five times renal secretion. These studies demonstrate that the rabbit uteroplacental unit is a rich source of PGE and suggest that production of the vasoactive lipid may have a key role in regulating UPBF during pregnancy.

Animals↗
PubMed1975

The measurement of nephron filtration rate and absolute reabsorption in the proximal tubule of the rabbit kidney.

Micropuncture studies were performed in the rabbit to determine nephron filtration rate and absolute fluid reabsorption in the proximal tubule in order to compare the latter value with data obtained with the in vitro microperfusion technique. New Zealand white rabbits, 2-2.8 kg, were studied. Nephron filtration rate was 21 nl/min (n equal to 48) and absolute reabsorption along the length of the accesible portion of the proximal convoluted tubule was 10.3 nl/min. Correcting this value for tubular length gives a fluid reabsorption of approximately 1.9 nl/mm per min. In view of the marked difference between the in vivo and in vitro techniques and the various sources of error with each, this is reasonably similiar to the value of 1.3 nl/mm per min obtained in the isolated proximal convoluted tubule.

Animals↗
PubMed1974

Studies of the mechanism of oliguria in a model of unilateral acute renal failure.

To further evaluate the mechanism of the oliguria of acute renal failure, a model was utilized in which intense and prolonged vasoconstriction produced the unilateral cessation of urine flow. The radioactive microsphere method was used to measure total and regional blood flow before and after the intrarenal infusion of norepinephrine, 0.75 mug/kg/min, for 2 h in the dog. In the control kidney, renal blood flow increased 32% 48 h after norepinephrine in association with a fall in the fractional distribution of flow to the outer cortex. In the experimental kidney, total renal blood flow fell from 190 ml/min before norepinephrine to 116 ml/min at 48 h (P < 0.025) with a uniform reduction in cortical blood flow. After the administration of 10% body wt Ringer's solution, there was a marked redistribution of flow to inner cortical nephrons in both the control and experimental kidney. In addition, there was a marked increase in total blood flow in both kidneys. On the experimental side, flow rose to 235 ml/min, a value greater than in either the control period (P < 0.05) or at 48 h after norepinephrine (P < 0.001). However, in spite of this marked increase in blood flow, there was essentially no urine flow from the experimental kidney. In separate studies, the animals were prepared for micropuncture. In all studies, the surface tubules were collapsed, and there was no evidence of tubular obstruction or leakage of filtrate. Over 99% of the 15-muM spheres were extracted in one pass through the experimental kidney. An analysis of the forces affecting filtration suggested that an alteration in the ultrafiltration coefficient may be responsible, at least in part, for the anuria in this model. In this regard, transmission and scanning electron microscopy revealed a marked abnormality in the epithelial structure of the glomerulus. It is suggested that a decrease in glomerular capillary permeability may be present in this model of acute renal failure.

Acute Kidney Injury↗
PubMed1973

Mechanism of the redistribution of renal cortical blood flow during hemorrhagic hypotension in the dog.

Studies were performed to define the mechanisms involved in the redistribution of renal cortical blood flow to inner cortical nephrons which occurs during hemorrhagic hypotension in the dog. The radioactive microsphere method was utilized to measure regional blood flow in the renal cortex. Renal nerve stimulation decreased renal blood flow 40% but had no effect on the fractional distribution of cortical blood flow. Pretreatment with phenoxybenzamine, phentolamine, propranolol, or atropine did not alter the redistribution of cortical flow during hemorrhage. A reduction in renal perfusion pressure by aortic constriction caused a qualitatively similar alteration in regional blood flow distribution as occurred during hemorrhage. When perfusion pressure was kept constant in one kidney by aortic constriction followed by hemorrhage, no redistribution occurred in the kidney with a constant perfusion pressure while the contralateral kidney with the normal perfusion pressure before hemorrhage had a marked increase in the fractional distribution of cortical flow to inner cortical nephrons. Additionally, retransfusion had no effect on the fractional distribution of flow in the kidney in which perfusion pressure was maintained at the same level as during hemorrhage while in the contralateral kidney in which pressure increased to normal there was a redistribution of flow to outer cortical nephrons. These studies indicate that the redistribution of renal cortical blood flow which occurs during hemorrhage is not related to changes in adrenergic activity but rather to the intrarenal alterations which attend a diminution in perfusion pressure.

Animals↗
PubMed1973

A comparison of the segmental analysis of sodium reabsorption during Ringer's and hyperoncotic albumin infusion in the rat.

Studies were designed to compare the segmental analysis of sodium reabsorption along the nephron during volume expansion with either 10% body weight Ringer's or 0.6% body weight hyperoncotic albumin. Total kidney and nephron glomerular filtration rate increased similarly with both, but urinary sodium excretion (12.7 vs. 4.0 mueq/min, P < 0.001) and fractional sodium excretion (5.0 vs. 1.6%, P < 0.001) increased to a greater extent with Ringer's. Fractional reabsorption of sodium in the proximal tubule was diminished in both groups but to a significantly greater extent during Ringer's (P < 0.005). Absolute reabsorption was inhibited only in the Ringer's group. Delivery of filtrate out of the proximal tubule was greater in the Ringer's studies, 45 vs. 37 nl/min (P < 0.001). However, both fractional and absolute sodium delivery to the early and late distal tubule were not significantly different in the two groups. Fractional reabsorption in the collecting duct decreased from 96% in hydropenia to 31% during Ringer's but fell only slightly to 80% in the albumin studies. Absolute collecting duct reabsorption was also greater in the albumin studies, 0.55 vs. 0.21 neq/min (P < 0.001), which could totally account for the difference in urinary sodium excretion between the two groups. (22)Na recovery in the final urine after end distal microinjections was 71% during Ringer's infusion and 34% during albumin (P < 0.001). From these data we conclude that: (a) Ringer's solution has a greater inhibitory effect on proximal tubular sodium reabsorption, and (b) in spite of this effect, differences in mucosal to serosal collecting duct sodium transport are primarily responsible for the greater natriuresis during Ringer's infusion.

Albumins↗