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T F Ferris

Publications and source records attributed to T F Ferris.

At least 73 records · Page 4Linked to original sources
PubMed1972

The effect of bradykinin on proximal tubular sodium reabsorption in the dog: evidence for functional nephron heterogeneity.

In a previous study we have found that acetylcholine, a renal vasodilator, inhibits fractional and absolute reabsorption of sodium in the proximal tubule of the dog. To delineate whether this effect on proximal tubular sodium reabsorption was related to alterations in renal hemodynamics or to a direct tubular action of the drug, free-flow micropuncture studies were performed in the dog in which the tubular fluid to plasma inulin ratio and nephron filtration rate were determined before and during the administration of a structurally different renal vasodilator, bradykinin. This agent increased sodium excretion from 12 to 96 muEq/min and decreased total kidney filtration fraction from 0.35 to 0.25. However, sodium reabsorption in the proximal tubule of the superficial nephrons was unchanged during bradykinin administration. Since it has been shown that a decrease in filtration fraction and presumably peritubular capillary protein concentration will decrease proximal tubular sodium reabsorption, studies were performed to determine whether the fall in total kidney filtration fraction seen with both vasodilators is paralleled by a similar change in the circulation of superficial nephrons. The results of these studies indicate that neither agent altered superficial nephron capillary protein concentration, hematocrit, or filtration fraction. In contrast, a decrease in capillary protein concentration, hematocrit, and filtration fraction was consistently demonstrated during the intrarenal infusion of 7.5-15 ml/min of Ringer's solution while an increase in these parameters occurred during the i.v. administration of norepinephrine, 60 mug/min. In the Ringer's infusion studies, both fractional and absolute sodium reabsorption in the proximal tubule were decreased concomitant with the fall in capillary protein concentration and hematocrit. THIS DATA SUGGESTS THAT: (a) the hemodynamic effect of renal vasodilatation is not the same in the circulation of all nephrons; (b) the inhibitory effect of acetylcholine on proximal tubular sodium reabsorption is due to a direct tubular action; (c) a decrease in capillary protein concentration and/or hematocrit does decrease proximal tubular sodium reabsorption; (d) although proximal reabsorption of sodium is unchanged in the superficial nephrons during bradykinin administration, a decrease in reabsorption may be present in deeper nephrons in which filtration fraction is decreased.

Absorption↗
PubMed1972

Uterine blood flow and uterine renin secretion.

Experiments were carried out in pregnant nephrectomized rabbits to determine the relationship between uterine blood flow and uterine renin secretion. Uterine blood flow was measured by the percentage distribution of radioactive microspheres injected into the left ventricle which lodged in uterus and placenta, and cardiac output was measured by dye dilution. In 40 animals, 24 hr after nephrectomy, uterine blood flow was 4.7+/-0.4% of cardiac output and absolute flow 32.4+/-3 ml/100 g per min. Plasma renin activity (PRA) in uterine vein, 994+/-182 ng/100 ml per hr, was higher than in carotid artery, 832+/-143 (P < 0.025). With reduction of uterine blood flow from 4.7+/-0.5 to 1.95+/-0.3% of cardiac output and absolute flow from 30.8+/-4.6 to 8.8+/-2 ml/100 g per min, uterine vein PRA rose from 1434+/-234 to 4430+/-300 (P < 0.001), and carotid artery PRA from 1009+/-200 to 2300+/-350 (P < 0.01). Hemorrhagic hypotension caused uterine vein PRA to increase from 913+/-293 to 3638+/-1276 (P < 0.001) and carotid artery PRA from 774+/-252 to 1730+/-433 (P < 0.01). Uterine blood flow expressed as a percentage of cardiac output remained constant after hemorrhage, 5.5+/-0.9 and 6.3+/-0.8%, although absolute flow fell from 37+/-7.7 to 29+/-3.6 ml/100 g per min because of the large fall in cardiac output which occurred.Angiotensin, 10 ng/kg per min, caused no significant change in blood pressure or cardiac output but increased uterine blood flow from 4.1+/-0.6 to 8.4+/-1% (P < 0.005) of cardiac output with absolute flow increasing from 37.4+/-7 to 73.2+/-10 ml/100 g per min (P < 0.001). The increase in uterine blood flow during angiotensin was abolished by the prior administration of propranolol. Isoproterenol, 0.5 mu/min, increased uterine blood flow from 3.5+/-0.6 to 6.4+/-1.2% of cardiac output (P < 0.02) with absolute flow increasing from 25+/-5 to 51+/-12 ml/100 g per min (P < 0.05). Norepinephrine, 500 ng/min, caused no significant change in uterine blood flow. These findings suggest that uterine renin might be involved in regulating uterine blood flow, secretion being increased in response to a reduction in flow with the resultant rise in circulating or local angiotensin, through beta adrenergic stimulation, increasing uterine blood flow.

Angiotensin II↗
PubMed1971

Effect of renal vasodilatation on the distribution of cortical blood flow in the kidney of the dog.

Studies were performed to evaluate the validity of using the radioactive microsphere technique to measure regional blood flow in the renal cortex. A technique was developed in which the renal cortex was divided into four equal zones, and the fractional and absolute distribution of blood flow in these zones was determined. It was consistently found that approximately 70% of the renal blood flow was distributed to the two outer cortical zones with the remaining 30% going to the two inner cortical zones. In addition, there was a reproducible pattern of distribution of blood flow in different areas of the same kidney after a single injection of microspheres and in the same area of the kidney after multiple injections of microspheres. Using this method, the distribution of renal blood flow was determined before and during the intrarenal administration of either acetylcholine (40 mug/min) or bradykinin (5 mug/min). Both agents decreased the per cent of blood flow to outer cortical zone 1, caused no change in zone 2, and increased the fractional blood flow in inner cortical zones 3 and 4. When this data was evaluated in terms of total blood flow, there was no change in zone 1, an increase in zone 2 commensurate with the change in total blood flow, and a marked increase in inner cortical zones 3 and 4 which accounted for 60 and 65% of the increase in total blood flow during acetylcholine and bradykinin administration, respectively.Therefore, the natriuresis of renal vasodilatation is associated with a redistribution to inner cortical nephrons.

Acetylcholine↗
PubMed1969

Toxemia of pregnancy in sheep: a clinical, physiological, and pathological study.

Toxemia was induced in 13 of 20 pregnant ewes by the stress of a change in environment and food deprivation late in pregnancy. Of the toxemic ewes, eight developed prominent neurological findings with convulsions, motor weakness, and blindness, whereas five ewes developed azotemia without neurological signs. Proteinuria and azotemia occurred in all but one of the toxemic animals. Seven animals did not develop clinical or laboratory evidence of toxemia. Hypertension did not occur with the onset of toxemia but all toxemic animals showed glomerular changes by light and electron microscopy. These abnormalities, which were similar to those seen in human preeclampsia, included endothelial cell swelling, focal reduplication of the basement membrane, and fusion of the epithelial cell foot processes. The toxemia could not be attributed to changes in hematocrit, plasma glucose, Na, Cl, CO(2), K, Ca, fibrinogen, arterial pH, lactate, or pyruvate concentrations. Cardiac output fell only in ewes with prominent neurological signs. Plasma renin rose strikingly in animals developing toxemia, without change in substrate concentration. In contrast to human and other species, sheep uterus and amniotic fluid contained no detectable quantities of renin. Thus in response to stress the pregnant ewe develops a toxemia which in the absence of hypertension has clinical and pathological similarities to human preeclampsia.

Adrenal Glands↗