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F H Epstein

Publications and source records attributed to F H Epstein.

At least 145 records · Page 8Linked to original sources
PubMed1985

Surface ultrastructure of the gill arch of the killifish, Fundulus heteroclitus, from seawater and freshwater, with special reference to the morphology of apical crypts of chloride cells.

The surface ultrastructure of the gill arches of the killifish, Fundulus heteroclitus, adapted to seawater or freshwater, was found to be similar to that reported for other euryhaline teleosts. Two rows of gill filaments (about 42 filaments per row) extended posterolaterally, and two rows of gill rakers (about 10 rakers per row) extended anteromedially from each arch. Leaf-like respiratory lamellae protruded along both sides of each filament, from its base to its apex. The distributions, sizes, and numbers of various surface cells and structures were also determined. All surfaces were covered by a mosaic of pavement cells, which measured about 7 X 4 microns and exhibited concentrically arranged surface ridges. Taste buds were especially prominent on the rakers and the pharyngeal surfaces of the first and second gill arches, but were often replaced by horny spines on the third and fourth gill arches. Apical crypts of chloride cells occurred mostly on the surfaces of the gill filaments adjacent to the afferent artery of the filament. In seawater adapted killifish, crypts resembled narrow, deep holes along the borders of adjacent pavement cells, had openings of about 2 microns2, and occurred at a frequency of about 1 per 70 microns2 of surface area. In freshwater fish, the crypts usually had larger openings (about 10 microns2), occurred less frequently (1 per 123 microns2), and exhibited many cellular projections in their interiors. Changes in crypt morphology may be related to the ion transport function of chloride cells.

Adaptation, Physiological↗
PubMed1985

[Coronary heart disease: epidemiologic-genetic aspects].

Coronary heart disease and the risk factors which predispose to it aggregate in families. How much of this clustering of disease is "explained" by the familial resemblance in predisposing factors? The published reports which bear on this question fall into six distinct study designs: prospective studies, persons at high or low risk or persons with and without a positive family history as points of departure, case-control studies, studies of patients who had a coronary angiogram and studies in different ethnic groups. The findings of the 16 investigations reviewed suggest that there are as yet unidentified factors - genetic, environmental or both - which are responsible for familial clustering of coronary heart disease, apart from the three main risk factors (serum lipids, blood pressure, smoking) and diabetes. Future research must put greater emphasis on studies of families rather than individuals and on closer collaboration between epidemiologists and geneticists, in order to fill these gaps in knowledge. It is likely that the individual predisposition to coronary heart disease is due in part to genetic influences which remain to be discovered in the course of such studies. They would help in identifying susceptible person in the population with greater precision than is now possible. The "high-risk strategy" of coronary heart disease prevention will become more efficient as more specific and sensitive tests of disease prediction are developed. In the meantime, preventive programmes must be put into action on the basis of what is already known, on the level of both the high-risk and the community-wide mass strategy.

Coronary Disease↗
PubMed1985

Switzerland's participation in MONICA.

Switzerland is currently participating in the multicenter study "Monitoring of Trends and Determinants in Cardiovascular Disease - MONICA". Incidence of acute myocardial infarction will be studied over a period of ten years in a target population. The results will be compared with changes in medical care and the spread of known risk factors for cardiovascular disease in the population. This paper describes how the different data will be registered in Switzerland and how far the work has progressed up to now.

Adult↗
PubMed1985

Trends in total mortality and mortality from heart disease in 26 countries from 1950 to 1978.

Death rates for total mortality and for non-rheumatic heart disease and hypertension ('heart disease') are described for men and women ages 45-64 in six time periods during 1950-78 for 26 countries. Rates for men in high-rate countries are three times those in low-rate countries. This variation is more striking for men than women. There were marked increases for heart disease in men in most countries, but in 13 countries there was a slowing or reversal of that trend in the 1960's or 1970's or acceleration of an already downward trend. In 22 countries long-term declines for heart disease occurred in women. There was a widening of the north/south gradient in Europe and of the male/female ratio of heart disease mortality. Countries with high heart disease death rates in men had high ratios of heart disease to total death. Other countries experienced a rise in proportionate mortality. In women, proportionate mortality for heart disease remained flat or declined in most countries. In spite of these changes in rates, each country seems to have a range for heart disease mortality that is characteristic of its population and environmental setting so that profound changes in rates do not substantially alter their relative ranking. Our intent is to stimulate the search for reasons why heart disease mortality recently declined in some countries but not in others (already begun in the WHO-sponsored MONICA programme). Our forthcoming monograph on international mortality trends for the major causes of death will be a next step in this process.

Australia↗
PubMed1985

Na-K-Cl cotransport in chloride-transporting epithelia.

The elasmobranch rectal gland has served as a useful model to study features of Na-K-Cl cotransport that are common to many chloride-transporting epithelia. These include: (1) dependence on a Na+ gradient created by Na-K-ATPase; (2) high intracellular Cl- concentration; (3) characteristic inhibitor profile including inhibition by loop diuretics and barium but not by amiloride, SITS, DIDS, or carbonic anhydrase inhibitors; and (4) remarkable energy efficiency of transepithelial transport (25-30 NaCl/l 02). The mechanism by which this is accomplished is clarified by kinetic analysis of experiments with isolated perfused rectal glands of Squalus acanthias in which perfusate concentrations of Na and Cl are systematically varied. These show a Hill coefficient of one for Na+ and two for Cl-, suggesting that one Na+, one K+, and two Cl- interact with the cotransport carrier. Nitrate can substitute for Cl- to some extent, and it itself weakly transported. The loop diuretic bumetanide behaves like a competitive inhibitor of Cl-. The teleological significance of the neutral cotransport of two Cl- with one Na+ and one K+ is that it enables transporting epithelia like the rectal gland, cornea, salivary gland, and thick ascending limb of Henle's loop to double the efficiency of their Na-K-ATPase pump.

Adenosine Triphosphate↗
PubMed1985

Effect of vasoactive intestinal peptide on isolated perfused rat kidney.

Vasoactive intestinal peptide, a polypeptide neurotransmitter, stimulates salt secretion by the mammalian intestine and the rectal gland of the dogfish shark. Because of the recent identification of vasoactive intestinal peptide in renal nerves, the present study was undertaken to investigate its effects on the isolated perfused rat kidney. The addition of vasoactive intestinal peptide to the recirculating perfusate produced a significant increase in urine volume, fractional excretion of sodium, chloride, and potassium, as well as osmolar clearance when compared with control kidneys. These changes associated with addition of vasoactive intestinal peptide occurred without any significant changes in perfusion flow, renal vascular resistance, or inulin clearance. These experiments strongly suggest an action of vasoactive intestinal peptide on renal tubular reabsorption.

Animals↗
PubMed1985

Primary role of volume expansion in stimulation of rectal gland function.

Chloride secretion by the in vivo rectal gland of the shark is stimulated by the intravascular infusion of salt solutions of varying osmolar and sodium concentration. In a cross-perfused and denervated rectal gland, the infusion of a small amount of a hypertonic salt solution raises plasma osmolality but does not increase plasma volume in the donor fish. Under these conditions, rectal gland chloride secretion is not stimulated. A subsequent infusion of isotonic shark Ringer solution increases plasma volume 50%, decreases plasma osmolality, and produces a fourfold increase in chloride secretion and a threefold decrease in vascular resistance within the gland. Both the vasodilatory and secretory responses also follow the infusion of a hypotonic shark Ringer solution. The data further support the hypothesis that the rectal gland of the shark is involved in the regulation of intravascular volume rather than in osmoregulation.

Animals↗
PubMed1985

Mode of action of somatostatin to inhibit secretion by shark rectal gland.

The rectal gland of the spiny dogfish Squalus acanthias is stimulated to secrete chloride by vasoactive intestinal peptide (VIP) in a way that is inhibited by somatostatin. The mechanism of inhibition by somatostatin was studied in isolated perfused rectal glands and separated rectal gland cells. Somatostatin did not alter the specific binding of VIP to rectal gland cells but inhibited their accumulation of adenosine 3',5'-cyclic monophosphate (cAMP) in response to VIP. In isolated perfused glands, somatostatin inhibited the stimulation of secretion produced by VIP, adenosine, and forskolin, as well as by dibutyryl cAMP plus a phosphodiesterase inhibitor. The results support the hypothesis of both a proximal and a distal locus, in the cascade of events leading from adenylate cyclase activation to cellular response, at which somatostatin exerts an inhibitory effect.

Adenosine↗
PubMed1985

Atriopeptin stimulation of rectal gland function in Squalus acanthias.

The rectal gland of the shark plays a significant role in the homeostasis of extracellular volume. Regulation of rectal gland function is under hormonal control, but the precise identity of the humoral mediator is unknown. Atriopeptin stimulates rectal gland chloride secretion in vivo. This stimulation of epithelial transport is accompanied by systemic and local hemodynamic effects. Atriopeptin also stimulates chloride secretion by the in vitro perfused rectal gland, an effect that is not accompanied by hemodynamic changes. Extracts of shark heart, but not muscle, brain, kidney, or intestine, contain a heat-stable trypsin-sensitive substance capable of in vitro stimulation of rectal gland chloride secretion. Electron micrographic analysis reveals multiple neurosecretory-like granules in atrial cardiocytes that are only rarely seen in ventricular cardiocytes. By using the in vitro perfused gland as a biologic assay, serum obtained after extracellular volume expansion reveals the presence of a rectal gland stimulatory factor that is not present in serum before expansion. These results are consistent with the hypothesis that atriopeptin is present in shark cardiocytes and is released during volume expansion. The atriopeptin stimulates rectal gland chloride secretion, providing a negative feedback mechanism for the regulation of extracellular volume.

Animals↗
PubMed1985

Disparate mechanisms for hypoxic cell injury in different nephron segments. Studies in the isolated perfused rat kidney.

Hypoxic injury was evaluated morphologically in the proximal tubule and in the medullary thick ascending limb of isolated rat kidneys perfused for 90 min without O2 or with various metabolic inhibitors. Inhibition of mitochondrial respiration (with rotenone, antimycin, oligomycin) or of intermediary metabolism (with monofluoroacetate, malonate, 2-deoxyglucose) caused reduction in renal oxygen consumption, renal function, and ATP content comparable with those elicited by oxygen deprivation. Metabolic inhibition produced hypoxiclike injury in the first portions of the proximal tubule, S1 and S2 ("clubbing" of microvilli, mitochondrial swelling), and the extent of damage was correlated with the degree of ATP depletion. In the third portion of the proximal tubule, S3, hypoxiclike damage (cytoplasmic edema or fragmentation) occurred most consistently when both aerobic and anaerobic metabolism were inhibited simultaneously. In the medullary thick ascending limb, none of the metabolic or mitochondrial inhibitors used could reproduce the injury of oxygen deprivation. Thus, the proximal tubule and the thick ascending limb have markedly different responses to cellular energy depletion, suggesting disparate mechanisms for hypoxic injury along the nephron.

Adenosine Triphosphate↗
PubMed1985

Compliance with salt restriction as a limiting factor in the primary prevention of hypertension.

It is an important but still unresolved question whether reduction of salt intake in the offspring of hypertensives (a high risk group) prevents the development of the disease. Therefore, 178 offspring (14-26 years old) of hypertensives were enrolled in a 2-year pilot trial aimed mainly at a reduction in salt consumption. For the intervention group (n = 99) a behavioural approach was chosen with extensive counselling by experienced dietitians. The controls (n = 79) received no continuous dietary advice. Both groups showed a small decline in sodium intake over time, but the differences between the two groups were not significant. Division into subgroups with and without sodium reduction revealed no differences in blood pressure. We conclude that the inherent resistance to any change of lifestyle among healthy subjects may require new and more comprehensive motivational approaches.

Adolescent↗
PubMed1984

Impairment of extrarenal potassium disposal by alpha-adrenergic stimulation.

Since beta-adrenergic stimulation enhances extrarenal potassium uptake, we postulated an opposite effect of the alpha-adrenergic nervous system. Seven healthy subjects were given intravenous potassium chloride (0.5 mmol per kilogram of body weight), in the presence and absence of the alpha-agonist phenylephrine. After potassium chloride alone, the potassium level rose to 0.64 +/- 0.03 mmol (mean +/- S.E.M.); phenylephrine augmented the rise (0.93 +/- 0.09 mmol, P less than 0.025) and prolonged it, without changing urinary potassium excretion. Subsequent administration of potassium and phenylephrine together with the alpha-antagonist phentolamine blocked the rise in the potassium level due to phenylephrine and shortened the duration of elevation, again without affecting urinary potassium excretion. No changes in plasma renin and aldosterone levels or in serum insulin concentrations occurred, to account for these findings. Stimulation of alpha-adrenergic receptors impairs extrarenal disposal of an acute potassium load--the opposite effect of beta-adrenergic stimulation. The alpha-adrenergic effect may act to preserve a normal serum potassium level or may contribute to hyperkalemia under certain circumstances, such as vigorous exercise.

Adult↗