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Biomedical subjects

P U Feig

Publications and source records attributed to P U Feig.

11 recordsLinked to original sources
PubMed1992

Potassium supplementation attenuates experimental hypertensive renal injury.

The long-term roles of dietary sodium and potassium on the renal end-organ damage of hypertension were investigated in Wistar-Kyoto (WKY) and in spontaneously hypertensive (SHR) rats. Eight rats from each strain were maintained since 1 month of age on one of four dietary combinations of either low (0.4%) or high (6.0%) NaCl and low (0.51%) or high (7.6%) KCl providing sodium/potassium molar ratios of 1:1, 1:15, 15:1, and 15:15, respectively. Urinary sodium/potassium excretion ratios confirmed the proportion of salts consumed. Systolic blood pressures (SBP) were similar at 5 months of age and at the completion of the study at 9.5 months; SBP was significantly higher in SHR than in WKY rats and was not attenuated by dietary potassium supplementation of a magnitude that raised plasma potassium concentrations. Albumin excretion rate (AER) was also higher in SHR than in WKY rats (P less than 0.0001). In SHR, AER rose further with high sodium intake (P less than 0.035) but, contrary to SBP, was ameliorated by an equimolar addition of potassium (P less than 0.01). Morphologic lesions were generally absent in WKY rats and were more common in SHR as a group (P less than 0.001). In all four SHR groups, the graded histopathologic injury correlated well with measured AER but a major improvement in hypertensive renal lesions occurred largely in the KCl-supplemented, salt-loaded SHR group. These results show a disassociation between the effects of dietary monovalent cations on the level of SBP and their effect on renal injury. Sodium aggravates renal injury and potassium protects against this renal effect of sodium independent of SBP effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Albuminuria↗
PubMed1991

Inverse changes in erythroid cell volume and number regulate the hematocrit in newborn genetically hypertensive rats.

Erythrocytosis and microcytosis have been described in strains of genetically hypertensive rats and in essentially hypertensive humans. Published discussion of these phenomena has centered around their relationship to observed alterations in ionic transport and the pathogenesis of hypertension. In presenting data for another strain of spontaneously hypertensive rats in which these findings are exhibited, we note that erythroid cell size decreases concurrently with the increase in cell numbers so that the hematocrit and the mean corpuscular hemoglobin concentration remain constant. Data from the literature support the hypothesis that erythroid cell size is inversely proportional to cell count in a large number of species. Erythrocytosis, as it develops in the neonatal rat, is a consequence of the marked immaturity of this species at birth. Erythrocytosis in the spontaneously hypertensive rat is not due to a difference in the affinity of its hemoglobin for oxygen or to significant tissue anorexia. Microcytosis in the spontaneously hypertensive rat is the consequence of a continuation of the linear volume decrease with age of its erythroid cells seen in the normotensive animals and may be accounted for by the production of smaller cells with concomitant regulation of individual cell volume.

Age Factors↗
PubMed1990

Increased platelet membrane sodium-proton exchange rate in spontaneously hypertensive rats.

It has been proposed that increased Na-H exchange activity is involved in the pathophysiology of genetic hypertension. We studied platelets of spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto (WKY), and domestic Wistar rats (DWR), since platelets have similarities to smooth muscle cells and have been shown to have potentially related ion metabolism abnormalities, such as increased intracellular calcium activity. We determined the exchange rate by the intracellular acidification-dependent, extracellular sodium-dependent volume increase. The rate of increase during the first 3 min is linear and is shown to be higher in SHR (0.475 X min-1) than in WKY (0.410 X min-1) or DWR (0.389 X min-1). We conclude that the Na-H activity is increased in platelets of SHR. Similar findings in lymphocytes and neutrophils of SHR, and analogous findings in platelets of humans with essential hypertension, suggest that this abnormality is expressed by several cell types, some of which may be involved in the pathophysiology of genetic hypertension in both rats and humans.

Animals↗
PubMed1979

Disposition of intravenous potassium in anuric man: a kinetic analysis.

The disposition of a constant-rate (0.3 mEq/kg/hr) intravenous potassium load was studied in anuric, chronic hemodialysis patients. Changes in plasma potassium concentration could be adequately described by a two-compartment kinetic model under both isohydric conditions and during acute metabolic alkalosis. From 63 to 92% of the infused potassium left the extracellular fluid (ECF) in isohydric studies, and from 73 to 97% left the ECF in alkalanizing studies. Cellular uptake of the infused potassium was less when the plasma potassium concentration was higher. Plasma aldosterone levels rose but insulin levels did not increase during infusions. In a juvenile-onset diabetic subject, the impairment of cellular potassium uptake at higher plasma potassium was magnified so that infused potassium was virtually confined to the ECF compartment until exogenous insulin was given. This implies a permissive rather than a regulatory role for endogenous insulin in facilitating cellular entry of excess potassium.

Anuria↗
PubMed1977

Dependence of the driving force of the sodium pump on rate of transport.

The driving force for active transport of Na+ in the isolated toad bladder, ENa, was measured as the reciprocal slope of the change in conductance with change in short-circuit current after stimulation with antidiuretic hormone. The base-line short-circuit current was altered by change in ambient Na+ concentration or addition of amiloride, maneuvers which alter availability of Na+ at the site of active transport. In the absence of a chemical gradient for Na+ across the bladder, ENa was found to be inversely related to the rate of Na+ transport, a finding incompatible with the simple electrical analogue that has been proposed for the system. The results provide additional support for the view that ENa measured in this way has both energetic and kinetic components.

Amiloride↗
PubMed1976

Vasculitis with urticaria, hypocomplementemia, and multiple system involvement.

A patient with cutaneous necrotizing vasculitis had chronic urticaria associated with multiple system involvement including arthralgias, glomerulonephritis, myositis, pseudotumor cerebri, and adenopathy. Persistent hypocomplementemia is noted with classic pathway activation. The syndrome recognized in this patient and those few individuals reported previously seems to constitute a distinct category of collagen-vascular disease.

Adult↗