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Biomedical subjects

H G Preuss

Publications and source records attributed to H G Preuss.

At least 55 records · Page 3Linked to original sources
PubMed1993

A review of persistent, low-grade lead challenge: neurological and cardiovascular consequences.

Although acute toxicity following heavy intake of lead (Pb) is a well-established clinical entity, the harmful effects of persistent, low-dose challenge, a situation commonly found among the general population, is uncertain. The major dangers of persistent, low-dose challenge that have been hypothesized are controversial: first, mentation and behavioral perturbations and second, development of hypertension with its consequences on the cardiovascular system. Accordingly, one cannot exclude some contributions from persistent Pb exposure to chronic disease and the aging process. Despite these potential adversities, many sources for Pb contact still remain with us. Current estimates are that 10-50% of American children (over 3-4 million) harbor unsafe levels according to present-day standards. Therefore, it is reasonable to conclude that more work is needed in this area. Clearcut evidence concerning the deleterious influence of Pb on the nervous and/or cardiovascular-renal systems would lead to greater attempt to lessen exposure, to ameliorate symptomatology by providing supplemental agents which obviate the unwanted effects of Pb (iron, calcium, zinc), and to consider therapy with binding agents, like CaNa2EDTA, in the afflicted.

Animals↗
PubMed1993

Nutrition and diseases of women: cardiovascular disorders.

Studies of prevention, diagnosis, and intervention for coronary heart disease and hypertension have either been conducted largely in men, or gender differences have not always been fully sought. This has added to a general perception that coronary artery disease is basically a male affliction despite the fact that coronary artery disease is the leading cause of death among women, especially elderly women. Many risk factors among women are similar to men, i.e., high blood pressure (BP), elevated serum cholesterol levels, and cigarette smoking; however, women compared to men have greater incidence of diabetes mellitus, congestive heart failure, and hypertension as they become older. The risk of cardiovascular disorders can be reduced by postmenopausal estrogen replacement, exercising sufficiently, and ceasing smoking. In addition, good nutrition, taking into consideration the proper amount and forms of calories, sodium, potassium, calcium, magnesium, and macronutrients to maintain an ideal lipid profile and BP, is helpful in preventing cardiovascular perturbations.

Adult↗
PubMed1993

Comparative nephrotoxicity of tetraplatin and cisplatin in rats.

Cisplatin, a useful therapeutic agent against many forms of cancer, possesses significant nephrotoxicity, necessitating a search for agents with similar therapeutic profiles but with less potential for renal damage. Since tetraplatin, another platinum analog being evaluated in phase I clinical trials, has a favorable therapeutic profile when compared to cisplatin, we examined the comparative nephrotoxicity of tetraplatin and cisplatin in rats when both compounds were administered at equimolar doses. Based on various parameters, we found that tetraplatin was less nephrotoxic. In vivo injections of equimolar doses of tetraplatin caused a much lesser rise in serum urea nitrogen and creatinine when compared to cisplatin. In vitro, renal slice accumulation of 3H-p-aminohippurate and 14C-tetraethylammonium was significantly decreased after cisplatin but not after tetraplatin. Morphological damage in the kidneys was more severe after cisplatin compared to tetraplatin. We conclude through in vivo and in vitro methodology that tetraplatin is significantly less nephrotoxic than cisplatin at comparable therapeutic doses.

Animals↗
PubMed1993

Hypertension: a review with emphasis on therapeutics with ACE inhibitors.

Hypertension, more prevalent with aging, is a major risk factor for cardiovascular disorders. Accordingly, it is important to decrease blood pressure and maintain it in an acceptable range to lessen morbidity and mortality. When nonpharmacological therapy fails, drug therapy should be instituted. The ideal drugs lower blood pressure, have few adverse side effects, and may have additional benefits on coexisting maladies. ACE (angiotensin-converting enzyme) inhibitors are excellent first-line drugs because they have few adverse effects and may have additional benefits on cardiac and renal status. This overview discusses many aspects of hypertension and its therapy, but emphasizes use of ACE inhibitors in the elderly.

Age Factors↗
PubMed1993

Basics of renal anatomy and physiology.

A kidney contains over 1 million functioning units called nephrons. Each nephron is composed of a glomerulus and tubule. The glomerulus acts to filter the blood free of cells and large proteins, producing an ultrafiltrate composed of the other smaller circulating elements. The ultrafiltrate enters the tubule, which is highly specialized at various segments, to produce the final urine by removing substances from the tubular fluid (reabsorption) or adding substances to the tubular fluid (secretion). Filtration, reabsorption, and secretion keep the organism in balance in terms of water, minerals, electrolytes, and hydrogen ion concentration and eliminate the toxic substances produced by the body. The major known hormonal functions of the kidney influence blood pressure, calcium metabolism, and red blood cell production.

Animals↗
PubMed1993

Fundamentals of clinical acid-base evaluation.

The final diagnosis of acid-base perturbations relies on laboratory analyses. The major direct tools of assessment are arterial pH and PCO2 and serum electrolytes. From these values, a diagnosis of metabolic acidosis, respiratory acidosis, metabolic alkalosis, and respiratory alkalosis with or without an excess anionic gap and with or without a proper compensatory response is made.

Acid-Base Imbalance↗
PubMed1993

Assessment of renal function--glomerular and tubular.

The tests most commonly used to estimate the status of renal function via alterations in glomerular filtration rate (GFR) are plasma creatinine concentration (PCr), blood, urea, nitrogen (BUN), and creatinine clearance (CCr). Unfortunately, these tests have some drawbacks. Nevertheless, they are quite useful to clinicians aware of their limitations, especially in many instances when it may be unnecessary or impractical to have precise measurements. Accordingly, serial measurements of PCr, especially when related to simultaneous BUN determinations, or CCr, may suffice. However, the functional status of the kidneys often needs to be corroborated by more precise methods when subtle changes in renal function are detected or when clinically indicated.

Animals↗
PubMed1992

Blood pressure responses to sucrose ingestion in four rat strains.

Among four strains examined, spontaneously hypertensive rats (SHR) show a marked (20 mm Hg, P less than .01) systolic blood pressure elevation (SBP), Sprague-Dawley (SD) and Wistar-Kyoto (WKY) rats developed a moderate elevation (8 mm Hg, P less than .01), and a normotensive Wistar rat (WAM) had a lesser SBP elevation (6 mm Hg, P = NS) after excess sucrose ingestion. The SBP elevations found in SHR were noted at 2 and 4 weeks after starting the dietary treatments. Corresponding with SBP changes, plasma renin activity (PRA), aldosterone, and neuropeptide Y (NPY) concentrations all decreased with the high sucrose-low protein diet compared to the low sucrose-high protein diet, while circulating insulin levels were unchanged. Although norepinephrine (NE) and epinephrine (E) excretion tended to be higher in the rats eating the high sucrose-low protein food, the differences were not statistically significant. The differences in these parameters could influence the SBP in SHR, SD, and WKY, but virtually similar qualitative and quantitative blood and urinary findings were found in WAM, a strain of rat that showed no significantly increased SBP. Removing one kidney increases the CHO-induced SBP response of WKY to levels comparable to those seen in SHR, converting a moderate responder to a highly sensitive one. We conclude that under well-controlled conditions there are obvious differences in the SBP response to the macronutrients in the diets of various rat strains and that SHR possess some intrinsic mechanism(s), most likely associated with renal metabolism, which make this strain more sensitive to refine CHO-induced SBP elevations.

Administration, Oral↗
PubMed1992

High sucrose diets increase blood pressure of both salt-sensitive and salt-resistant rats.

We examined the effects of a diet relatively high in sugar and low in protein content on systolic blood pressure (SBP) in rats with known pressure responses to salt (NaCl) in order to compare "sugar/protein sensitivity" to "salt sensitivity." Dahl salt-sensitive (DSS) and salt-resistant (DSR) rats were fed one of two low salt diets containing either high sugar (sucrose 51.5% w/w)/low protein (14.6% w/w) or low sugar (sucrose 12.5% w/w)/high protein (52.2% w/w) content. After 3 weeks, the DSS ingesting the high sugar diet/low protein diet developed significantly elevated SBP relative to DSR eating the same high sugar/low protein diet and the DSS and DSR consuming the low sugar/high protein diet. After 2 to 3 months, the SBP of DSR eating the high sugar diet began to rise markedly and eventually both DSS and DSR ingesting the high sugar/low protein diet maintained similarly elevated SBP, significantly higher than DSS and DSR ingesting the low sugar/high protein diet. When Fischer 344 rats, a normotensive, salt-resistant rat strain, were fed the high sucrose/low protein diet, SBP also rose significantly into hypertensive ranges over 2 to 3 months. Since the SBP of DSR and Fischer 344 rats are not influenced to any great extent by high salt intake, even after prolonged exposure, the SBP rise associated with the high sugar/low protein diet may be via a mechanism different from salt-induced hypertension. However, it is also possible that the high sugar/low protein diet creates in DSS and DSR the situation responsible for salt induction in DSS.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1991

Development of sugar-induced blood pressure elevation after uninephrectomy in a resistant rat strain.

Certain rat strains acutely increase blood pressure (BP) when given diets high in NaCl. Prior results showed that "salt-sensitive" rat strains, at least the ones studied, also increase BP in response to sugar loading. To examine this relationship further and learn more about the pathogenesis of sucrose-induced BP elevations, we examined the effects of unilateral nephrectomy (uninephrectomy) on sucrose-induced BP changes. The rationale is based upon the findings that renal mass removal sensitizes BP response to salt loading. Over 15 weeks, augmented sugar (sucrose) consumption by Long-Evans (LE) rats did not increase BP markedly compared to rats consuming a diet relatively low in sugar unless uninephrectomy was performed. The differences in BP caused by the high sugar diet in a uninephrectomized rat could not be explained adequately by alterations in catecholamine excretion, plasma renin activity, excesses in blood volume, or the other parameters examined. However, salt-induced hypertension has been attributed to the presence of circulating substances affecting ion transport. Among the dietary groups, there was a significant correlation between the ability of plasma to depress PAH and TEA renal slice uptake and the difference in BP. This is consistent with the presence of a circulating factor affecting cell transport that has its greatest activity in the high sugar-uninephrectomy group of LE rats. We conclude that reducing renal mass potentiates sugar-induced BP elevation similar to salt-induced BP elevation in a normally resistant rat strain, and the rise of BP may be caused by a circulating factor.

Aging↗
PubMed1991

Blood pressure in unilaterally nephrectomized rabbits: a correlation with serum renotropic activity.

Over 40 years ago, Grollman reported that unilateral nephrectomy (UN) in rabbits precipitated hypertension and suggested that liberation of a pressor substance by an ischemic or damaged kidney could not be causative. Because others were unable to corroborate that UN in rabbits led to increased blood pressure (BP), we followed 7 rabbits after UN and 4 rabbits after a sham operation. At 7-10 days postoperatively, BP increased from the baseline average of 83 to an average of 97 mm Hg in the UN rabbits (p less than 0.01). In contrast, BP did not change significantly after sham operation. Measurements of blood chemistries, serum insulin levels and digoxin-like substances showed no significant changes after UN which would explain the BP rise, but plasma renin activity (PRA) rose from 11.4 to 30.3 ng/ml/h, (p less than 0.05). However, similar elevations occurred in sham-operated rabbits that showed no significant change in BP, i.e. 10.6-26.2 ng/ml/h. Measurement of serum renotropic activity after UN, but not after sham operation, also showed a significant elevation above baseline 97.6% (p less than 0.001). The renotropic activity 7-10 days after UN unlike PRA correlated significantly with the changes in BP (r = 0.87, p less than 0.001). We conclude that BP rises after UN in rabbits, confirming Grollman's findings. The correlative rise in BP and serum renotropic activity may play an important role in the BP elevation after UN.

Animals↗
PubMed1991

Effects of canrenone on RRM-sucrose hypertension in WKY.

Ingestion of a diet high in sucrose content by WKY rats having reduced renal mass (RRM) via a unilateral nephrectomy causes a significant elevation of BP--greater than might be expected from either condition alone. The same findings occur whether the added sucrose calories replace protein or fat. The elevated BP differential remained throughout the 6 months of the study. In some ways, these results resemble a well recognized model of hypertension produced by the removal of 70-80% of renal mass plus excess salt consumption (RRM-salt). When the RRM-sucrose WKY were given canrenone, an agent which is a digoxin antagonist, the BP decreased significantly simulating previous findings in RRM-salt. Therefore, like the RRM-salt model, evidence suggests that the RRM-sucrose model is also caused, at least in part, by a digoxin-like factor (DLF).

Animals↗
PubMed1991

Correlation of renal organic anion and cation transport with blood pressure in SHR.

In 1974, we found that sera from SHR suppressed renal PAH transport (PSEBM 145:97, 1974). Since a "natriuretic factor" depresses PAH as well as Na transport, we proposed that "natriuretic factor" was elevated in SHR. Our current investigation amplifies the previous study. On a given day, one spontaneously hypertensive rat (SHR) and one rat from a normotensive strain [Wistar Kyoto (WKY) or Sprague-Dawley (SD]) were examined together. SHR sera compared to WKY/SD sera significantly depress PAH (organic anion) and TEA (organic cation) uptake by rat renal slices. The ability of SHR sera to depress uptake correlated significantly with the BP: the sera with the greatest depressive influence on renal PAH and TEA uptake came from the SHR with the highest BP (PAH r = 0.89, p less than 0.0001; TEA = r = 0.76, p less than 0.01). Subsequent separation of serum on Sephadex 25 localized the factor to the same fraction as "natriuretic hormone". A similar correlation was found between the ability of the fraction to depress the 2 transports and the height of the BP. The serum factor did not inhibit ATPase activity. In contrast to the serum effects, renal slices removed from SHR showed increased rather than decreased PAH and TEA transport which significantly correlated with the BP. The slices with the highest uptakes came from the SHR with the highest BP. The high uptake of organic ions by the SHR renal slices could be an adaptive response to the serum factor or vice versa. We postulate that a serum factor which depresses PAH and TEA transport and is not "ouabain-like" may play a role in the BP elevation of SHR.

Acid-Base Equilibrium↗
PubMed1990

Influence of oat bran on sucrose-induced blood pressure elevations in SHR.

To determine whether oat fiber influences BP, we gave spontaneously hypertensive rats (SHR) a diet high in sucrose and low in protein (calories: sucrose 52%, protein 15%, fat 33%) or a diet low in sucrose and high in protein (calories: sucrose 13%, protein 52%, fat 35%). The amount of fat in these particular diets has not been shown to influence BP, so we modified the 2 diets by replacing fat with oat bran (10% w/w). Accordingly, we examined 4 groups of 5 rats consuming different diets: high sucrose, high sucrose + oat bran, low sucrose, and low sucrose + oat bran. Not unexpectedly, SHR consuming the diet high in sucrose had a significantly higher BP after 2 weeks than those consuming the diet low in sucrose. The significant difference in BP continued over the next 3 weeks. At the end of 6 week duration of study, we found the following BP: SHR ingesting the high sucrose diet, 217 mm Hg +/- 5 (SEM) vs SHR consuming the low sucrose diet, 187 mm Hg +/- 4 (SEM) p less than .0001]. SHR eating the low sucrose diet and consuming supplemental bran showed no significant change in BP after 6 weeks compared to SHR eating the basic diet alone, 188 mm Hg +/- 6 (SEM); however, 5 SHR consuming the high sucrose diet with added oat bran showed a significantly lower BP 200 mm Hg +/- 2 (SEM) than SHR ingesting the basic high sucrose diet devoid of oat bran [p less than .01]. We conclude that addition of oat bran to the diet can ameliorate sucrose-induced BP elevations in SHR.

Analysis of Variance↗
PubMed1990

Effect of sodium and potassium ingestion on renal growth in rats.

To determine whether differences in dietary Na and K intake influence renal growth and compensatory renal growth following unilateral nephrectomy (uni), rats were given 2 diets for 2 weeks which differed only in Na-K concentrations. Diet 1 (High Na, Low K) contained 1.0% Na, 0.36% K and diet 2 (Low Na, High K) contained 0.05% Na, 2.0% K. Half of the rats consuming diets 1 and 2 for 1 week received uni and the other half of sham operation (sham). The rats were followed for another week while consuming the experimental diets. Uni and sham rats on diet 1 showed significant increase in blood pressure (BP) (136 +/- 4 v 126 +/- 3 mm Hg, P less than .05). Uni itself did not alter blood pressure. Body weight and heart rate were unchanged by diet or operation. Kidney weight, renal RNA, protein, RNA/DNA, and protein/DNA increased significantly after uni but the differences were not affected by diet. Serum blood urea nitrogen (BUN) and creatinine were not markedly different among any group of rats suggesting no major renal damage. We conclude that dietary changes of Na-K which cause no obvious renal damage even though BP is elevated moderately do not influence renal growth or compensatory renal growth. Based on RNA, DNA and protein metabolism, the form of growth (hypertrophy or hyperplasia) is also not influenced by renal electrolyte handling.

Analysis of Variance↗
PubMed1990

Excess sucrose and glucose ingestion acutely elevate blood pressure in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) were fed 6 different diets. The baseline diet (I) derived equal calories from sucrose, proteins, and fats. Three other diets (II, III, VI) derived the majority of calories from refined CHO, sucrose or glucose, with decreases in calories from proteins or fats. The last two diets (IV, V) were relatively low in sucrose with a higher percentage of the total calories from proteins and fats, respectively. From 3 to 15 weeks on the diets, the highest average BP was in rats consuming high concentrations of sucrose or glucose (II, III, VI). Urinary excretory rates of norepinephrine (NE) at 5, 10 and 15 weeks and epinephrine at 5 and 10 weeks were significantly elevated in rats ingesting diets high in refined CHO, and NE positively correlated with blood pressure (BP) at 5 and 10 weeks of the study. At the end of the study, serum insulin levels were not different, but plasma renin and serum glucagon levels were lower in SHR consuming the diets with high CHO concentrations. We conclude that equally elevated BP are seen with relatively high intakes of either sucrose or glucose, whether the balance of calories is derived from lessening fat or protein. This is secondary, at least in part, to alterations in NE metabolism.

Animals↗
PubMed1990

Long-term effects of excess sucrose ingestion on three strains of rats.

We placed groups of spontaneously hypertensive rats (SHR), Wistar-Kyoto rats (WKY) and a local strain of normotensive Wistar rats on 5 different diets. Our baseline diet (I) derived a near equal number of calories from sucrose, proteins and fats, ie, 1/3 of total calories was provided by each macronutrient. Two other diets (II,III) derived the majority of calories from sucrose with less calories from proteins or fats respectively. The last two diets (IV,V) were relatively low in sucrose with a higher percentage of the total calories from proteins or fats respectively. The rats were assigned to the special diets at 3 months of age. They have now been ingesting these diets a total of 12 months. In SHR, the diets highest in sucrose calories (II,III), in contrast to diets I,IV and V, were associated with a markedly increased blood pressure (BP) at 3 months. The difference of approximately 20 to 30 mm Hg has held over 12 months. In contrast, the normotensive Wistar rats consuming diets II and III showed significant differences in BP (approximately 10 mm Hg) only after 12 months. The response of WKY was intermediate. Some clearcut elevation of BP, although not statistically significant, in WKY consuming diets II and III was present by 3 months. This difference became greater with time (20 mm Hg at 12 months). Consistent changes in body weights between the rats on the different diets were lacking. We conclude that excess ingestion of sucrose can cause chronic elevations in BP, the pattern of which varies among rat strains.

Analysis of Variance↗