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Biomedical subjects

H G Preuss

Publications and source records attributed to H G Preuss.

At least 19 recordsLinked to original sources
PubMed1996

Association of macronutrients and energy intake with hypertension.

Hypertension, a major public health problem, becomes more prevalent during aging. Epidemiological studies suggest that environmental factors such as nutrition may play a major role in blood pressure (BP) regulation. It is generally accepted that obesity and sodium/alcohol consumption are important factors, and many believe that calcium, magnesium and potassium consumption are regulatory as well. Less emphasis has been placed on whether macronutrients influence blood pressure significantly. This review focused on the ability of excess calories and consumption of carbohydrates, fats, and proteins to regulate blood pressure.

Dietary Carbohydrates↗
PubMed1995

Effects of chromium and guar on sugar-induced hypertension in rats.

Ingestion of sugars (sucrose, fructose, glucose) by various rat strains is associated with perturbations in the glucose/insulin system and higher systolic blood pressure (SBP). The association suggests causality, because alterations in insulin metabolism have been found in essential hypertension and many experimental forms of hypertension. To test the hypothesis that sugar-induced SBP elevation is secondary to perturbed insulin metabolism, we examined in 2 experiments effects of chromium and guar, substances known to affect insulin metabolism, on SBP of Spontaneously Hypertensive Rats (SHR). In both studies, sucrose compared to starch ingestion caused significant elevation of SBP; but addition of 2 chromium nicotinate complexes and guar prevented development of sugar-induced SBP elevations. The basal, genetic hypertension of the SHR was not affected by either nutrient. An additional finding in the first study was that sugar-consuming SHR supplemented with chromium had greater BW and increased organ weight (kidney, spleen, and liver) than nonsupplemented SHR. Accordingly, we have shown that two different mechanisms known to ameliorate insulin perturbations, use of chromium and guar, prevent sugar-induced SBP elevations. Since essential hypertension may be due to insulin perturbations and high dose chromium supplementation seems nontoxic, this may prove to be a useful means to lower blood pressure (BP) in some essential hypertensives, as well as diabetic hypertensives. Soluble fiber in the form of guar is also quite effective in favorably influencing sugar-induced SBP elevations.

Animals↗
PubMed1994

Effects of high sugar diets on renal fluid, electrolyte and mineral handling in rats: relationship to blood pressure.

OBJECTIVE: We examined whether sugar-induced systolic blood pressure (SBP) elevations in rats may develop, in part, through a mechanism common to salt-induced hypertension, i.e., renal retention of water and salt. DESIGN: Spontaneously hypertensive rats (SHR) ate four diets: two high (> 50% of calories) and two low (< 12% of calories) in sugar (sucrose). SBP, various urinary parameters, and the renal angiotensin and prostaglandin systems were assessed. RESULTS: SHR consuming diets high in sugar showed significantly decreased urinary volume and excretion of electrolytes, which coincided with increasing SBP. When low sugar diets replaced high sugar diets, SBP and urinary parameters rapidly returned to baseline. SHR received captopril while consuming high sugar diets, and both SBP and urinary parameters assumed baseline values, comparable to ones seen in SHR consuming low sugar diets. A direct angiotensin II receptor antagonist (DuPont 753) did not influence SBP. However, we found decreased PGE2 excretion in SHR consuming excess sugar. CONCLUSIONS: Salt and water retention occur early during sugar-induced hypertension due to reduced renal excretion, consistent with some part in the pathogenesis. The effects of high sugar diets on SBP were not due to angiotensin II inhibition, however, decreased availability of vasodilatory prostaglandins may play a role in the renal events and sugar-induced hypertension in SHR.

Animals↗
PubMed1994

Early lead challenge and subsequent hypertension in Sprague-Dawley rats.

OBJECTIVE: The consequences of chronic, low grade lead (Pb) burden from earlier exposure on development of hypertension (HT) and cardiovascular disease is, at best, controversial, even though many epidemiological studies suggest the possibility. Accordingly, we examined ability of a short-term Pb challenge to cause later developing HT in rats. METHODS: We gave 12 newly weaned Sprague-Dawley rats (SD) a 1% Pb acetate solution to drink for 6 weeks, while 12 control rats drank water. The rats were further subdivided into groups consuming high and low amounts of sugar. All rats were followed for 4 months after cessation of the Pb challenge. RESULTS: Early Pb challenge caused no significant changes in body weight (BW) from controls; however, systolic blood pressures (SBP) of rats initially receiving Pb continued to rise significantly above their respective dietary controls for months after cessation of challenge. While a high sugar diet alone was associated with elevated SBP, high sugar consumers also challenged with Pb had the highest SBP. Protein excretion did not increase, suggesting, along with other evidence, a lack of significant renal damage. CONCLUSIONS: Previous exposure to Pb can cause subsequent chronic elevations in SBP.

Animals↗
PubMed1994

Interplay between sugar and salt on blood pressure in spontaneously hypertensive rats.

Previous experience showed that sucrose ingestion exceeding 50% of total calories consistently increased systolic blood pressure (SBP) in rats, but ingesting 36 or 13% of calories as sucrose did not. In fact, the mean SBP of rats ingesting 36% of calories as sucrose was not different from rats ingesting 13% of calories as sucrose. This was not the case in the present study where the dietary salt content was increased. Adding dietary salt (NaCl) to raise low concentrations of Na (0.14% wt/wt) to higher concentrations (0.80% wt/wt) in diets with 36 and 13% of calories from sucrose significantly elevated SBP in spontaneously hypertensive rats eating both diets, but significantly more in the former. Accordingly, an interplay exists between sugar and salt in SBP regulation, and it is suggested that amounts of sugar characteristically consumed by an average human are capable of increasing BP. Composition of diets, especially with respect to sugar and salt, should be considered when interpreting results from studies on various aspects of hypertension.

Animals↗
PubMed1993

Comparative pharmacological, toxicological and antitumoral evaluation of free and liposome-encapsulated cisplatin in rodents.

The systemic toxicity and efficacy of cisplatin (CDDP) were examined in vitro and in vivo. Procedures were performed before and after the antineoplastic agent was encapsulated into multilamellar liposomes (L-CDDP). In vitro cytotoxicity evaluation in L1210 murine leukaemia and NIH OVCAR human ovarian cancer cells showed IC50 values of 0.14 and 0.05 micrograms/ml with CDDP or L-CDDP, respectively. In vivo, mice injected intravenously with L-CDDP had plasma levels of platinum 4-fold higher than with CDDP. The t1/2 alpha was 2 h and the t1/2 beta exceeded 48 h with L-CDDP; whereas a t1/2 alpha of 15 min and t1/2 beta of 12 h was observed with CDDP. The values of platinum in liver, spleen, kidneys, lungs and heart were substantially higher in L-CDDP-treated compared to CDDP-treated mice. Cytotoxic evaluation of both agents was tested in vitro (murine L1210 leukaemia and NIH OVCAR cell line) and in vivo (male CD2F1 mice). CDDP and L-CDDP showed similar cytotoxicity in tissue culture. At the highest dose given, 12 mg/kg intraperitoneally (i.p.), L-CDDP showed higher antitumour efficacy demonstrated by an increased life span of the mice. The CDDP treatment at the highest dose was lethal to all the tumour bearing mice. The nephrotoxicity in rats (blood urea nitrogen and creatinine evaluation) of L-CDDP administered i.p. was significantly less than with CDDP. In addition, the ability of kidney slices to transport organic anions [para-aminohippurate (PAH)] and consume O2 was substantially decreased in rats treated with free CDDP compared to L-CDDP. Accordingly, the liposomal encapsulation of CDDP attenuates its nephrotoxicity, but allows maintenance of antitumour efficacy and may be a potentially effective modality in clinical settings.

Animals↗
PubMed1993

Rabbit and human renotropin are not epidermal growth factor.

Sera obtained from rabbits and humans after unilateral nephrectomy (uni sera) compared with sera obtained preoperatively (control sera) significantly stimulate 3H-thymidine incorporation into the DNA of cultured renal tissue from the respective species. In contrast, rabbit liver cells in culture are not stimulated by the uni sera compared with control sera obtained from rabbits. Mouse epidermal growth factor (EGF) added to tissue cultures significantly stimulates both kidney and liver cells of rabbits and kidney cells of humans. Antiserum against EGF overcomes, at least to some extent, the enhancing effect of EGF under all circumstances, but does not influence the stimulatory ability of uni serum obtained from rabbit and human kidney cells from the respective species. In addition, the activity of EGF was not different in the presence of uni and control sera. This study corroborates the presence of renotropic activity in the sera of rabbits and humans after removal of functioning renal mass and shows that this activity is not derived from EGF, nor does it work by potentiating some aspect of the EGF system.

Animals↗
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↗