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Biomedical subjects

F C Luft

Publications and source records attributed to F C Luft.

At least 415 records · Page 23Linked to original sources
PubMed1990

Effect of hypertension and type II diabetes on renal function in an urban population.

End-stage renal disease is a devastating complication of essential hypertension and type II diabetes mellitus, conditions that commonly occur together. We and others have previously suggested that the outcome of both conditions may be influenced by more aggressive treatment. We examined a large general medicine outpatient population; 72% were black and 41% were diabetic (95% type II). Decreased renal function, defined as a serum creatinine greater than or equal to mg/dL, developed in 18.1%. A multivariable logistic regression analysis identified glucose control, systolic blood pressure level, and male gender as indicators of decreased renal function. These data suggested that both glucose and blood pressure control may decrease the frequency of impaired renal function. However, when these variables were controlled, blacks still had almost twice the risk for renal dysfunction of whites. The data draw attention to, and elucidate the exceptionally high incidence of renal dysfunction in hypertensive blacks with or without diabetes. Further, they may explain the inordinate numbers of blacks with hypertension requiring dialysis. Prospective trials to test the efficacy of blood pressure and glucose control on the course of renal disease in hypertensive and/or type II diabetic patients are warranted.

Adult↗
PubMed1990

Increased sodium-lithium countertransport in black non-insulin-dependent diabetic hypertensives.

Black hypertensive diabetics have been shown to exhibit elevated intracellular calcium which may stimulate Na/H antiport. Since Na/Li countertransport appears to be a functional mode of Na/H antiport, we measured erythrocyte Na/Li countertransport in nondiabetic normotensive and hypertensive blacks and whites and hypertensive non-insulin-dependent diabetic blacks. Na/Li countertransport was significantly lower in the blacks than in the whites (0.170 +/- 0.017 v 0.230 +/- 0.017 mmol/L/h, P less than .02), but there was no significant difference between the black hypertensives and normotensives. In contrast, black hypertensive diabetics exhibited a significant increase in Na/Li countertransport compared to normotensive and hypertensive nondiabetic blacks (0.252 +/- 0.032 v 0.170 +/- 0.017, P less than .02. Thus, these data indicate that the activity of this antiporter is elevated in black diabetics, possibly further contributing to the development of hypertension in this population.

Adult↗
PubMed1990

Putative mechanism of blood pressure reduction induced by increases in dietary calcium intake.

An increase in dietary calcium intake lowers blood pressure in spontaneously hypertensive rats and in some patients with arterial hypertension. The mechanisms by which this decrease come about are not clear. A membrane-stabilizing effect wrought by an increase in extracellular calcium would appear unlikely, since the increases in extracellular calcium concentration with increased dietary intake are minimal. Calcium regulatory hormones may be the mediators, and a cybernetic framework has been suggested. Striking defects have been reported in the calcium handling and hormonal household of the spontaneously hypertensive rat. However, a clear cut relationship in terms of a hormonal "template" has not yet been identified in prospective experiments. Data have been presented to show that increased calcium intake has a direct effect on regulatory areas in the brain. However, the mechanisms by which such a response would be mediated are entirely unknown. Increased calcium intake may induce natriuresis. It has been suggested that increased calcium intake helps the "salt sensitive"; however, prospective studies to this effect have not been presented. Increased calcium intake may induce phosphaturia. However, the evidence that blood pressure lowering effects are mediated by phosphate depletion are unconvincing. Some evidence suggests that increased calcium intake may influence local regulatory processes which in turn influences cell integrity and growth. At this point, a unifying hypothesis is not available. However, the clues to various possibilities are intriguing.

Animals↗
PubMed1990

Renal and hemodynamic effects of atrial natriuretic peptide in patients with cirrhosis.

The effects of anaritide, a 25-amino-acid synthetic analogue of ANP, were evaluated in 28 patients with cirrhosis complicated by ascites and/or edema. Each patient received two doses of the agent, as well as an infusion of placebo. Six different doses were tested ranging from 0.015-0.300 microgram/kg/min. The infusions lasted for 2 hours and were flanked by both baseline and recovery periods. There was a significant effect of placebo on urinary sodium and chloride excretion rates but no effect on urine flow rate. In response to anaritide, the urine flow rate increased at 0.03, 0.06, 0.075, and 0.100 microgram/kg/min. The sodium and chloride excretion rates increased at all doses except the highest dose. There was no definite effect of anaritide on urinary potassium, calcium, and phosphate excretion rates. There was also no significant effect on creatinine clearance. The mean arterial pressure decreased in response to the 0.060, 0.075, and 0.100 microgram/kg/min doses. In addition, five of the patients receiving the highest dose (0.300 microgram/kg/min) had decreases in their systolic pressures to 90 mm Hg or less. In conclusion, anaritide is natriuretic and diuretic in patients with cirrhosis complicated by ascites and/or edema. Its effect, however, on arterial pressure may limit its therapeutic potential in this patient population.

Atrial Natriuretic Factor↗
PubMed1990

Sodium bicarbonate and sodium chloride: effects on blood pressure and electrolyte homeostasis in normal and hypertensive man.

To test the hypothesis that NaCl and NaHCO3 have divergent effects on blood pressure, we carried out a randomly allocated, placebo-controlled, crossover trial in 10 mildly hypertensive and 10 normal subjects. They ingested a fixed daily basal diet of 60 mmol sodium and chloride, 60 mmol potassium and 14 mmol calcium. After balance was achieved (4 days), the subjects were randomly assigned to drink 3 liters/day of a NaHCO3-containing mineral water (26.2 mmol/l sodium and 33.03 mmol/l HCO3) or a control solution containing equimolar amounts of cations as the chloride salt for 7 days (total daily sodium 138 mmol). All urine was collected. Blood pressure was determined by an automated device. One month later the opposite regimen was followed. NaCl did not influence blood pressure, whereas NaHCO3 decreased systolic blood pressure (by 5 mmHg) in the hypertensive subjects. Both regimens decreased plasma renin activity in the hypertensive subjects but did not consistently influence plasma aldosterone or catecholamines. However, urinary calcium excretion, which was greater in hypertensives than in normotensives, and greater in white than in black subjects, increased consistently with NaCl but not with NaHCO3. The excretion of urate was not influenced by the regimens; however, urate excretion was consistently greater in whites than in blacks. The data show that NaCl increases calcium excretion whereas NaHCO3 does not, even at modest levels of intake. NaCl and NaHCO3 may therefore differ in their effects on blood pressure.

Adult↗
PubMed1989

[The Intersalt study: results and perspectives].

The recently published Intersalt Study comprising 10,079 participants from 52 study centers in 32 countries demonstrated that the simple linear relationship so far postulated for the association between electrolytes and hypertension is history. In addition overweight and alcohol consumption make an independent contribution to the level of individual blood pressures. The study results have to be interpreted carefully in the framework of a differentiated epidemiologic analysis.

Adult↗
PubMed1989

Inverse regulation of alpha-2 and beta-2 adrenoceptors in salt-sensitive hypertension: an hypothesis.

A high salt diet leads to up-regulation of alpha-2 adrenoceptors and down-regulation of beta-2 adrenoceptors in normotensive subjects. Although the increase in blood pressure with a high salt diet is not related to the magnitude of the alpha-2 or beta-2 adrenoceptor changes alone, it is related to the increase in the ratio of the receptor changes (operative alpha/beta adrenoceptor ratio). An increase in the operative alpha/beta adrenoceptor ratio with a high salt intake results in vasoconstriction and reduced vasodilatation at resistance vessels, as well as increased renal proximal tubular sodium reabsorption. An influence of heredity on this relationship is supported by four lines of evidence: 1) salt-sensitivity of blood pressure occurs predominantly in subjects with a family history of hypertension; 2) studies in twin children document the influence of genetic variance on salt-sensitivity of blood pressure; 3) subjects with a family history of hypertension have a significantly lower salivary sodium concentration and an altered urinary sodium excretion after salt loading compared to subjects with no such history; 4) salt-sensitivity of blood pressure may be associated with specific genetic markers. On the basis of these observations, we propose the hypothesis that enhanced inverse alpha-beta-adrenoceptor regulation in response to a high salt intake may be responsible for salt sensitivity in the normal population, and may contribute to the development of essential hypertension in susceptible individuals. This alteration is likely to be genetically mediated.

Down-Regulation↗
PubMed1989

Renal disease in hypertensive adults: effect of race and type II diabetes mellitus.

To test the hypothesis that race is a predictor of hypertensive renal disease, we examined a general medicine clinic population of 6,880 hypertensive patients who were treated for at least 1 year (mean, 5.2 years). Their mean age was 55.8 years; 70% were women, 72% were black, and 41% were diabetic (95% type II). Many were already under treatment at the time of enrollment. Their mean blood pressure at entry was 150/92 mmHg; during treatment it was 142/86 mmHg. Decreased renal function, defined as a serum creatinine greater than or equal to 2 mg/dL, developed in 18.1%. A multivariable logistic regression analysis identified diabetes, glucose control, systolic blood pressure levels, heart failure, and male gender as indicators of decreased renal function. These data suggested that glucose and blood pressure control may decrease the frequency of impaired renal function. However, when these variables were controlled, blacks still had almost twice the risk for renal dysfunction (91% greater risk) than whites (P less than 0.0001). With increasing creatinine values, the percentage of black patients increased progressively. The data draw attention to and elucidate the exceptionally high incidence of renal dysfunction in blacks with or without diabetes. Further, they may explain the inordinate numbers of blacks with hypertension requiring dialysis. Finally, these retrospective data suggest that prospective trials to test the effect of blood pressure and glucose control on the course of renal disease in hypertensive and/or type II diabetic patients are warranted.

Black People↗
PubMed1989

The effect of dietary interventions to reduce blood pressure in normal humans.

Changes in electrolyte intake have been advocated to lower the prevalence of hypertension in the normal population. To elucidate the potential impact of such strategies, we conducted a comprehensive analysis of data from three interventions, namely, salt (NaCl) restriction, calcium (Ca) supplementation, and potassium (K) supplementation in normal volunteers. Eighty-two adults lowered their Na intake from 157 +/- 6 S.E. to 68 +/- 3 mEq/day for 12 weeks. Population mean systolic and diastolic blood pressure decreased less than or equal to 2 mm Hg. Ca supplementation, 1.5 g daily for 12 weeks in 37 men, decreased blood pressure compared to 38 men receiving placebo. Ca supplementation, 1 g daily for 8 weeks in an older group of 44 normal subjects, decreased supine diastolic and standing systolic blood pressure. K supplementation with a nonchloride salt in 64 normal adults for 4 weeks had no effect on systolic or diastolic blood pressure even though urinary excretion was increased by 20 mmol/day. The responses to all interventions were Gaussian in distribution. A potentially adverse effect on blood pressure in some normal individuals cannot be excluded on the basis of the currently available data. Although all three interventions may benefit some hypertensive and some normal individuals, the data from these relatively short-term cross-sectional studies are insufficient to warrant generalized dietary recommendations for the normal population.

Adult↗
PubMed1989

Effects of oral calcium, potassium, digoxin, and nifedipine on natriuresis in normal humans.

Many factors influence renal sodium excretion and blood pressure. We tested the independent effects of dietary calcium (Ca; 500 mg twice daily), potassium (KCl; 20 mEq three times daily), sodium-potassium dependent ATPase inhibition (digoxin), calcium channel blockade (nifedipine), and placebo, on acute natriuresis in 14 normal subjects while receiving 150 mEq/d sodium diets and 2 L normal saline intravenously over four hours. Each subject received each regimen in random sequence. Sodium balance before infusion was not different among the regimens. Plasma renin activity (PRA) was increased in subjects receiving nifedipine, while the plasma aldosterone concentration (PA) was not different among the regimens. None of the regimens influenced the clearance of inulin or paraaminohippurate (PAH) either before or after saline infusion. Only KCl and nifedipine affected sodium excretion compared to controls. KCl and nifedipine increased the amount of sodium excreted after the infusion was terminated. In the case of nifedipine, this natriuresis was sufficient to increase the 24-hour sodium excretion on that day to above that of the other regimens. The data support the notion that potassium and nifedipine may decrease blood pressure by facilitating sodium excretion. Nifedipine may also uncouple renin from aldosterone. Oral calcium supplementation and sodium-potassium dependent ATPase inhibition did not facilitate natriuresis.

Administration, Oral↗
PubMed1989

Genetic and environmental approaches to the prevention of hypertension.

While the familial and genetic nature of hypertension has long been recognized, the mechanisms involved are not clear. Recent studies suggest that an environmental factor, increased dietary sodium intake, may be required for the expression of this genetically determined form of hypertension. The evidence for this conclusion is based on physiological studies of humoral factors, renal function and the blood pressure response to sodium and volume expansion and reduction in several carefully characterized human populations.

Humans↗
PubMed1989

Red-cell sodium-lithium countertransport and fractional excretion of lithium in normal and hypertensive humans.

To examine the relations between erythrocyte sodium-lithium countertransport and renal proximal tubular sodium handling, we measured countertransport, and then subjected 30 normal and 32 hypertensive subjects, both white and black, to provocative maneuvers of volume expansion and contraction. The fractional excretions of sodium and lithium were measured simultaneously. In agreement with previous studies, we found that countertransport in erythrocytes was elevated in hypertensive patients compared with normal subjects. We also observed that whites have a higher level of countertransport than blacks. In the basal state, we found that fractional sodium excretion of hypertensive patients was no different than in normal subjects, whereas the fractional lithium excretion of hypertensive persons was increased compared with normotensive values. Volume expansion with 2 1 0.9% saline administered intravenously during a 4-hour period provoked an exaggerated natriuresis and a greater increase in fractional lithium clearance in hypertensive patients compared with the control group. With volume expansion and contraction, fractional lithium clearance and countertransport were directly correlated. Our data suggest that hypertensive persons do not have increased proximal tubular sodium reabsorption compared with normal subjects. Further, the exaggerated natriuresis of hypertension is, in part, the result of increased distal solute delivery. The fact that our hypertensive patients were older may partially explain the discrepancies between this report and previous observations.

Biological Transport↗
PubMed1989

Angiotensin-induced hypertension in the rat. Sympathetic nerve activity and prostaglandins.

To elucidate mechanisms of angiotensin II (Ang II)-related hypertension, we infused angiotensin (76 ng/min s.c.) into rats with minipumps for 10-14 days. Control rats received sham pumps. We measured blood pressure by tail-cuff, and the excretion of aldosterone and prostaglandins (PG) (PGE2, prostacyclin derivative 6kPGF1 alpha, and thromboxane [Tx] derivative TxB2). Angiotensin II increased blood pressure by 20 mm Hg by day 2 and by 90 mm Hg by day 10. Aldosterone excretion increased from 10 to 70 ng/day in Ang II rats by day 7. Urine PGE2 did not increase in angiotensin rats; however, both 6kPGF1 alpha and TxB2 excretion increased with angiotensin. Control rats had no changes in any of these parameters. A sympathetic component was tested in a separate group of angiotensin rats that received phenoxybenzamine (300 micrograms/kg/day) during angiotensin infusion; their increase in blood pressure of 40 mm Hg at 10 days was less than in those rats with angiotensin alone but more than in control rats. Phenoxybenzamine did not influence the angiotensin-induced increases in excretion of 6kPGF1 alpha or TxB2. Additional groups of conscious angiotensin and control rats were equipped with splanchnic nerve electrodes on day 14 for recording of sympathetic nerve activity. Angiotensin rats had greater basal sympathetic nerve activity than the control rats. Incremental methoxamine injections demonstrated altered baroreceptor reflex function in rats receiving angiotensin. We conclude that increased blood pressure with chronic angiotensin infusion is accompanied by increased production of aldosterone and increased sympathetic tone. The latter may be modulated by PG.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Hypothalamic GABA and sympathetic regulation in spontaneously hypertensive rats.

The posterior hypothalamus contains a sympathoexcitatory system that can be modulated by changes in GABAergic tone. We tested the hypothesis that the GABAergic mechanism in the posterior hypothalamus is altered in spontaneously hypertensive rats (SHR) compared with the Wistar-Kyoto (WKY) control rats. Blood pressure and heart rate were continuously measured in the conscious state; blood samples were obtained for determination of plasma catecholamine concentrations. Bilateral microinjections of the GABAA receptor antagonist bicuculline methiodide into the posterior hypothalamus increased heart rate and blood pressure in a dose-related fashion and increased plasma catecholamine concentrations in both SHR and WKY rats. The responses were not significantly different between the two strains of rats. Microinjections of the GABAA receptor agonist muscimol in this same region caused dose-related decreases in both heart rate and blood pressure in SHR and WKY rats. Although the decreases in heart rate caused by muscimol were not significantly different between the SHR and WKY rats, the decreases in blood pressure were significantly greater in SHR compared with WKY rats. Further, microinjection of muscimol caused a significant decrease in plasma catecholamines in SHR but not in WKY rats. These data indicate that in SHR and WKY rats the posterior hypothalamus contains a sympathoexcitatory mechanism that is tonically inhibited by GABA. The ability of muscimol to decrease plasma catecholamines selectively in SHR and to cause greater decreases in blood pressure, suggests that the GABAergic mechanisms in the posterior hypothalamus of the SHR and WKY rats may differ.

Animals↗
PubMed1989

Hypertension in dialysis patients: does CAPD provide an advantage?

We considered the hypothesis that CAPD is a superior treatment to HD in patients with dialysis-refractory hypertension. We compared 12 HD patients to 22 CAPD patients entered to our program over a one year period. All had been treated for hypertension before dialysis. We found that systolic blood pressure decreased in CAPD patients compared to HD patients, even though medications were more commonly reduced in CAPD patients compared to HD patients. Ten CAPD patients required no medications after one year's treatment. These preliminary data in this small pilot study support the notion that CAPD is superior to HD in blood pressure management of hypertensive patients. A large, multicenter study may be warranted to determine if CAPD favorably influences the risk of cardiovascular complications in dialysis patients compared to HD.

Blood Pressure↗
PubMed1989

Salt and hypertension: recent advances and perspectives.

Dietary sodium intake has long been considered important in the genesis and maintenance of hypertension. This view is predicated on the results of epidemiologic observations, experiments in animals, investigations at the cellular level, and the results from dietary intervention trials. In the past decade a considerable body of new evidence has been gathered. A comprehensive, world-wide epidemiologic investigation involving over 10,000 subjects found significant relationships between sodium excretion and blood pressure levels and between sodium excretion and the slope of increase in blood pressure with age. The relationships, however, are not as straight-forward as previously proposed. Investigations in animals and in human subjects emphasize the genetic nature of salt sensitivity of blood pressure. A putative genetic marker has been suggested in human studies. At the cellular level, increases in sodium-lithium countertransport, sodium-hydrogen exchange, and cytosolic calcium level have been identified. Cytosolic calcium level was found to increase in lymphocytes in response to a high-salt diet in salt-sensitive individuals with hypertension, yet the identification of a circulating inhibitor of sodium-potassium--dependent adenosine triphosphatase remains elusive. Dietary intervention trials of salt restriction in patients with hypertension are generally disappointing. Active research is elucidating the role of sodium intake and hypertension at all levels. The data to date, however, still do not allow sweeping conclusions or generalizations.

Blood Pressure↗