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Biomedical subjects

P Boer

Publications and source records attributed to P Boer.

At least 127 records · Page 7Linked to original sources
PubMed1981

Renin and body fluid volumes in chronic renal disease. Relations between arterial pressure, plasma renin activity, blood volume, and extracellular volume in chronic renal disease, as compared with essential hypertension.

In 47 patients with hypertension and chronic renal insufficiency (CRI) and 38 patients with essential hypertension (EH), the following parameters were measured under moderate salt restriction: plasma volume (PV), blood volume (BV), extracellular fluid volume (ECFV), ratio of blood volume to insterstitial fluid volume (BV/IV), recumbent plasma renin activity (PRA), increase in PRA upon standing (delta PRAst), creatinine clearance (Ccr), and mean arterial pressure (MAP). Mean PRA, ECFV, and MAP values did not differ significantly between the two groups. In the CRI group, MAP showed a weak positive correlation with ECFV (r = 0.34). Mean PV, BV and BV/IV ratio were significantly higher than in the EH group, whereas delta PRAst was markedly blunted (p less than 0.001) and showed a weak correlation with Ccr (r = 0.33). This suggests that patients with CRI on a moderate Na intake have a decreased tissue compliance which results in a relative elevation of BV. On the other hand, although MAP was not significantly correlated with either BV or IV, a negative correlation (r = -0.31) was found between MAP and BV/IV, indicating that elevation of the blood pressure (BP) tends to depress BV. These oppositely directed effects may explain the failure so far to establish a relationship between BP in renal disease and any haemodynamic parameter or combination of such parameters.

Blood Pressure↗
PubMed1981

Lesch-Nyhan syndrome in an Arab family. Detection and biochemical manifestation of heterozygosity.

A large Arab family affected with the rare X-linked Lesch-Nyhan syndrome is reported on. Two hemizygous boys, two and nine years of age, had the classical biochemical and clinical-neurological syndrome. The activity of erythrocyte hypoxanthine-guanine phosphoribosyltransferase (HGPRT) was below the detectable limit (greater than 0.1% of normal). They were mentally and physically retarded and exhibited spasticity and choreoathetosis; the older of the two also exhibited self-mutilation. The mother and three of her seven daughters, all clinically asymptomatic, were proven to be heterozygous for HGPRT deficiency, by demonstration of an increased rate of de novo purine synthesis in cultured skin fibroblasts. Erythrocyte HGPRT activity was normal in the three heterozygous daughters, but was significantly reduced in the mother. However, in all four heterozygotes, erythrocyte HGPRT/adenine phosphoribosyltransferase ratio was lower than in all other family members. All heterozygotes had blood uric acid levels within the normal range, although higher than in the normal women in the family. The ratio uric acid/creatinine concentration in the urine was significantly elevated in one of the heterozygotes, and in the upper normal limit in two others, indicating excessive purine production.

Adolescent↗
PubMed1980

One and three doses of propranolol a day in hypertension.

In 26 patients with essential hypertension who were on continuous chlorthalidone therapy, 1 and 3 daily doses of propranolol were compared in a crossover study. Plasma propranolol levels and heart rates had larger daily fluctuations on single-dose therapy than on 3 times daily; plasma renin activity was more constant. There was no significant difference in blood pressures. Once-daily propranolol dosage was well tolerated and possibly gave less rise to the troublesome side effect of vivid dreaming.

Adolescent↗
PubMed1980

Lipid-mediated glycosylation of endogenous proteins in isolated plasma membrane of Saccharomyces cerevisiae.

A highly purified plasma membrane fraction from Saccharomyces cerevisiae was obtained by centrifugation on discontinuous sucrose and Urografin gradients. This plasma membrane fraction was capable of glycosylating endogenous proteins. It is shown that glycolipids play an intermediate role in these glycosylation reactions; with uridine 5'-diphosphate-N-acetylglucosamine as sugar donor the intermediate lipids possessed stability towards alkali and chromatographic mobilities similar to polyprenyl diphosphate N-acetylglucosamine and polyprenyl diphosphate di-N-acetylchitobiose.

Cell Fractionation↗
PubMed1980

Observations on plasma renin substrate in the nephrotic syndrome.

Literature data on renin in the nephrotic syndrome are conflicting: renin values are reported to be elevated as the rule, but sometimes normal or low; data on renin substrate are scanty and pointing to low values. In the present study, plasma renin activity (PRA) and plasma renin substrates (PRS) were measured in 27 episodes of the nephrotic phase in 24 patients with nephrotic syndrome with various lesions. 10 patients were reinvestigated after remission; 1 patient could be followed during development of the edema phase as well as during prednisone-induced remission. During the nephrotic phase, PRS was suppressed in 8%, normal in 44 and elevated in 48%, while PRA was suppressed in 41%, normal in 48 and elevated in 11% of the patients. After remission, PRA increased in 70% and PRS decreased in 20 and increased in 50% of the cases. The purpose of this study was to investigate PRA and PRS in nephrotic patients; it is concluded that low PRS and high PRA are not as characteristic for the nephrotic syndrome as they are generally thought to be.

Adult↗
PubMed1980

De novo synthesis of purine nucleotides in human blood platelets.

Human blood platelets were found to carry the complete pathway of de novo purine nucleotide synthesis. The rate of purine synthesis was gauged by the rate of incorporation of precursor (14C)formate into purines. The effect on formate incorporation of several compounds known to inhibit purine synthesis de novo was studied. Adenine, orotic acid and azaserine inhibited purine synthesis, but hypoxanthine and allopurinol did not. Platelet content of phosphoribosylpyrophosphate (PRPP) and of ribose-5-pes. Incubation of intact platelets with high inorganic phosphate concentrations caused an increase in platelet PRPP content but did not affect R-5-P content or the rate of purine synthesis de novo.

Adenine↗
PubMed1980

The determination of acid phosphatase of prostatic origin with the Automatic Clinical Analyzer (ACA, DuPont).

A critical evaluation of the determination of acid phosphatase of prostatic origin with the Du Pont ACA is reported. Th affinity of the enzyme towards certain substrates, and the specificity of sodium thymolphthalein monophosphate as a substrate for prostatic acid phosphatase were investigated. The validity of this method, which is supposed to be specific for prostatic phosphatase is, however, limited; clinical data showed that related human acid phosphatase interfere and decrease the specificity of the determination.

Acid Phosphatase↗
PubMed1980

Oral contraceptives and responsiveness of plasma renin activity and blood pressure in normotensive women.

In young normotensive women (5 without and 5 with chronic oral contraceptives (= o.c.) cardiovascular homeostasis was challenged by isoproterenol and ergometer exercise, at normal and at resitricted sodium intake. Blood pressure and plasma renin activity (= PRA) did not differ between the 2 groups. Plasma renin substrate was markedly elevated in the o.c. group. Sodium restriction induced similar changes in body weight, urinary sodium excretion, systolic blood pressure and PRA; diastolic blood pressure decreased only in the non-o.c. group (by 6 mm Hg). In both groups isoproterenol and exercise induced similar changes in heart rate and blood pressure, except that after sodium restriction both stimuli caused larger decreases in diastolic blood pressure in the o.c. group. At both levels of sodium intake, PRA increased slightly less during exercise in the o.c. group; following restriction PRA response to isoproterenol was significantly less in the o.c. group. These results indicate that following chronic use of o.c. PRA responsiveness is normal or somewhat blunted. The different responses of diastolic blood pressure to sodium restriction and subsequent isoproterenol or exercise point to subtle changes in the inter-action of aodium and pressor mechanisms during chronic o.c. use.

Adult↗
PubMed1980

Activity of adenosine deaminase and of purine nucleoside phosphorylase in peripheral lymphocytes from patients with acquired immunological disorders.

The activity of adenosine deaminase (ADA) and of purine nucleoside phosphorylase (PNP) was determined in the peripheral lymphocytes of patients with diseases associated with acquired partial dysfunction of the immune response. Increase ADA activity was found in patients with Waldenstrom's macroglobulinemia and in some patients with non-Hodgkin's lymphoma. Increased PNP activity was found in patients with non Hodgkin's lymphoma whereas decreased PNP activity was fund in patients with connective tissue disorders. The alternations found in ADA and PNP activities probably reflect changes in the lymphocyte subpopulations and do not seem to have an etiological role in the pathogenesis of the disturbed immune response.

Adenosine Deaminase↗
PubMed1980

Observations on the blood pressure lowering mechanism of diuretics.

The haemodynamic effects of short-time (3-7 days) and longer (2-3 months) periods of saliuretic treatment were investigated in several groups of patients with uncomplicated essential hypertension. Short-time salt depletion results in decrease of cardiac index, extracellular and blood volumes and marked increases in plasma renin activity (PRA) and noradrenaline excretion, while blood pressure (BP) becomes "renin dependent"as assessed by an angiotensin I antagonist (P 113). The BP decrease was only moderate and variable, due to increased peripheral resistance, and could not be related either to control PRA values or degree of subsequent elevation. After longer treatment periods, all of the above-mentioned changes are still present, but less pronounced while BP decreases further. At that time a clear distinction can be made between the patients who do and those who do not "respond" with a BP drop. The non responders tend to remain in a salt and fluid depleted state with a renin dependent BP, while in the responders the initially induced hemodynamic changes have largely, but not completely, disappeared.

Blood Pressure↗
PubMed1979

Atenolol and chlorthalidone on blood pressure, heart rate, and plasma renin activity in hypertension.

The antihypertensive effect of atenolol, with and without chlorthalidone, on hypertension was assessed in an outpatient as well as in an inpatient study. In the outpatient study atenolol alone induced decreases in systolic and diastolic BP amounting to 20 and 15 mm Hg. Maximal response of BP and HR developed within a week at the lowest dose used (100 mg twice daily). Combined atenolol-chlorthalidone treatment decreased lying and standing systolic BP by 7 and 14 mm Hg more than atenolol alone, but diastolic BP was decreased little more. In the inpatient study the addition of atenolol to chlorthalidone therapy in a dose of 100 mg twice daily resulted in a maximal decrease in BP within 3 days. At this dose PRA was lowered only slightly. Larger doses did not lead to any significant further decrease in BP, whereas PRA fell progressively. Our results indicate that, in contrast to nonselective blockade, specific beta-1-adrenoceptor blockade by atenolol is capable of inducing a distinct antihypertensive effect, unrelated to suppression of PRA. The decrease in PRA after larger doses of atenolol was not accompanied by a further decrease in BP. Because diuretic-induced renin release plays a role in the maintenance of the BP, our findings suggest that at higher dosages a hypertensive effect of the beta blocker compensated for the hypotensive effect of the decrease in PRA.

Adult↗
PubMed1979

Effects of atenolol and propranolol when added to long-term antihypertensive diuretic therapy.

The antihypertensive effects of atenolol and propranolol were compared in a double-blind crossover study of 19 patients with essential hypertension (World Health Organization, I and II) who were receiving long-term diuretic treatment (chlorthalidone, 50 mg daily) during the study. After a 3-wk placebo period, a beta-adrenergic antagonist was administered once daily (atenolol, 50 mg daily, or propranolol, 80 mg daily) for a week. If the MAP was more than 108 mm Hg at the end of the week, dosage of the beta-blocker was doubled the following week; when necessary, doubling was repeated to a maximum dose of 640 mg propranolol and 400 mg atenolol daily. Fifty milligrams atenolol had a greater effect than 80 mg propranolol and was as effective as 160 mg propranolol. The dose-response curve flattened off after 160 mg propranolol and 50 mg atenolol daily. The two highest doses of atenolol lowered MAP more than the highest doses of propranolo. Heart rate slowing was the same for both drugs and did not correlate with the fall in blood pressure. PRA was suppressed by all doses of propranolol, whereas atenolol suppressed PRA only at the 2 highest doses, (200 and 400 mg daily). With the lower propranolol doses, the percent MAP change correlated weakly with the percent PRA change (80 mg--r = 0.41, p less than 0.1; 160 mg--r = 0.64, p less than 0.05). Side effects were minimal, and were noted only with 640 mg propranolol; with this exception, the percentage of patients with no complaints rose when placebo was replaced by beta-blockers.

Administration, Oral↗
PubMed1979

Clonidine withdrawal. Mechanism and frequency of rebound hypertension.

1. The frequency and pathophysiology of the clonidine withdrawal syndrome was studied in fourteen hypertensive patients on chronic clonidine therapy. 2. After sudden cessation of clonidine (900 microgram daily) almost all of the patients showed an excessive increase of the heart rate and blood pressure. Seven of the fourteen patients had subjective symptoms, in three severe enough to require interruption of observation by therapeutic intervention 12 to 60 h after the last dose of clonidine. After clonidine withdrawal, NAE increased to abnormally high values in correlation with the blood pressure (P less than 0.01) and heart rate (P less than 0.001), whereas PRA even decreased initially, probably secondary to the rise of the blood pressure, and only rose, although not significantly, 48 h after withdrawal. PRA was not correlated with NAE, heart rate, or blood pressure. 3. It is concluded that the clonidine withdrawal phenomenon is a frequently occurring and potentially dangerous syndrome. Overactivity of the sympathetic nervous system is mainly responsible, without the mediation of the renin angiotensin system. This also explains our experience that adrenergic beta-receptor blocking drugs do not prevent the rise in BP, although they alleviate some of the symptoms.

Adult↗