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Biomedical subjects

W Siess

Publications and source records attributed to W Siess.

At least 91 records · Page 5Linked to original sources
PubMed1982

Plasma catecholamines, platelet aggregation and associated thromboxane formation after physical exercise, smoking or norepinephrine infusion.

To study the possible role of catecholamines in platelet activation, platelet aggregation stimulated by ADP, collagen, arachidonic acid and L-epinephrine, thromboxane B2 (TXB2) formation and plasma levels of catecholamines and renin were studied in healthy men both before and after 6 days of propranolol treatment (40 mg three times daily) under control conditions and during sympathoadrenergic stimulation by physical exercise (200 W) or smoking. Exercise markedly increased plasma norepinephrine from 128 +/- 28 to 998 +/- 418 pg/ml (+/- SD), and plasma renin activity from 1.0 +/- 0.5 to 4.2 +/- 1.8 ng AI/ml . hour. Smoking predominantly increased plasma epinephrine, from 47 +/- 25 to 154 +/- 76 pg/ml. Propranolol did not consistently influence these variables, but blunted the circulatory response to exercise and smoking. Despite the marked increases of plasma catecholamines after both stimuli with and without beta blockade, platelet aggregation stimulated by ADP, 1-epinephrine, collagen and arachidonic acid and associated TXB2 formation were not enhanced. Moreover, as already suggested by a trend toward reduced aggregability in these settings, plasma norepinephrine levels in the same range (745 +/- 368 pg/ml) due to infusion (5 micrograms/min) significantly reduced platelet aggregation with low-dose collagen (0.25-0.75 micrograms/ml), I-epinephrine (0.2-1.0 microM) and ADP (0.5-1.5 microM). These data do not support a role of endogenous catecholamines in initiating platelet activation and TXB2 formation.

Adult↗
PubMed1982

Very low levels of 6-keto-prostaglandin F1 alpha in human plasma.

Two stable derivatives of PGI2, its nonenzymatic hydrolysis product (6-keto-PGF1 alpha) and an enzymatic metabolite (6, 15-diketo-PGF1 alpha), were determined in human plasma and urine. These compounds were measured by RIA after separation on rp-HPLC. Previous purification of the samples on rp-HPLC markedly enhanced the specificity of the RIA determinations of those compounds in plasma and urine. The PGI2 derivative 6-keto-PGF1 alpha was detected in both plasma (4.7 +/- 3.2 pg/ml, mean +/- S.D., n=34) and urine (166 +/- 61 pg/ml, n=9). No gender differences of the plasma or urinary levels of 6-keto-PGF1 alpha were found. The PGI2 metabolite 6,15-diketo-PGF1 alpha was not measurable in plasma or urine (less than 1 and less than 10 pg/ml, respectively, n=4). Thus this compound may not be a major endogenous metabolite of PGI2 in man. When [3H]PGI2 was added to citrated blood immediately after venipuncture, it was recovered entirely as [3H]6-keto-PGF1 alpha after rp-HPLC. Therefore any circulating PGI2 would be measured as 6-keto-PGF1 alpha by our method. The results obtained suggest that PGI2 could be present in human venous blood under physiological conditions, but only in very low concentrations. (J Lab Clin Med 99:388, 1982.)

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Stimulated platelet aggregation, thromboxane B2 formation and platelet sensitivity to prostacyclin - a critical evaluation.

Platelets have been implicated in the development of atherosclerotic and thrombotic vascular diseases. Evaluation of platelet aggregation in relation to endogenously formed compounds which affect platelet function may provide information of clinical and pharmacological relevance. We describe a method in which thromboxane B2 (TXB2) formation was analyzed following stimulation of platelet-rich plasma (PRP) with ADP, 1-epinephrine, collagen, and arachidonic acid. In addition, we determined platelet sensitivity to prostacyclin following ADP- and collagen-induced platelet aggregation. The parameters under study were found to depend on the platelet count in PRP, on the type and dose of the aggregating agent used, and on the test time after blood sampling. By standardization of these variables, a reliable method was established which can be used in clinical and pharmacological trials.

Adenosine Diphosphate↗
PubMed1981

Effects of very low versus standard dose acetyl salicylic acid, dipyridamole and sulfinpyrazone on platelet function and thromboxane formation in man.

The effects of three conventional antiplatelet regimes, dipyridamole 3 X 75 mg/day (D), sulfinpyrazone 4 X 200 mg/day (S), acetylsalicylic acid 3 X 330 mg/day combined with dipyridamole 3 X 75 mg/day (ASA + D), and very low dose acetylsalicylic acid 100 mg/day (ASA) on platelet function were studied in man following 4 days of treatment. D and S slightly increased mean minimal ADP concentration for irreversible aggregation (n.s.), S reduced aggregation and thromboxane (TXB2) formation on low dose collagen (2P less than or equal to 0.05), ASA and ASA + D increased platelet count (2P less than or equal to 0.05), increased bleeding time (n.s. for ASA, 2P less than or equal to 0.05 for ASA + D), abolished irreversible aggregation on ADP, suppressed TXB2 formation on all (2P less than or equal to 0.001) and aggregation on lower concentrations of collagen (2P less than or equal to 0.01) and abolished aggregation and TXB2 formation on arachidonic acid (2P less than or equal to 0.001). Very low dose ASA suppresses platelet aggregation and TXB2 formation on several stimuli of possible physiologic significance. In the light of a recently proposed critical balance of vascular antiaggregatory prostacyclin and platelet proaggregatory TXA2 very low dose ASA might offer advantages over conventional dosage of ASA and should be evaluated in thromboembolic disorders.

Adenosine Diphosphate↗
PubMed1980

Platelet-membrane fatty acids, platelet aggregation, and thromboxane formation during a mackerel diet.

Eicosapentaenoic acid (C20:5 omega 3), which is present in high concentration in certain salt-water fish, may reduce the incidence of cardiovascular disease in Greenland Eskimos by reducing platelet aggregation and adhesion. Changes in platelet and plasma fatty acids, platelet aggregation, and thromboxane (TX) formation were studied in 7 healthy White men who had been on a mackerel diet for 1 week. Platelet aggregation had TX synthesis after low-dose collagen stimulation in platelet-rich plasma were reduced. This could be due to the marked change of the ratio of C20:5 to arachidonic acid (C20:4 omega 6) in platelet membranes. When the men were on the mackerel diet, their C20:5 level in platelet membranes and in plasma increased and that of C20:4 dropped. Both fatty acids were released during platelet aggregation. The reduction in the amount of C20:4 liberated and/or a diminished conversion of C20:4 to TXA2 by competitive inhibition of the platelet cyclo-oxygenase by the released C20:5 could be responsible for the decreased platelet aggregation.

Animals↗
PubMed1979

Formation and action of prostaglandins in the kidney.

The kidney has a high capacity to produce a spectrum of different acting prostaglandins (PG). In vivo and in vitro studies have shown that renal formation of PG's, possibly in the vasculature of the cortex represents an essential step in the mechanisms regulating the secretion of renin. PG's formed in the cortex seem to participate also in the control of renal vascular resistance and glomerular filtration rate. PGE2 formed in the medulla modulates the hydroosmotic action of antidiuretic hormone and influences the kidney's capacity for urine concentration. Renal PG formation is reduced by high NaCl intake and enhanced by low NaCl intake and in hypokalemic states. These findings make renal PG's good candidates for participation in the regulation of salt and water balance and in the control of blood pressure. Due to the close connection with the renin angiotensin system, alterations in renal PG formation might be involved in the etiology of high and low renin states. Thus, an impairment in the renal cortical production of vasodilating and renin-stimulating PG's could constitute the common denominator for both the reduced renin secretion and the increased vascular resistance which have been reported to be associated in essential hypertension.

Animals↗
PubMed1979

[Prostaglandins in cardiovascular and renal function. Biochemical, physiological and clinical findings (author's transl)].

Prostaglandins (PG) are highly unsaturated, cyclic fatty acids with 20 carbon atoms which are biosynthesized from dihomo-gamma-linolenic, arachidonic and eicosapentaenoic acids. These fatty acids are either ingested or are biosynthesized from linoleic and linolenic acids, respectively. The PG-precursor fatty acids are liberated from membrane phospholipids by phospholipase A and are converted to prostaglandins by the multienzyme complex PG-synthetase. The activity of the PG-system is influenced by extracellular hormonal, neural and mechanical stimuli and by intracellular factors such as ion-concentration and activity of the enzymes adenyl- and guanylcyclase. Prostaglandins are tissue hormones or autacoids which act on their receptors near their site of synthesis and degradation. The prostaglandin family constitutes a group of more than 10 natural occurring compounds showing a variety of biological actions. In arteries and veins the different PG:s have vasodilating as well as vasoconstricting effects. In addition, they are involved in the regulation of vascular smooth muscle proliferation. Within the kidney PG:s have vascular and tubular actions. They antagonize the effect of ADH, mediate renin secretion and are involved in the control of electrolyte balance. In the regulation of platelet aggregation and platelet adhesion PG:s have opposite functions: Prostacyclin which is synthesized in the vascular wall antagonizes the aggregating action of Thromboxane A2 which is formed in the platelets. A defect or an imbalance in the production of PG:s in the vascular wall, in platelets or in the kidney is assumed to play a pathogenetic role in a variety of cardiovascular and renal diseases such as in hypertension, atherosclerosis, persistent ductus arteriosus and Bartter's syndrome.

Arteriosclerosis↗
PubMed1979

Urinary prostaglandins and kallikrein in essential hypertension.

1. Urinary prostaglandins (PG), kallikrein and plasma renin activity (PRA) were measured in 35 patients with essential hypertension and 22 normotensive controls before and 15 min after frusemide (40 mg intravenously). 2. PGE2 and kallikrein excretion rates were lower in hypertensive subjects, and failed to rise to the same extent after frusemide. PGF2 alpha excretion was not significantly different in the two groups of patients either before or after frusemide. PRA rose less in the hypertensive subjects after frusemide. 3. These findings support the view that there is an abnormality of renal vasodilator systems (PGE2 and kallikrein) in essential hypertension.

Adult↗
PubMed1978

[Pathogenetic, pathophysiological and biochemical aspects of essential hypertension (author's transl)].

Hereditary and environmental factors are involved in the pathogenesis of essential hypertension. Obesity, salt intake and stress are predominant among the environmental influences. Autonomous nervous dysfunction, increased contractility of vascular smooth muscle cells and impaired renal handling of sodium are major abnormalities in essential hypertension. At present it cannot be decided if alterations in the activities of systemic or renal hormonal systems reflect primary defects or adaptive changes in the regulation of blood pressure. In any case the kidney is regarded to have a key position in the long term increase of blood pressure in essential hypertension. Recent studies in essential hypertensive patients suggest that renin release decreases as renal vascular resistance increases. Studies from our laboratory have shown that renal prostaglandins are intrinsic to the renin release mechanism from the kidney. Additionally, there is evidence that renal prostaglandin synthesis is disturbed in essential hypertension, either primarily or secondarily, leading to unresponsive renin secretion. Further studies on the interrelationships of other hormonal systems and on hormone-receptor interactions in the vascular wall are necessary to delineate more precisely the mechanisms which are operative in the pathogenesis and manifestation of essential hypertension.

Adrenal Cortex Hormones↗
PubMed1977

Radioimmunological and biological measurement of prostaglandins in rabbit urine: decrease of PGE2 excretion at high NaCl intake.

The estimation of prostaglandin (PG) E2 and of PGF2alpha by radioimmunoassay is described in detail. PGE2 was measured after conversion to either PGB2 or PGF2alpha and the results compared to bioassay. The methods were used to follow the excretion of PGE2 and PGF2alpha after salt loading in rabbits. A marked reduction of PGE2 levels was observed at high NaC1 intake, while PGF2alpha excretion remained unchanged.

Animals↗