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Background: The leading cause of death among elderly women is cardiovascular (CV) disease in the United States and in Western Europe as well. The protective effect of postmenopausal hormone replacement therapy (HRT) on coronary heart disease has been verified in epidemiologic studies. There are no data available on the rate of HRT use in Eastern Europe. Our goals were to study the rates of HRT in Eastern Europe, to compare them to those of the United States and Western Europe, as well as to compare their CV mortality rates.Methods: The use of HRT in Eastern Europe was calculated from sales records obtained from all pharmaceutical companies that ship HRT preparations to the given area. Data on HRT in Western countries were taken from the literature. Mortality rates were obtained from the World Health Organization.Results: The rate (mean +/- SD) of HRT in Eastern Europe was 2.88 +/- 2.67%, whereas 12.67 +/- 9.97% in Western Europe and the United States, p < .05. The cardiovascular mortality rate per 100,000 women older than 45 years in Eastern Europe was higher (1766 +/- 158.3) than in the Western countries (1155 +/- 164.1, p < .001).Conclusions: The rate of HRT is markedly lower. whereas CV mortality rates are notably higher in Eastern Europe than in the United States or Western Europe. Because HRT seems to be underutilized in Eastern Europe, to increase its use might be an important tool to improve CV mortality rates. However, due to the risks associated with HRT, other measures to prevent coronary heart disease, such as smoking cessation programs, and other efforts should also be considered in Eastern Europe. [ABSTRACT FROM AUTHOR]

Segmental remodeling of resistance arteries, inhibition of angiogenetic processes, their rarefaction by AngiotensinII and hypertension are accepted facts. Less is known about alterations in resistance artery network geometry potentially induced by them. Female rats were infused with 100 ng/kg/min AngiotensinII with osmotic minipumps for four weeks that raised mean arterial blood pressure from 98 ± 3 to 125 ± 7 mmHg. Geometry of the left coronary artery system was studied on plastic casts and on in situ microsurgically prepared, saline infused video-microscoped networks (n = 13 and 11 controls and hypertensives, respectively). Parallel running branches, broken course of larger branches, multiple branchings and branch crossings have been identified (13 and 74 such deformities, in control and hypertensive networks, respectively, p < 0.01). Bifurcation angles increased with increasing asymmetry of daughter branches but not in hypertensives. Dividing the whole network (theoretically) into several hundreds of 50μm long ring units, ring frequency peaked at 200μm diameter in normal networks. This peak diminished and was replaced by a peak at 300μm in hypertensives (p < 0.01). In controls, diameter of vascular units decreased at a fairly even rate with flow distance from the orifice. The 350, 200, 150μm diameter units were found with highest frequencies at flow distances around 2.5, 5.5 and 7.5mm, respectively. This regular pattern disintegrated in hypertensives. Higher blood flow routes were needed to cover the same distance from the orifice (p < 0.01). Shrinkage and diminishment of many parallel connected 200μm segments, concomitant enlargement of many larger segments accompanied with morphological deformities can be expected to contribute to elevated vascular resistance., (© 2020 Published by Elsevier Ltd.)

Background: the European Union of Medical Specialists (UEMS-GMS) recommendations for training in Geriatric Medicine were published in 1993. The practice of Geriatric Medicine has developed considerably since then and it has therefore become necessary to update these recommendations., Methods: under the auspices of the UEMS-GMS, the European Geriatric Medicine Society (EuGMS) and the European Academy of Medicine of Ageing (EAMA), a group of experts, representing all member states of the respective bodies developed a new framework for education and training of specialists in Geriatric Medicine using a modified Delphi technique. Thirty-two expert panel members from 30 different countries participated in the process comprising three Delphi rounds for consensus. The process was led by five facilitators., Results: the final recommendations include four different domains: 'General Considerations' on the structure and aim of the syllabus as well as quality indicators for training (6 sub-items), 'Knowledge in patient care' (36 sub-items), 'Additional Skills and Attitude required for a Geriatrician' (9 sub-items) and a domain on 'Assessment of postgraduate education: which items are important for the transnational comparison process' (1 item)., Conclusion: the current publication describes the development of the new recommendations endorsed by UEMS-GMS, EuGMS and EAMA as minimum training requirements to become a geriatrician at specialist level in EU member states., (© The Author(s) (2019). Published by Oxford University Press on behalf of the British Geriatrics Society.)

Objective: Hypertension causes adverse remodeling and vasomotor alterations in coronaries. Hormones such as estrogen may help counterbalance some of these effects. The aim of this study was to analyze the effects of ovariectomy and estrogen therapy in a rat model of menopausal hypertension induced by angiotensin II (AII)., Methods: We investigated diameter, tone, and mechanics of intramural coronaries taken from ovariectomized female rats (n = 11) that received chronic AII treatment to induce hypertension, and compared the results with those found in female rats that were also given estrogen therapy (n = 11). The "hypertensive control" group (n = 11) underwent an abdominal sham operation, and received AII. After 4 weeks of AII treatment, side branches of left anterior descendent coronary (approximately 200 μm in diameter) were isolated, cannulated with plastic microcannulas at both ends, and studied in vitro in a vessel chamber. The inner and outer diameter of the arteries were measured by microangiometry, and spontenuous tone, wall thickness, wall cross-sectional area, tangential stress, incremental distensibility, circumferential incremental elastic modulus, thromboxane agonist-induced tone, and bradykinin-induced dilation were calculated., Results: In hypertension, intramural small coronaries show inward eutrophic remodeling after ovariectomy comparing with hypertensive controls. Estrogen therapy had an opposite effect on vessel diameter. Hormone therapy led to an increase in spontaneous tone, allowing for greater dilatative capacity., Conclusions: Estrogen may therefore be considered to counterbalance some of the adverse changes seen in the wall of intramural coronaries in the early stages of chronic hypertension.

Certain steroidal compounds have an antioxidant effect in humans. Our aim was to test whether the synthetic steroid tibolone and its metabolites are also able to display such a property. For this, granulocytes from healthy men and women were incubated for two hours with different concentrations (10(-7), 10(-8), 10(-9 )M) of either estradiol, tibolone, 3α-hydroxytibolone, 3β-hydroxytibolone, Δ(4)-tibolone, 3α-sulfated-tibolone, 3α-17β-disulfated-tibolone, 3β-sulfated-tibolone or 3β-17β-disulfated-tibolone. Superoxide anion generation of neutrophils was measured by photometry. Results of different steroids were given as percentages of their controls. A more simple superoxide generating system, the xanthine-xanthine oxidase reaction was also tested. We found that granulocyte superoxide production did not differ from the control using 10(-9 )M of steroids. Using 10(-8 )M concentration: estradiol (80.9 ± 2.5%); 3β-sulfated-tibolone (83.3 ± 4.7%); 3β-17β-disulfated-tibolone (81.0 ± 4.2%) caused a significant decrease in superoxide production, compared to the control. In addition at 10(-7 )M, 3β-hydroxytibolone and 3α-sulfated-tibolone also showed antioxidant effects. In the xanthine-xanthine oxidase system estradiol (67.4 ± 1.0%), 3α-sulfated-tibolone (85.8 ± 5.3%), 3α-17β-disulfated-tibolone (71.9 ± 2.5%), 3β-sulfated-tibolone (73.9 ± 5.0%), and 3β-17β-disulfated-tibolone (65.8 ± 3.4%) caused a significant decrease in superoxide production. Conclusively, although tibolone itself did not show significant antioxidant capacity, most of its active metabolites have antioxidant effects.

Steroid hormones influence the antioxidant processes of cells. However, the molecular mechanism of this effect is not fully clear. Our aim was to examine how steroid hormones affect the expression of certain genes that play a role in antioxidant processes. Blood was taken from ten healthy volunteers. Neutrophil granulocytes were separated and treated either with 17-β-estradiol, progesterone, testosterone, or cortisol. Whole RNA was isolated and reverse transcription was carried out in treated and control groups. Relative quantification was performed with SYBR Green assay and gene-specific oligonucleotides. We found that the expression of Mn-superoxide dismutase was significantly increased by 17-β-estradiol and testosterone, myeloperoxidase expression was significantly elevated by cortisol and progesterone, and the expression of NADPH oxidase was significantly decreased by progesterone. We conclude that the antioxidant effect of steroid hormones is in part carried out through transcriptional regulation of certain enzymes. Subsequent studies are required in order to examine the non-genomic, membrane receptor mediated effect of steroids on antioxidant processes.

Background: Weak androgens have an antioxidant effect in vitro which is represented as a beneficial change in the antioxidant status., Objective: Our aim was to clarify whether dehydroepiandrosterone (DHEA) and dehydroepiandrosterone-sulphate (DHEAS) oral administration results in beneficial antioxidant changes in Sprague-Dawley adult male rats in vivo., Methods: Groups of experimental animals were fed a high-fat or a normal-fat diet and treated with DHEA or DHEAS in the drinking fluid. The control group was fed a high-fat diet together with untreated drinking fluid. Total scavenger capacity (TSC) was measured before and after 4 weeks of treatment in blood samples using a chemiluminometric assay. Fat content, superoxide dismutase (SOD), catalase and glutathione S-transferase (GST) activity in the liver were determined by Sudan staining and spectrophotometric assessments, respectively, from the fresh frozen tissue., Results: DHEA and the DHEAS treatment showed significantly increased TSC in the groups fed a high-fat diet. The control group and the DHEA- or DHEAS-treated groups on normal diets showed no significant changes in TSC. The total score of liver fat content in the high-fat diet groups showed a marked positivity with Sudan staining, and the groups treated with DHEA or DHEAS had a markedly decreased amount of fat in the liver slides compared to the untreated group on the high-fat diet. Liver SOD activity was decreased in all high-fat diet groups and elevated only in the groups on a normal diet with DHEA or DHEAS treatment. Liver catalase and GST activities were decreased in the groups where TSC was significantly increased., Conclusion: Our results support the hypothesis that DHEA and DHEAS supplementation can improve the antioxidant status in lipid-rich dietary habits., (Copyright © 2010 S. Karger AG, Basel.)

The present study aimed to test whether, beyond the known antioxidant effect of estradiol, such a property is also possessed by estrone and estriol. For this purpose, an in vitro investigation of the effect of estrone and estriol on superoxide anion production by human neutrophil granulocytes was carried out. Blood samples were obtained from healthy volunteers and neutrophil granulocytes were separated for measurement of superoxide anion generation after incubation with estrone, estriol (10(-7), 10(-6) and 10(-5) M) and 17beta-estradiol (10(-7) M). Superoxide anion production of isolated neutrophil granulocytes was quantified by photometry and using the reduction of ferricytochrome-C. When adding estrone and estriol to neutrophil granulocyte suspensions, the production of superoxide anion fell (10(-5) M: 84.17 +/- 3.14% and 88.77 +/- 1.98% of control production, p < 0.01 and p < 0.05, respectively). Estradiol produced an antioxidant effect at lower concentration (10(-7) M: 72.91 +/- 7.94% of control production, p < 0.001). The weak estrogens estrone and estriol, similarly to estradiol, are also able to reduce the superoxide anion release in our experimental model. This may have importance in the antioxidant defense of biological systems.

The prevalence of ischemic heart disease is lower in premenopausal females than in males of corresponding age. This should be related to gender differences in coronary functions. We tested whether biomechanical differences exist between intramural coronary resistance arteries of male and female rats. Intramural branches of the left anterior descending coronary artery (uniformly approximately 200microm in diameter) were isolated, cannulated and studied by microarteriography. Intraluminal pressure was increased from 2 to 90mmHg in steps and steady-state diameters were measured. Measurements were repeated in the presence of vasoconstrictor U46619 (10(-6)M) and the endothelial coronary vasodilator bradykinin (BK) (10(-6)M). Finally, passive diameters were recorded in calcium-free saline. A similar inner radius and a higher wall thickness (41.5+/-2.9microm vs. 31.4+/-2.7microm at 50mmHg in the passive condition, p<0.05) resulted in lower tangential wall stresses in male rats (18.9+/-1.9kPa vs. 24.9+/-2.5kPa at 50mmHg, p<0.05). Isobaric elastic modulus of vessels from male animals was significantly smaller at higher pressures. Vasoconstrictor response was significantly stronger in male than in female animals. Endothelial relaxations induced by BK were not different. This is the first demonstration that biomechanical characteristics of intramural coronary resistance arteries of a mammalian species are different in the male and female sexes. Higher wall thickness and higher vascular contractility in males are associated with similar endothelial function and larger high-pressure elasticity compared to females. These gender differences in biomechanics of coronary resistance arteries of rats may contribute to our better understanding the characteristic physiological and pathological differences in humans.

Background: The prevalence of cardiovascular disorders is higher among men than in age-matched women. This is probably related, in part, to gender-dependent differences in coronary function including thromboxane-A(2) (TXA(2)) sensitivity. This question has been examined only on major, epicardial coronaries. The intramural small arteries directly responsible for supplying the myocardial arterioles with blood have been hardly accessible for investigation, owing to difficulties in their preparation. Vasoconstrictor TXA(2) excess generated by platelets and the vascular wall may play an important role in coronary ischemic events. In the present study we tested the vasoconstrictor reactivity of intramural coronary arteries to TXA(2)., Methods: Secondary, intramural branches of the left anterior descendent coronary artery of Sprague-Dawley rats (diameter: 200 microm) were placed into a vessel chamber. TXA(2) vasoconstrictor reactivity was measured on the basis of pressure-diameter curves in normal Krebs-Ringer solution and after addition of TXA(2) receptor agonist., Results: Vasoconstrictor response induced by TXA(2) agonist was twice as strong in males compared with females for the whole pressure range ( p < 0.001)., Conclusions: A gender-dependent difference was demonstrated in TXA(2)-induced contraction of intramural coronary artery segments. In some pathologic situations the enhanced TXA(2) release from platelets and injured vascular wall may cause greater vasoconstriction of intramural coronary arteries in males than in females.

Objectives: The consequences of female sex hormone deficiency and the effects of hormone replacement therapy are controversial because individual hormones and their derivates can result in partially antagonistic activities. This intricate system involving cerebral autoregulatory mechanisms caused by ovariectomy and female sex hormone replacement was studied in rats., Methods: The lower limit of cerebral blood flow autoregulation was determined by stepwise reduction of systemic arterial pressure while simultaneously measuring the changes of the hypothalamic blood flow (HBF) using the hydrogen gas-clearance method., Results: In ovariectomized rats resting HBF decreased substantially and the threshold of cerebrovascular autoregulation decreased to 40 mm Hg. Estrogen replacement prevents the former change and shifts the latter upwards. Similarly, progestin replacement restores autoregulation to the physiological levels found in control animals, whereas it has no influence on the ovariectomy-induced reduction of resting blood flow., Conclusions: Steady-state HBF and compensatory changes of regional cerebral vascular autoregulation are altered significantly following ovariectomy. Estrogen or progestin replacement has an opposite effect on these cerebral circulatory parameters. Our observations highlight the essential role of female sex hormones in hypothalamic autoregulation during hypotensive stress.

Objective: To test whether the menopause entails any changes in the myeloperoxidase activity of neutrophil granulocytes. The effects of hormone replacement therapy on myeloperoxidase activity and related changes in free radical production were also investigated., Design: Laboratory investigation of the effect of oestrogen on intracellular myeloperoxidase activity and release from human neutrophil granulocytes. Analysis of related changes in superoxide anion generation., Setting: 2nd Department of Medicine and 1st Department of Obstetrics and Gynaecology, Semmelweis University, Budapest., Samples: Intracellular myeloperoxidase activity (mean peroxidase index) was measured automatically in blood samples obtained for general laboratory work-up from 135 randomly selected patients in our department. Blood samples from 11 postmenopausal women were analysed before and during hormone replacement therapy. Blood samples from 20 healthy volunteers were obtained and neutrophil granulocytes separated for in vitro measurement of superoxide anion production after adding myeloperoxidase to the incubation media., Methods: The mean peroxidase index was measured using a Technicon H-3 instrument. myeloperoxidase release from neutrophils was quantified by ELISA technique. Superoxide production of isolated neutrophil granulocytes was measured by photometry., Main Outcome Measures: Intracellular activity of myeloperoxidase, concentration of myeloperoxidase-protein in supernatant of neutrophils, release of superoxide anion from neutrophil granulocytes., Results: 1. Intracellular myeloperoxidase activity in neutrophils was lower in postmenopausal women, than in females with regular cycles (-1.84 +/- 3.06 versus 1.59 +/- 3.55, P < 0,001). 2. In postmenopausal women intracellular myeloperoxidase activity and myeloperoxidase release increased during hormone replacement therapy (-5.54 +/- 6.63 versus -0.2 +/- 6.05; P < 0.001 and 52.74 mU/ml +/- 25.73 versus 251.4 +/-234.1 mU/ml; P < 0.05). 3. Adding myeloperoxidase to neutrophil granulocyte suspensions, the production of superoxide anion fell (e.g. adding 280 ng/ml myeloperoxidase: 77.9 +/- 14.04 % of control production, P < 0.001)., Conclusion: Hormone replacement restores the reduced myeloperoxidase activity in menopausal women. Adding myeloperoxidase to neutrophil granulocytes, the production of free radicals decreases.

Objective: The venous system may play a role in the development and progression of postmenopausal hypertension. In the present study, we investigated the effect of chronic angiotensin II-induced hypertension on the geometric, elastic, and contractile properties of the saphenous vein in sex hormone deficient and replaced female rats., Methods: Thirty Sprague-Dawley rats were ovariectomized (n = 10), ovariectomized and angiotensin-infused (n = 10), or ovariectomized plus angiotensin-infused and hormone replaced with estradiol and medroxyprogesterone (n= 10). After 4 weeks, the saphenous veins were removed and cylindrical segments of the vessels were placed into a microangiograph and cannulated at both ends. Intraluminal pressure versus outer diameter curves were registered in Krebs-Ringer solution, in maximal norepinephrine contraction, and in full papaverine relaxation., Results: In vivo venous tone of the saphenous vein in ovariectomized plus angiotensin-infused animals was significantly higher than in ovariectomized animals without angiotensin treatment (27.2 +/- 3.7% versus 5.3 +/- 2.1%, respectively; P <.05). Hormone replacement restored venous tone (9.6 +/- 3.4%; P <.01). In vitro pressure-induced myogenic tone was markedly reduced by chronic angiotensin infusion, which was partially reversed by hormone replacement. Passive incremental distensibility was lowered after angiotensin infusion independently of the sex hormone state., Conclusion: Hormone replacement improved venous contractility (rapid adaptation response), which was seen as decreased in vivo venous tone, but venous distensibility (chronic adaptation) was not improved by hormone replacement in our short-term study. We demonstrate beneficial short-term effects of hormone replacement on the venous system in our model of postmenopausal hypertension. Further studies might be warranted to see whether long-term benefits can be achieved.

Objective: To determine whether hormone replacement therapy can reverse established renal microvascular damage in type 2 diabetes and hypertension., Design: Prospective, single centre clinical trial., Setting: Outpatient clinics., Participants: Sixteen diabetic and hypertensive postmenopausal women (age 47-57 years), Methods: Administration of a cyclic combination of oestradiol and norgestrel orally for 3.5 monthly cycles., Results: Comparing the baseline values, mean (SD) 24-hour urine protein excretion was reduced from 0.452 g (0039) to 0.370 g (0.047) (P < 0.01) and creatinine clearance was increased from 1.68 mL/sec (0.11) to 1.77 mL/sec (0.08) (P < 0.05). Fasting plasma glucose also improved from 6.92 mmol/L (0.47) to 6.51 mmol/L (0.28) (P < 0.05), as did serum total cholesterol from 7.26 mmol/L (0.28) to 6.65 mmol/L (0.14) (P < 0.05). Blood pressure did not change significantly. Univariate linear regression analysis showed no significant correlation between the individual changes in blood pressure, fasting plasma glucose or serum cholesterol and the individual changes in proteinuria or creatinine clearance., Conclusions: This study shows that hormone replacement therapy may reduce proteinuria, and even improve creatinine clearance, in diabetic and hypertensive postmenopausal women. These effects are additive to nephroprotective therapy, and the mechanisms appear unrelated to conventional risk factors for vascular complications, such as high blood pressure, elevated plasma glucose or serum cholesterol.

Until recently, studies dealing with veins have almost always been the neglected part of vascular research. Recent data show an increasing rate of venous disease, and increasing evidence supports a role for veins in systemic diseases. The authors discuss and comment on findings of recent studies on venous drug reactivity. Alterations in venous reactivity to alpha- and beta-adrenergic, NO-dependent, and other drugs have been shown in many genetically determined and acquired conditions, such as hypertension, smoking, and aging. In some of them, the changes of venous responsiveness are most likely secondary to another process, while in others the they seem to play a primary role in the development of systemic disease states. Studying the drug reactivity of the venous system more extensively provides useful information for clinicians and researchers and will no doubt help to further knowledge of the normal and pathologic processes of the vasculature.

Bradykinin is a nonapeptide, whose mechanism of vasodilation is mediated chiefly through the release of endothelium-derived relaxing factor (EDRF). Diminished vasodilatory response to EDRF has been demonstrated in many pathologic states such as hypertension, atherosclerosis, diabetes, and long-term, heavy smoking. We studied whether the diminished EDRF-mediated vasodilatory response seen in chronic diseases can be demonstrated in young, clinically healthy smokers. We used the dorsal hand-vein compliance technique, an in vivo technique used to measure response to local infusions of vasoactive substances. Full dose-response curves to bradykinin (dosing range, 0.5-500 ng/min) were generated in 11 young, healthy smokers and 11 young, healthy nonsmokers by using hand veins preconstricted with phenylephrine (dosing range, 20-6,800 ng/min). In addition, after a washout period, a single maximal dose of a non-endothelium-dependent vasodilator, isoproterenol (300 ng/min) was infused. Our results demonstrated that smokers had a greater maximal venodilation to bradykinin than did nonsmokers (106 +/- 40% vs. 69 +/- 49%; p < 0.05). The log of the dose that produced half-maximal response to bradykinin was smaller in smokers: -0.10 +/- 0.93 (0.79 ng/min) versus 0.75 +/- 0.84 (5.6 ng/min); p < 0.05. There was no difference in the maximal dilatory response to isoproterenol: 80 +/- 45% (smokers) versus 89 +/- 50% (nonsmokers), nor was there a difference in the log dose of phenylephrine necessary to produce 80% constriction of the hand vein (2.7 +/-0.7 vs. 2.7 +/- 0.9 ng/min) between the two groups. We conclude that young, otherwise healthy smokers have a paradoxic hyperactive response to the endothelium-dependent vasodilator, bradykinin, but maintain a similar response to the nonendothelium-dependent vasodilator, isoproterenol as compared with nonsmokers. Their reactivity to the alpha1-adrenergic agonist phenylephrine was found to be intact. It is possible that a hyperactive response to EDRF in young smokers contributes to endothelium damage seen in chronic disease. To our knowledge, this is the first report on increased reactivity to bradykinin in short-term smokers.

Background: A considerable body of research has been accumulated regarding the pathogenesis and treatment of hypertension in Whites (Caucasians) and in Blacks. This research has led to more effective therapies geared specifically towards these ethnic groups. Unfortunately, very little information is available regarding the pathogenesis of hypertension and the effect of antihypertensive treatment in Native Americans (North-American Indians). Ethnic variability in the response to adrenergic mediated stimulation has been previously described, and reduced compliance of the venous system has been suggested among the possible mechanisms responsible for essential hypertension. The aim of this study was to compare venous responsiveness between Native Americans and Whites to vasoactive substances., Methods: The alpha1-adrenergic agonist, phenylephrine and the beta2-adrenergic agonist isoproterenol were studied in 10 Native American and White volunteers. The dorsal hand vein technique was used, which is a simple, relatively non-invasive method to study the response to vasoactive substances, in vivo., Results: The maximal venodilatory response to isoproterenol in the Native American group was 53.2+/-27.5%; while in the White group it was 103.4+/-66.0% (p<0.05). The maximal venoconstriction for phenylephrine in the Native American subject group was similar to that of the White group (85.4+/-24.0% vs. 89.4+/-10.9%) (p = n.s.)., Conclusions: Based on our findings, we can anticipate that Native Americans may respond differently to antihypertensive therapy. However, further investigation needs to be done with an eye towards the development of drug therapy and treatment strategies tailored to this specific population.

Soft tissue infections are among the rare manifestations of extra intestinal salmonellosis and occur more frequently in immunocompromised patients. Herein we report a case of a 51-year-old white male with type II. diabetes mellitus, diagnosed with supraclavicular abscess caused by Salmonella enteritidis. The patient denied any gastrointestinal symptoms, and stool cultures were negative. After incision, drainage, and administration of intravenous ampicillin (4 x 1.5 g/day for two weeks) the patient recovered completely. To our knowledge, this is the first reported case of cervical soft tissue abscess caused by Salmonella enteritidis without preceding gastrointestinal symptoms. We feel that the presence of diabetes was a risk factor for developing the infection.

The modulation of the production of prostacyclin and thromboxane from cat and cat aortic tissue slices by different vasoactive agents has been studied in order to reveal whether the release of these main two vasoactive prostanoids goes in parallel or may be controlled independently. Norepinephrine, isoproterenol, phentolamine, propranolol, angiotensin II, vasopressin, bradykinin, thrombin, verapamil, gallopamil, dopamine or methionin enkephalin were added to the incubation medium and 6-keto-PGF1 alpha (the stable metabolite of prostacyclin) and TxB2 (the stable metabolite of thromboxane) were determined in the supernatant by radioimmunoassay. The ratio of the release of prostacyclin and thromboxane was computed. Norepinephrine increased both prostacyclin and thromboxane release. Isoproterenol increased the ratio of prostacyclin and thromboxane released in cat aortic tissue slices. Phentolamine and propranolol had no effects. Angiotensin II induced a slight but statistically insignificant increase in the ratio of the two prostanoids released. Vasopressin increased thromboxane release only. Bradykinin stimulated the prostacyclin while thrombin stimulated the thromboxane release. Verapamil decreased both prostacyclin and thromboxane production. Gallopamil decreased prostacyclin release and increased thromboxane release from vessel wall slices in a certain concentration range causing a characteristic dose dependent minimum in the ratio of prostacyclin and thromboxane release. Dopamine separately increased prostacyclin release while enkephalin had no significant effect. The data obtained show that in vascular tissue some unidentified yet cytophysiological mechanisms might exist which specifically control the activities of the prostacyclin synthase and thromboxane synthase enzymes.

Persistent hypertension after nephrectomy is in most cases due to increased fluid volume. Endothelin-1 is a potent endogenous vasoconstrictor peptide. Its role in the development and maintenance of hypertension is not completely understood, but it might be significant in some cases. We report a case of stage IV hypertension after nephrectomy with elevated endothelin-1 levels and no volume overload.