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11. Human renal and systemic hemodynamic, natriuretic, and neurohumoral responses to different doses of L-NAME

Author

Broere, A., Meiracker, A.H. van den, Boomsma, F., Derkx, F.H.M., Veld, A.J. Man In't, and Schalekamp, M.A.D.H.

Subjects
Kidneys -- Physiological aspects, Hemodynamics -- Research, Natriuresis -- Regulation, Neurotransmitters -- Physiological aspects, Nitric oxide -- Physiological aspects, Esters -- Physiological aspects, Biological sciences
Abstract

The effects of varying degrees of acute systemic nitric oxide (NO) synthesis inhibition on renal and systemic hemodynamic, natriuretic and neurohumoral responses were investigated. Three different intravenous infusions of N(super G)-nitro-L-arginine methyl ester were studied for arterial pressure, renal blood flow, systemic vascular resistance, fractional sodium and lithium excretion, glomerular filtration rate and renal vascular resistance in healthy men. It was found that renal circulation is not more sensitive to the effects of NO synthesis inhibition than systemic circulation.

Published
1998

36. [From gene to disease; dopamine-beta-hydroxylase deficiency and orthostatic hypotension]

Author

Deinum, J., Meiracker, A.H. van den, Boomsma, F., Ittersum, F.J. van, Wevers, R.A., and Lenders, J.W.M.

Subjects
Genetic defects of metabolism [UMCN 5.1], Vascular medicine and diabetes [UMCN 2.2], Neuromuscular development and genetic disorders [UMCN 3.1]
Abstract

Contains fulltext : 58971.pdf (Publisher’s version ) (Closed access) The DBH gene encodes dopamine-beta-hydroxylase (DbetaH), the enzyme that catalyses the formation of norepinephrine from dopamine. Inactivation of this enzyme due to a mutation of the DBH gene causes a selective (nor)-adrenergic failure of the sympathetic nervous system. This manifests as a severe orthostatic syndrome in which sweating and a normal parasympathetic function are preserved. Several mutations of the DBH gene that cause this very rare syndrome have now been identified. Diagnosis is made on the basis of clinical features and the finding of increased plasma dopamine in the near-absence of norepinephrine. A sole finding of absent plasma DbetaH is insufficient, since about 4% of the population have absent DbetaH. This trait cosegregates with a polymorphism in the promoter region of the DBH gene and is not associated with sympathetic failure. The orthostatic syndrome of DbetaH deficiency can be treated with the non-natural amino acid L-dihydroxyphenylserine, which is decarboxylated to norepinephrine by the ubiquitous aromatic-L-amino acid decarboxylase.

Published
2004

37. Catecholamine handling in the porcine heart: a microdialysis approach

Author

LAMERIS, T.W., VAN DEN MEIRACKER, A. H., BOOMSMA, F., ALBERTS, G., DE ZEEUW, S., DUNCKER, D. J., VERDOUW, P. D., and MAN IN 'T VELD, A.J.

Subjects
Catecholamine metabolism -- Research, Swine -- Physiological aspects, Cardiology -- Research, Noradrenaline -- Physiological aspects, Biological sciences
Abstract

Lameris, T. W., A. H. van den Meiracker, F. Boomsma, G. Alberts, S. de Zeeuw, D. J. Duncker, P. D. Verdouw, and A. J. Man in 't Veld. Catecholamine handling in the porcine heart: a microdialysis approach. Am. J. Physiol. 277 (Heart Circ. Physiol. 46): H1562-H1569, 1999.--Experimental findings suggest a pronounced concentration gradient of norepinephrine (NE) between the intravascular and interstitial compartments of the heart, compatible with an active neuronal reuptake (U1) and/or an endothelial barrier. Using the microdialysis technique in eight anesthetized pigs, we investigated this NE gradient, both under baseline conditions and during increments in either systemic or myocardial interstitial fluid (MIF) NE concentration. At steady state, baseline MIF NE (0.9 [+ or -] 0.1 nmol/l) was higher than arterial NE (0.3 [+ or -] 0.1 nmol/l) but was not different from coronary venous NE (1.5 [+ or -] 0.3 nmol/l). Local U1 inhibition raised MIF NE concentration to 6.5 [+ or -] 0.9 nmol/l. During intravenous NE infusions (0.6 and 1.8 nmol [multiplied by] [kg.sup.-1] [multiplied by] [min.sup.-1], the fractional removal of NE by the myocardium was 79 [+ or -] 4% to 69 [+ or -] 3%, depending on the infusion rate. Despite this extensive removal, the quotient of changes in MIF and arterial concentration ([Delta]MIF/[Delta]A ratio) for NE were only 0.10 [+ or -] 0.02 for the lower infusion rate and 0.11 [+ or -] 0.01 for the higher infusion rate, whereas U1 blockade caused the [Delta]MIF/[Delta]A ratio to rise to 0.21 [+ or -] 0.03 and 0.36 [+ or -] 0.05, respectively. From the differences in [Delta]MIF/[Delta]A ratios with and without U1 inhibition, we calculated that 67 [+ or -] 5% of MIF NE is removed by UI. Intracoronary infusion of tyramine (154 nmol [multiplied by] [kg.sup.-1] [multiplied by] [min.sup.-1]) caused a 15-fold increase in MIF NE concentration. This pronounced increase was paralleled by a comparable increase of NE in the coronary vein. We conclude that U1 and extraneuronal uptake, and not an endothelial barrier, are the principal mechanisms underlying the concentration gradient of NE between the interstitial and intravascular compartments in the porcine heart. norepinephrine; spillover; pig; myocardial interstitium

Published
1999

38. Clinical pharmacological meeting

Author

Lubsen, J., Tijssen, J. G. P., Sluiter, H. E., Huysmans, F. Th. H., Thien, Th. A., Koene, R. A. P., Vincent, H. H., Derkx, F. H. M., Veld, A. J. Man in 't, Boomsma, F., Schalekamp, H. A. D. H., Hoefnagels, W. H. L., Lenders, J. W. M., Thien, Th., Smits, P., van 't Laar, A., v. Wijk, L. M., Kingma, J. H., Dunselman, P. H. J. M., v. Gilst, W. H., Lie, K. I., Wesseling, H., Lohman, J. J. H. M., Hooymans, P. M., Koten, M. L. P., Verhey, M. T. J. M., Merkus, F. W. H. M., Koopmans, P., Gribnau, F., Demacker, P., Jonkman, J. H. G., Van der Boon, W. J. V., Schoenmaker, R., Holtkamp, A., Hempenius, J., Edelbroek, P. M., Linssen, A. C. G., Zitman, F. G., Rooymans, H. G. M., de Wolff, F. A., Speth, P. A. J., Linssen, P. L. M., Wessels, J. H. C., Haanen, C., Elferink, F., van der Vijgh, W. J. F., van der Poort, S. E. J. M., Vermorken, J. B., Pinedo, H. M., Sonneveld, P., Nooter, K., van den Engh, G. J., Schurgers, N., de Blaey, C. J., and Crommelin, D. J. A.

Published
1984
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39. Abstracts of papers clinical pharmacological meeting

Author

Merkus, F. W. H. M., Gribnau, F. W. J., Thien, Th., Louwerenburg, Hans W., Kingma, J. Herre, van Gilst, Wiek H., Six, A. Jacob, de Graeff, Pieter, Wesseling, Harry, BoeLaert, J. R., Schurgers, M. L., Matthys, E. G., Belpaire, F., Daneels, R. F., de Cre, M. J., Boqaert, M. G., D'Haese, P. C., Verpooten, G. A., Lamberts, L. V., Liang, L., de Broe, M. E., de Meijer, P. H. E. M., Russel, F. G. M., Russel, A. J. M., van Ginneken, C. A. M., van Liedekerke, B. M., Lambert, W. E., Yousouf, M. A., de Roose, J. E., de Leenheer, A. P., Lambert, W., de Bersaques, J., Vanneste, L., de Leenheer, A., de Marie, S., Slaghuis, G., Rozing, P. M., Mattie, H., Poelma, F. G. J., Hilbers, H. W., Jansen, A. C. A., Tukker, J. J., Augusti, Jr, P., Verbeke, N., van Peer, A., Snoeck, E., Heykants, J., Bruynseels, J., Peeters, J., Amery, W., Rogiers, V., Vandenberghe, Y., Comet, M., Callaerts, A., Sonck, W., Guillouzo, A., Vercruysse, A., van Rooy, P., Rombaut, N., vanden Bussche, G., Tan, A. C. I. T. L., Jansen, T. L. Th. A., Termond, E. F. S., Kloppenborg, P. W. C., Thien, Th., Benraad, Th. J., van de Velde, V., Woestenbprghs, R., Hermens, W. A. J. J., Romeijn, S. G., Deurloo, M. J. M., Merkus, F. W. H. M., Musch, G., Massart, D. L., van Hengstum, M., Festen, J., van den Broek, W., Corstens, F., Beurskens, C., Hankel, M., de Smet, M., van Belle, S. J. P., de May, J., Storme, G. A., Kuppen, P. J. K., Schuitemaker, H., Veer, L. J. van't, van Oosterom, A. T., Schrier, P. I., de Bruijn, E. A., de Pooter, C. H., Tjaden, U. R., van Slooten, H., Roelevink, H. P., Smit, E., de Vries, E. G. E., Ijmker, J., Uges, D. R. A., Moors, M., Mertens, K., van Hecken, A., de Lepeleire, I., Verbesselt, R., Tjandra-Maga, T. B., de Schepper, P. J., Guelen, P. J. M., Jansen, T. J., Vrijhof, W. P., de Vos, D., Scharpé, S., Verkerk, R., Lsmeire, N., Zijlstra, I. F., Gribnau, F. W. J., Haaijer-Ruskamp, F. M., Post, D., Reddingius, P. F., Wesseling, H., Wollersheim, H. C. H., van den Meiracker, A. H., Veld, A. J. Man in 't, Admiraal, P., Boomsma, F., Derkx, F., Schalekamp, M. A. D. H., Schoors, D. F., Dupont, A. G., Claessen, F., Reljenga, J., Lenders, J. W. M., Thlen, Th., Laekeman, G., Muylle, L., van Hoydonck, A., Herman, A. G., and Peetermans, M. E.

Published
1988
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41. Abstracts of papers

Author

Belpaire, F., Derkx, F. H. M., Bryson, S. M., Kelman, A. W., Whiting, B., Modderman, E. S. M., Merkus, F. W. H. M., Hilbers, H. W., Zuidema, J., Raai jmakers, J. A. M., Terpstra, G. K., Wassink, G. A., Kreukniet, J., Tjandramaga, T. B., Verbesselt, R., van Hecken, A., Mullie, A., de Schepper, P. J., van Hooff, M. E. J., van Baak, M. A., Rahn, K. H., Colardyn, F., Clement, D., van Riel, P. L. C. M., van de Putte, L. B. A., Gribnau, F. W. J., HacRae, K. P., Vree, T. B., Hekster, C. A., Verpooten, G. A., Buntinckx, A. P., Verbist, L., de Broe, M. E., Vincent, H. H., Boomsma, F., Schalekamp, M. A. D. H., van de Donk, H. J. M., Duchateau, G. S. M. J. E., Paulus, G. J., Roels, F., Tulkens, P., Winograd, B., Oosterbaan, M. J. M., Boerema, H., van der Kleijn, E., Monbaliu, J., Tukker, J. J., de Blaey, C. J., van Peer, A., Woestenborghs, R., Heykants, J., Verlinden, M., Reyntjens, A., Dirks, R. J. M., Hallynck, Th., Pijck, J., Soep, H., Lagas, M., and Jonkman, J. H. G.

Published
1983
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44. Aldosterone-to-renin ratio as a screening test for primary aldosteronism--the Dutch ARRAT Study

Author

Pieter Jansen, Boomsma F, Ah, Den Meiracker, and Arrat, Dutch Investigators

Subjects
Clinical Trials as Topic, Drug Resistance, Spironolactone, Eplerenone, Renin-Angiotensin System, Risk Factors, Hyperaldosteronism, Hypertension, Prevalence, Humans, Mass Screening, Antihypertensive Agents, Mineralocorticoid Receptor Antagonists, Netherlands
Abstract

Since the introduction of the aldosterone-to-renin ratio (ARR ) as a screening tool for primary aldosteronism (PA), there has been a marked increase in the reported prevalence of this condition among hypertensive subjects. A meta-analysis from the literature shows a PA prevalence of almost 8% among hypertensive patients, with a twofold higher prevalence in referred patients as compared with primary care patients (9.0 vs 4.3%). However, the usefulness of the ARR remains subject of debate, because of doubts on its validity, and the many factors affecting the ARR , including posture, time of day of blood sampling, and use of antihypertensive medication. Furthermore, there is no clear cut-off value and it is unknown what population should be screened. Recently, The Dutch ARR AT Study was initiated. This is a multicentre, prospective trial aiming to evaluate the test characteristics of the ARR within a Dutch population of therapy-resistant hypertensive patients. The effect of antihypertensive medication on the ARR will be studied. Furthermore, from this study the prevalence of PA in this population will follow. Last, the blood pressure response to the selective aldosterone-receptor-antagonist eplerenone will be evaluated. The Dutch ARR AT Study will run until the end of 2009 and will contribute to the formulation of uniform guidelines for the screening for PA in the Netherlands.

Published
2008

45. Aldosterone-to-renin ratio as a screening test for primary aldosteronism--the Dutch ARRAT Study

Author

Jansen, P.M., Boomsma, F., Meiracker, A.H. van den, Deinum, J., and Lenders, J.W.M.

Subjects
Health aging / healthy living [IGMD 5], Cardiovascular diseases [NCEBP 14], Vascular medicine and diabetes [UMCN 2.2]
Abstract

Item does not contain fulltext Since the introduction of the aldosterone-to-renin ratio (ARR ) as a screening tool for primary aldosteronism (PA), there has been a marked increase in the reported prevalence of this condition among hypertensive subjects. A meta-analysis from the literature shows a PA prevalence of almost 8% among hypertensive patients, with a twofold higher prevalence in referred patients as compared with primary care patients (9.0 vs 4.3%). However, the usefulness of the ARR remains subject of debate, because of doubts on its validity, and the many factors affecting the ARR , including posture, time of day of blood sampling, and use of antihypertensive medication. Furthermore, there is no clear cut-off value and it is unknown what population should be screened. Recently, The Dutch ARR AT Study was initiated. This is a multicentre, prospective trial aiming to evaluate the test characteristics of the ARR within a Dutch population of therapy-resistant hypertensive patients. The effect of antihypertensive medication on the ARR will be studied. Furthermore, from this study the prevalence of PA in this population will follow. Last, the blood pressure response to the selective aldosterone-receptor-antagonist eplerenone will be evaluated. The Dutch ARR AT Study will run until the end of 2009 and will contribute to the formulation of uniform guidelines for the screening for PA in the Netherlands.

Published
2008

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