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Mechanismus und Bedeutung der arteriolären Media-Hypertrophie/Hyperplasie bei der arteriellen Hypertonie (1988)

Düsing, R. ; Göbel, B. ; Weißer, B. ; [et al.]

Springer

Journal of molecular medicine 66 (1988), S. 1151-1159

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ISSN: 1432-1440

Keywords: Arterial Hypertension, structural changes ; Arteriolar hypertrophy and hyperplasia ; Na+/Li+-exchange ; Na+/H+-antiport ; Phosphatidylinositol metabolism ; Growth factors

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Summary The most common haemodynamic abnormality in human essential hypertension is an increase in systemic vascular resistance. Morphologic substrate for increased flow resistance is a narrowing of the lumen of arteriolar resistance vessels. During the course of essential hypertension, this is associated with an increase in wall (mainly media) thickness due to hypertrophy and hyperplasia of vascular smooth muscle cells. In contrast to concepts interpreting media thickening strictly as structural adaptation to increased perfusion pressure, various lines of evidence also point to pressure independent factors. In this context, extracellular factors such as “growth factors” as well as alterations in the activity of intracellular messenger systems must be considered. Recent studies suggest that substances generally known to act as vasoconstrictors such as angiotensin II, noradrenaline and arginine-vasopressin may also stimulate vascular smooth muscle cell growth and proliferation. Intracellular messenger systems with possible significance in the response to trophins and/or mitogens of vascular smooth muscle cells are phospholipase C, protein kinase C and the Na+/H+-antiport. These systems have been demonstrated to be altered in hypertension supporting the concept that one endogenous factor in human essential hypertension with pathophysiological significance, at least in a subgroup of patients, may be an enhanced reactivity of vascular smooth muscle cells to trophic and mitogenic stimuli. In this context, intracellular messenger systems such as phospholipase C, protein kinase C and/or the Na+/H+-antiport may play an important pathophysiological role.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF01727661

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Synthese von [2]-Catenanen aus [2]-Rotaxanen (1988)

Schill, Gottfried ; Schweickert, Norbert ; Fritz, Hans ; [et al.]

Weinheim : Wiley-Blackwell

Berichte der deutschen chemischen Gesellschaft 121 (1988), S. 961-970

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ISSN: 0009-2940

Keywords: Chemistry ; Inorganic Chemistry

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Chemistry and Pharmacology

Description / Table of Contents: Synthesis of [2]-Catenanes from [2]-RotaxanesStarting from the rotaxane 18a a mixture of catenane 21 and rotaxane 23 is obtained by attaching a polymethylene bridge between the methylene groups in α-position of the sulfonyl groups. The isocyclic catenane 28 containing a 28- and a 46-membered ring is obtained from the catenane 21 by splitting the bonds between the bridgehead atoms and the sulfonyl groups. The 1H-, 13C-NMR, and mass spectra of this compounds are discussed.

Notes: Ausgehend von dem Rotaxan 18a wird durch Angliederung einer Polymethylenbrücke zwischen den beiden zu den Sulfonylgruppen α-ständigen Methylengruppen ein Gemisch von Catenan 21 und Rotaxan 23 synthetisiert. Aus 21 wird nach Spaltung der Bindungen zwischen den Brückenkopfatomen und den Sulfonylgruppen das isocyclische Catenan 28, bestehend aus einem 28-und einem 46-gliedrigen Ring, erhalten. Die 1H-, 13C-NMR-Spektren und Massenspektren dieser Verbindung werden diskutiert.

Additional Material: 1 Ill.