[Paracetamol and metamizol in the treatment of chronic pain syndromes].

In a medline search (covering 1966 to Sept. 1996) 32 clinical studies were identified, in which the efficacy of paracetamol or matamizol per se, or in comparison to other analgesics, in various chronic pain states, such as migraine, dysmenorrhoea, arthritis and osteoarthritis pain and cancer pain had been examined. In patients with migraine (4 studies) several other analgesics (ibuprofen, mefenamic acid, flupirtin) were slightly more effective than paracetamol, however, the efficacy of paracetamol itself had not been assessed.

Flow versus pressure in the control of renin release in conscious dogs.

In Goldblatt hypertension, renal artery stenosis reduces renal arterial pressure (RAP) and renal blood flow (RBF) and thereby increases plasma renin activity (PRA) levels. Although it is clear that reduction in RAP stimulates renin, the decrease in RBF may contribute to higher PRA as well. However, it has hitherto never been possible to dissociate a decrease in RBF from a concomitant decrease in RAP.

Presence of renin within intramitochondrial dense bodies of the rat adrenal cortex.

It has been suggested that tissue-specific expression of the genes of the renin-angiotensin system (RAS) leads to local generation of angiotensin (ANG) II with specific physiological implications. We demonstrate here that an intracellular RAS exists in adrenal glomerulosa cells; 60 h after bilateral nephrectomy and hemodialysis, renin and prorenin were eliminated from the circulation, whereas intra-adrenal renin content increased (control rats: 2 +/- 0.5 ng ANG I.

Contribution of a 12 kDa protein to the angiotensin II-induced stabilization of angiotensinogen mRNA: interaction with the 3' untranslated mRNA.

Several authors have shown that angiotensin II stimulates hepatic angiotensinogen synthesis in vivo, ex vivo and in vitro. In previous studies we have demonstrated that this effect of angiotensin II depends mainly on a transient inhibition of adenylyl cyclase and is the consequence of a stabilization of angiotensinogen mRNA. In the present study we describe the isolation of a polysomal 12 kDa protein which, in band shift and cross link assays, shows a specific affinity to the 3' untranslated region (3' UTR) of angiotensinogen mRNA and prevents enzymatic degradation of angiotensinogen mRNA in a cell-free incubation system.

A role for podocytes to counteract capillary wall distension.

In a previous study of the changes in glomerular structure in the isolated perfused kidney (IPK), perfusion at high pressures lead to an enlargement of the glomerular tuft and to the formation of giant capillaries. The present paper analyzes the morphological and dimensional changes of the peripheral glomerular capillary wall under these circumstances. The enlargement of glomerular capillaries at high pressure perfusion was accompanied by a considerable increase in the surface area of the glomerular basement membrane (GBM).

Mechanism by which angiotensin II stabilizes messenger RNA for angiotensinogen.

The most important specific regulatory mechanism for hepatic angiotensinogen synthesis and secretion is its stimulation by angiotensin II, the effector peptide of the renin-angiotensin system. In the circulating system, this octapeptide is thought to stimulate hepatic angiotensinogen synthesis through a positive feedback loop. In the present study, we have identified the intracellular mechanisms leading to an increase in angiotensinogen messenger RNA (mRNA) and secretion.

Angiotensinogen: an acute-phase protein?

Angiotensinogen has been assumed to be an acute-phase protein, because some forms of acute inflammation, eg, the injection of lipopolysaccharide or cellite or partial hepatectomy, increased the hepatic synthesis of angiotensinogen. In addition, the well-characterized nephrectomy-induced stimulation of angiotensinogen was thought to represent an acute-phase reaction. To evaluate this hypothesis, we examined changes in angiotensinogen secretion by the isolated perfused rat liver after the systemic administration of turpentine or lipopolysaccharide as well as in response to nephrectomy or sham nephrectomy.

Angiotensin II stimulates the synthesis of angiotensinogen in hepatocytes by inhibiting adenylylcyclase activity and stabilizing angiotensinogen mRNA.

Angiotensin II stimulates the hepatic synthesis and secretion of angiotensinogen, the substrate of renin. In the present study performed on freshly isolated rat hepatocytes we demonstrate that this effect of angiotensin II is mainly related to a transient inhibition of adenylylcyclase. Agents known to decrease intracellular cAMP (angiotensin II, vasopressin, guanfacine) or the cAMP-antagonist Rp-adenosine-3',5'-cyclic phosphothioate stimulated, whereas cAMP-stimulating agents (isoproterenol, forskolin, glucagon) or the cAMP-agonist Sp-adenosine-3',5'-cyclic phosphothioate inhibited angiotensinogen synthesis.

Modulation of tissue angiotensinogen gene expression by glucocorticoids, estrogens, and androgens in SHR and WKY rats.

Local or tissue renin angiotensin systems are thought to participate in cardiovascular regulation. However, little information is available on the mechanisms by which renin and angiotensinogen synthesis and secretion are regulated in these tissues. In view of the importance of steroid hormones in the regulation of hepatic angiotensinogen, we have examined the effects of dexamethasone, ethinyl estradiol, or dihydrotestosterone on angiotensinogen gene expression in peripheral or cerebral tissues of Wistar Kyoto (WKY) or spontaneously hypertensive rats (SHR).

Endothelium-derived NO stimulates pressure-dependent renin release in conscious dogs.

The effect of blocking the formation of endothelium-derived relaxing factor/nitric oxide (EDNO) on pressure-dependent renin release (RR) was studied in six conscious foxhounds with chronically implanted catheters in the abdominal aorta and the renal vein. Renal blood flow (RBF) was measured with an ultrasonic transit-time flowmeter. RR was determined by multiplying the renal venous-arterial plasma renin activity difference with renal plasma flow.

Tissue distribution of angiotensinogen mRNA during experimental inflammation.

It has been proposed that angiotensinogen is an acute phase protein, because its plasma concentrations increase during some forms of acute inflammation. However, this is not a consistent finding. Furthermore, no specific function of circulating angiotensinogen in the inflammatory reaction is known.

Angiotensin II and dexamethasone regulate angiotensinogen mRNA by different mechanisms.

Angiotensinogen synthesis and secretion in the liver is regulated by glucocorticoids and angiotensin II. In isolated hepatocytes in suspension culture, both dexamethasone and angiotensin II induced an increase in angiotensinogen mRNA (2.5- and 4-fold, respectively) with half maximal stimulation at 20 and 200 nM, respectively.

Increased adrenal renin in transgenic hypertensive rats, TGR(mREN2)27, and its regulation by cAMP, angiotensin II, and calcium.

The newly established rat strain TGR(mREN2)27 is a monogenetic model in hypertension research. Microinjecting the mouse Ren-2d renin gene caused it to become a stable part of the genome. The rats are characterized by fulminant hypertension, low plasma active renin, suppressed kidney renin, high plasma inactive renin, and high extrarenal transgene expression, most prominently in the adrenal cortex.

The response of hepatic angiotensinogen secretion to experimental inflammatory stimuli. A comparison with acute-phase proteins.

Angiotensinogen is thought to be an acute-phase protein, since its plasma concentrations increase in response to some inflammatory conditions, e.g. partial hepatectomy, nephrectomy or lipopolysaccharide (LPS) injection.

Is arterial pressure a determinant of renal prostaglandin release?

The effect of changes in renal perfusion pressure (RPP) on renal prostaglandin (PG) release was investigated in conscious dogs (n = 10). PGE2, PGF2 alpha, and 6-keto-PGF1 alpha levels in renal venous and aortic plasma were measured in response to controlled reductions of RPP by an inflatable cuff implanted around the renal artery. PG plasma concentrations were determined by gas chromatography-negative ion chemical ionization mass spectrometry.

[Not Available].

Different therapeutic modalities are available for the treatment of rheumatic pain. The most important one, besides physiotherapy, is medication with analgesics and adjuvant drugs. Analgesics are given orally and by a stepwise approach in keeping with the principles of cancer pain therapy.

Physiological concentrations of ANP exert a dual regulatory influence on renin release in conscious dogs.

The influence of physiological increments in circulating atrial natriuretic peptide (ANP) on renin release was determined in conscious dogs. Renin stimulus-response curves (RSRCs) were obtained by controlled reductions of renal perfusion pressure (RPP) under control conditions and during intrarenal or intravenous ANP infusions. Under all experimental conditions, the RSRCs were characterized by a plateau, a threshold pressure (Pth), and a steep slope below Pth.

Effects of neuropeptide-Y on renal function and its interaction with sympathetic stimulation in conscious dogs.

1. The effects of neuropeptide-Y (NPY) on renal function were investigated in conscious foxhounds. 2.

Role of the renin-angiotensin system in the adaptation to high salt intake in immature rats.

The response of the renin-angiotensin system, extracellular fluid volume, plasma volume, plasma sodium and mean arterial blood pressure to an increase in salt intake (8% NaCl in the diet for 10 days) was compared in immature (20 days) and adult (80 days) rats which were either sham-operated or uninephrectomised. Salt feeding induced a significant increase in plasma sodium in immature animals, and a greater suppression of the renin-angiotensin system in immature than in adult rats, although extracellular fluid volume, plasma volume and blood pressure remained unchanged. Following uninephrectomy, however, the renin-angiotensin system was maximally suppressed in both age groups and in younger animals extracellular fluid volume, plasma volume and blood pressure were significantly increased.

Influence of pulsatile perfusion upon renin release from the isolated perfused rat kidney.

It is well established that renin release from the juxtaglomerular epithelioid cells in the media of the afferent arteriole strongly depends on the mean renal perfusion pressure, whereas a possible influence of the pulsation of blood pressure on renin release has only occasionally been investigated, and the results are contradictory. Such an influence on renin release cannot be excluded because pulsation is known to modulate arterial baroreceptors and vascular tone in some resistance vessels. In the isolated perfused rat kidney, we found a pulsation amplitude-dependent inhibition of renin release that could be blocked either by vasodilatation or by calcium channel blockade.