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O Vonend

Publications and source records attributed to O Vonend.

6 recordsLinked to original sources
PubMed2006

Alpha(2A)-adrenoceptors regulate sympathetic transmitter release in mice kidneys.

BACKGROUND AND PURPOSE: In the present study, a rodent model was used to investigate whether the alpha(2A)-adrenoceptor (alpha(2A)) represents the presynaptic autoinhibitory receptor regulating sympathetic transmitter release in the kidney. Moreover, the potential role of alpha(2A) as a heteroceptor regulating adenosine triphosphate (ATP) release was tested. EXPERIMENTAL APPROACH: Kidneys from wild-type (WT) and alpha(2A)-knockout (KO) mice were isolated and perfused. Renal nerves were stimulated with platinum-electrodes. Endogenously released noradrenaline (NA) was measured by HPLC. The perfusion pressure was monitored continuously. KEY RESULTS: Renal nerve stimulation (RNS) induced a frequency (1,2,5,7.5,10,15 Hz)-dependent release of NA in WT mice (994+/-373, 2355+/-541, 6375+/-950, 11626+/-1818, 19138+/-2001 pg NA g(-1) kidney (means+/-s.e.m.)). There was a 2.7-fold (5 Hz) increase of NA release in alpha(2A)-KO mice. In WT animals alpha-adrenoceptor blockade by phentolamine increased RNS-induced NA release in a concentration-dependent manner up to 350% of control. No facilitation by phentolamine was observed in alpha(2A)-KO mice. Pressor responses to 1 Hz and 2 Hz were resistant to alpha(1)-adrenoceptor blockade (0.03 microM prazosin) but abolished by P(2) receptor blockade (5 microM PPADS). Blockade of alpha(2)-adrenoceptors (1 microM rauwolscine) increased these purinergic pressor responses to 296+/-112% (1 Hz) in WT but not in alpha(2A)-KO mice. Exogenous ATP (100 microM) increased basal but not RNS-induced NA release. CONCLUSIONS AND IMPLICATIONS: alpha(2A)-Adrenoceptor-activation inhibits NA and ATP release from renal sympathetic nerves. Pressor responses to RNS at higher stimulation frequencies (>2 Hz) are mediated by NA. At lower frequencies neuronally released ATP seems to be the predominant transmitter mediating renovascular resistance.

Adenosine Triphosphate↗
PubMed2005

Dihydrotachysterol therapy for hypoparathyroidism: consequences of inadequate monitoring. Five cases and a review.

BACKGROUND: The half synthetic Vitamin D analogue dihydrotachysterol (DHT) is widely used for hypocalcaemic hypoparathyroidism following surgical removal of parathyroids. Such treatment generally initiated by surgeons right after surgery has to be continued in clinical practice. Unfortunately, the required careful monitoring of calcium metabolism is often lacking and as demonstrated may lead to life-threatening conditions. PATIENTS AND METHODS: Here we report on five patients referred to our nephrology unit because of unknown impairment of renal function during therapy with DHT. All patients had clinical signs of hypercalcaemia. Since most symptoms are nonspecific they were not perceived by primary care physicians. In fact DHT treatment was continued for 4 - 50 years. In all cases calcium levels were determined after inadequate long intervals ranging from 3.08 to 4.97 mmol/l. Creatinine levels ranged from 277 to 365 micromol/l. All patients suffered from symptoms of severe hypercalcaemia, three of them needing intensive care unit treatment. RESULTS: All patients were treated effectively with a regimen consisting of intravenous saline, a loop diuretic, and application of bisphosphonates. As confirmed by renal biopsy persisting alleviation of renal function was due to calcifications. After discontinuation of DHT therapy patients were safely switched to shorter acting vitamin D derivates maintaining a normal calcium level. CONCLUSIONS: In comparison to short acting vitamin-D derivates hypercalcaemic episodes with DHT appear to last longer and may therefore occur with higher incidence. A future option could be the use of synthetic parathyroid hormone (s-PTH) recently shown to be safe and effective. Nevertheless a customized therapy and careful monitoring is indispensable in any case to prevent irreversible organ damage.

Aged↗
PubMed2003

The pattern of distribution of selected ATP-sensitive P2 receptor subtypes in normal rat kidney: an immunohistological study.

Using immunohistological techniques and available polyclonal antibodies, we have identified several ATP-sensitive P2 receptor subtypes in specific structures of the normal rat kidney. Of the P2 receptor subtypes examined, P2X1, P2X2 and P2Y1 receptors were found in the smooth muscle layer of intrarenal vessels. The P2Y1 receptor was also found on glomerular mesangial cells, the brush border membrane of the proximal straight tubule and on peritubular fibroblasts. In the cortex, P2Y4 receptors were found on the tubule epithelium of the proximal convoluted tubule, and P2Y2 receptors on glomerular epithelial cells (podocytes). P2X4 and P2X6 receptors were present throughout the renal tubule epithelium from the proximal tubule to the collecting duct. P2X5 receptors were expressed on medullary collecting duct cells and the apical membrane of the S3 segment of the proximal tubule. Possible functions of these receptor subtypes in normal rat kidney are discussed.

Adenosine Triphosphate↗
PubMed1999

Neuropeptide Y and ATP interact to control renovascular resistance in the rat.

Neuropeptide Y (NPY) and ATP are cotransmitters of norepinephrine (NE). Modulation of ATP-mediated purinergic neurotransmission by NPY was investigated in rat perfused kidney. Beta,gamma-Methylene-L-ATP (beta,gamma-mATP; 1.0 to 1.5 microM, n = 8), NE (0.1 microM, n = 8), and NPY (0.1 microM, n = 14) increased perfusion pressure by maximally 12 +/- 1, 17 +/- 2, and 9 +/- 1 mmHg, respectively. In the presence of NPY, responses to ATP and NE were dramatically enhanced. Renal nerve stimulation in the presence of the alpha-adrenoceptor antagonist phentolamine (1 microM) induced pressor responses of 54 +/- 5 mmHg (n = 6). Alpha-blockade-resistant responses were abolished by the P2-purinoceptor blocker suramin (300 microM) and thus mediated by ATP. Purinergic responses were also reduced significantly (50%) by the NPY-Y1 receptor blocker BIBP 3226 (1 microM). NPY (0.1 microM) potentiated purinergic pressor responses and enhanced ATP release from 0.7 +/- 0.2 to 4.1 +/- 0.9 pmol (n = 4) associated with a significant increase of soluble ATPase activity. All NPY effects were prevented by BIBP 3226. Pressor responses to renal nerve stimulation delivered at short time intervals, mimicking enhanced sympathetic drive to the kidney, were not constant but showed a progressive rise, which was prevented by BIBP 3226. In this study, it is suggested that purinergic vasoconstriction in rat kidney depends on concomitantly released NPY. NPY by itself is only a weak vasoconstrictor but acts as a modulator of renal vascular resistance by enhancing the effects of its sympathetic cotransmitters, especially during sympathetic overactivity.

Adenosine Triphosphatases↗