Drugs online research references
J Urol. 1996 Mar;155(3):1104-7.
Tachykinin NK-2 receptors in child urinary bladder.
Zeng XP, Burcher E.
School of Physiology and Pharmacology, University of New South Wales, Sydney, Australia.
PURPOSE: Although NK-2 receptors mediate contractions to tachykinins in adult detrusor muscle, little is known about the functions of tachykinins in child urinary bladder. Here we have used highly selective agonists and antagonists to examine NK-2 receptors in child detrusor muscle. MATERIALS AND METHODS: Specimens of urinary bladder from 23 children (0 to 10 years0 were obtained at operation for vesicoureteric reflux. Strips of detrusor muscle were mounted in organ baths in Krebs solution containing phosphoramidon (10 microM.), and isometric tension was recorded. Contractile responses were elicited by tachykinins and selective agonists in the presence and absence of autonomic inhibitors and of tachykinin NK-2 receptor antagonists. RESULTS: The NK-2 receptor agonists neurokinin A (NKA), neuropeptide gamma and [Lys5, MeLeu9, Nle10]-NKA(4-10) contracted the isolated child detrusor, with pD2 values of 7.7, 7.2 and 7.3. The maximum response to NKA was greater than that to the other 2 agonists. No age-related differences were seen. Selective agonists for NK-1 receptors ([Sar9, Met(O2)11]-SP and septide) and NK-3 receptors (senktide) were ineffective contractile agents. Responses to NKA were unaffected by phentolamine (5 microM.), propranolol (3 microM.), tetrodotoxin (1 microM.) and indomethacin (1 microM.), indicating a direct action on smooth muscle. The tachykinin NK-2 receptor antagonists SR 48968 and MEN 10627 caused a concentration-dependent antagonism of responses to NKA, with apparent pKB values of 9.4 and 8.1. CONCLUSIONS: Neurokinin A appears to act directly on NK-2 receptors on detrusor muscle of infant and child urinary bladder, without involvement of neural or indirect contractile mechanisms. Potency of antagonists was similar to that seen in other tissues. However, agonist potency was significantly lower in the isolated detrusor from children, compared with our previous study in adult detrusor. This discrepancy may be related to age-related differences in NK-2 receptors or in contractile mechanisms; alternatively it may be a result of the reflux condition.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8583573&dopt=Abstract
J Mal Vasc. 1995;20(4):288-9.
[Medical treatment of aortic aneurysms using beta-blockers]
[Article in French]
Chakkour K, Gouny P, Nussaume O, Vayssairat M.
Service de Chirurgie Vasculaire et Thoracique, Hopital Rothschild, Paris.
There is no known treatment capable of avoiding extension and rupture of aneurysms of the abdominal aorta. There has however been much work recently suggesting a favourable effect of beta-blockers. Early work with experimental animal models of aortic aneurysms showed that Propranolol has a protective effect on extension and rupture of these aneurysms. Studies of the biochemistry of the aortic wall have shown that Propranolol has an independent effect on blood pressure, stimulation lysyl-oxidase and production of intermolecular elastin bridges which strengthen the arterial wall. In man, Propranolol slows the progressive dilatation of the aorta in Marfan's disease. These data on atherosclerosis aneurysms are only part of the picture, but 3 studies have shown that slower widening of the aorta diameter is related to treatment with beta-blockers. In conclusion, the surgical indications for aneurysms in 1995 are unchanged from those in 1994. In cases where surgery is not indicated (patient refusal, operative risk too high, small aneurysms) could comprise a study group for a randomized evaluation against placebo of the effect of beta-blockers. A controlled study is required before therapeutic strategies can be modified.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8586949&dopt=Abstract
J Neurophysiol. 1995 Nov;74(5):1911-9.
Actions of norepinephrine on rat hypoglossal motoneurons.
Parkis MA, Bayliss DA, Berger AJ.
Department of Physiology and Biophysics SJ-40, University of Washington School of Medicine, Seattle 98195.
1. We used conventional intracellular recording techniques in 400-microns-thick slices from the brain stems of juvenile rats to investigate the action of norepinephrine (NE) on subthreshold and firing properties of hypoglossal motoneurons (HMs). 2. In recordings in current-clamp mode, 50 or 100 microM NE elicited a reversible depolarization accompanied by an increase in input resistance (RN) in all HMs tested (n = 74). In recordings in single-electrode voltage-clamp mode, NE induced a reversible inward current (INE) accompanied by a reduction in input conductance. The average reversal potential for INE was -104 mV. The NE responses could be elicited in a Ca(2+)-free solution containing tetrodotoxin, indicating that they were postsynaptic. 3. The NE response could be blocked by the alpha-adrenoceptor antagonist prazosin, but not by the beta-adrenoceptor antagonist propranolol, and could be mimicked by the alpha 1-adrenoceptor agonist phenylephrine but not by the alpha 2-adrenoceptor agonist UK 14,304 or by the beta-adrenoceptor agonist isoproterenol when alpha-adrenoceptors were blocked. 4. Substitution of barium for calcium in the perfusion solution blocked the increase in RN in response to NE without completely blocking the depolarization. Replacement of sodium chloride with choline chloride in the barium-substituted perfusion solution blocked the remaining depolarization. 5. The neuropeptide thyrotropin-releasing hormone (TRH), which also depolarizes and increases the RN of HMs, occluded the response of HMs to NE. 6. NE altered HM firing properties in three ways: it always lowered the minimum amount of injected current needed to elicit repetitive firing, it increased the slope of the firing frequency versus injected current relation in 8 of 14 cells tested, and it increased the delay from the onset of the depolarizing current pulse to the first evoked spike in all cells tested. 7. We conclude that NE acts directly on alpha 1-adrenoceptors to increase the excitability of HMs. It does this by reducing a barium-sensitive resting potassium current and activating a barium-insensitive inward current carried primarily by sodium ions. A portion of the intracellular pathway for these actions is shared by TRH. In addition, there is evidence that NE alters HM firing patterns by affecting currents that are activated following depolarization.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8592184&dopt=Abstract
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