Drugs online research references
Kidney Int. 1996 Mar;49(3):626-33.
Regulation of renin release is impaired after nitric oxide inhibition.
Chatziantoniou C, Pauti MD, Pinet F, Promeneur D, Dussaule JC, Ardaillou R.
INSERM U.64, Hopital Tenon, Paris, France.
The aim of the present study was dual: first to establish that a preparation of afferent arterioles freshly isolated from the rat kidney is a suitable model to study renin release and synthesis, and second to investigate the effect(s) of nitric oxide (NO) inhibition on renin release in this model. Purification of renal microvessels was based on iron oxide infusion into the kidneys and separation of the afferent arterioles from glomeruli and connective tissue with a magnet. These microvessels express preprorenin mRNA, contain renin granules and release renin as evidenced by RT-PCR, immunocytochemistry and measurement of renin activity, respectively. Renin secretion was increased in isolated afferent arterioles after in vivo treatment with the diuretic furosemide (+300%) or in vitro treatment with the adenylyl cyclase activator forskolin (+50%), indicating that this vascular preparation responds appropriately to regulators of the renin-angiotensin system. Furthermore, in afferent arterioles isolated from control rats, renin release was positively correlated with total renin content (r = 0.85). In afferent arterioles isolated from rats chronically treated with the NO-synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), forskolin was ineffective in modifying renin release despite stimulation of cAMP levels. In addition, the correlation between renin release and tissue renin content was disrupted. Similar results were obtained when cortical slices were used instead of afferent arterioles, suggesting that this defect in the regulation of renin release is independent of the presence of macula densa cells. To verify that the lack of regulation of renin release after L-NAME treatment was due to NO inhibition, the NO donor 3-morpholino-syndonimin-hydrochloride (SIN-1) was administered in afferent arterioles or cortical slices from kidneys of L-NAME-treated rats. In both preparations, SIN-1 reversed the L-NAME effect and re-established the responsiveness of renin release to forskolin and the relationship between renin release and renin content. These data indicate that the adenylyl cyclase-mediated mechanism regulating renin release is impaired when NO synthesis is inhibited.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8648902&dopt=Abstract
Med Pregl. 1996;49(5-6):206-10.
[Early aggressive treatment in severe craniocerebral injuries]
[Article in Croatian]
Vulekovic P, Momcilovic A, Popovic L, Gvozdenovic L, Kojadinovic Z.
Neurohirurska klinika, Institut za hirurgiju, Medicinski fakultet, Novi Sad.
A series of 33 severely head injured patients, Glasgow Coma Scala score 8 or less, was studied prospectively. All patients were treated by the same protocols and by the physician. Intracranial pressure was monitored in all patients by ventricular puncture. Some degree of increased intracranial pressure (more than 10mmHg) was present at admission to the intensive care unit in 52% of cases. Increases in over 20mmHg during the monitoring period were seen in 15 patients (45%). In 5 patients (15%) he was over 20mmHg, but controlled in intensive care unit with combination of dexamethasone, hyperventilation, normothermia, furosemide and mannitol. In this group mortality rate was 80%. In 10 patients (30%) intracranial hypertension was uncontrollable despite intensive measures, in this group all patients died. The mortality rate in patients with intracranial pressure less than 20mmHg during the monitoring period was significantly lower, 25%. Uncontrollable intracranial hypertension is a serious prognostic sign; all affected patients in our series died. Even intracranial pressure more than 20mmHg, which could be controlled, was associated with high mortality rate (80%). By early aggressive treatment based on intracranial pressure monitoring we can diminish the incidence of intracranial hypertension and reduce overall mortality rate in patients with severe head injury.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8692097&dopt=Abstract
Life Sci. 1996;59(13):1015-24.
Tachyphylaxis to furosemide in isolated airways of guinea pigs.
Iwamoto LM, Wilson VL, Lavallee SL, Fujiwara N, Ayau EL, Nakamura KT.
Dept of Pediatrics, Kapiolani Medical Center for Women and Children, Honolulu, HI 96826, USA.
This in vitro study was conducted to determine whether tachyphylaxis of guinea pig airway to furosemide occurs under conditions that produce tachyphylaxis to the beta 2-adrenoceptor agonist, salbutamol. Isometric tension was measured in tracheal rings bathed in HEPES buffer from 4-6 d newborn guinea pigs of either sex, and 6 wk old males. Paired rings were first incubated with furosemide, 30 or 300 microM, or control for 60 min, washed, then constricted with 3 microM acetylcholine. At stable contraction, relaxation to furosemide (30 microM-1 mM) was measured. For comparison, similar experiments were performed with 10 microM salbutamol incubation for 30 min. 86Rb uptake, a marker for K+ transport and Na-K-Cl cotransport activity, was also measured in these airway segments. Pre-exposure to these airway relaxants did not affect contractile force generation by acetylcholine. Tracheal desensitization to both salbutamol and furosemide was observed. Partial recovery of furosemide induced relaxation was seen one hour after desensitization. Pre-exposure to 300 microM furosemide did not inhibit the decrease in 86Rb uptake normally observed with furosemide. In summary, we found that: 1) tachyphylaxis of guinea pig airway relaxation occurred with both salbutamol and furosemide under similar experimental conditions; however 2) inhibition of 86Rb uptake by furosemide was not affected by prior exposure. Taken together, these results suggest that furosemide induced airway relaxation could be affected by repeated or prolonged exposure, but this response may not be associated with changes in furosemide-sensitive Na-K-Cl cotransporter activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8809220&dopt=Abstract
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