Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mannitol is an osmotic diuretic with properties that suit it to a variety of clinical situations. Despite the paucity of controlled studies that precisely define optimal use, a consensus based on published work and clinical experience may be reached. Mannitol can be used prophylactically, as a diagnostic aid, or as therapy for the oliguric state. The diuretic properties of mannitol are also useful in patients with refractory edema or intoxications by aspirin, barbiturates, or bromide. As an extracellular solute, the drug may ameliorate intracranial hypertension or symptoms of dialysis dysequilibrium. The renal and systemic effects of this versatile agent are discussed.
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PMID:Mannitol. 678 63

The influence of alterations in sodium intake on blood pressure and indices of peripheral sympathetic activity was studied during the development of hypertension in the SHR. Male SHRs were given a diet containing either low (0.05%), normal (0.29%) or high (3.4%) sodium content beginning at 7 weeks of age. Systolic blood pressure was measured weekly by the tail cuff method in conscious animals. Three weeks after initiation of the diets 24 hour urines were collected for analysis of catecholamines. Plasma catecholamines were measured and the blood pressure response to ganglionic blockade (hexamethonium bromide, 30 mgm/kg) determined. High sodium resulted in a marked increase in the severity of hypertension that was associated with an increase in plasma and urinary norepinephrine concentration and an exaggerated depressor response to ganglionic blockade. In addition, a highly significant positive correlation was seen between plasma norepinephrine concentration and systolic blood pressure. The results are compatible with the hypothesis that the increase in blood pressure in the SHR maintained on a high sodium intake is in part due to an increase in peripheral sympathetic activity.
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PMID:Sodium-neural interactions in the development of spontaneous hypertension. 710 38

The effect of acute 25% decrease in mean arterial pressure (MAP) produced by sodium nitroprusside (SNP) infusion on mean intracerebral and cerebral perfusion pressures was examined in 7 swine with intracranial hypertension. All animals were anesthetized (alpha-chloralose), paralyzed (pancuronium bromide), orotracheally intubated and mechanically ventilated to maintain normocapnia. An epidural balloon was incrementally inflated to produce the desired brain tissue pressure (BTP) which was measured by an intracerebral microtransducer implanted contralateral to the balloon. MAP was measured from the carotid artery; cerebral perfusion pressure (CPP) was calculated as: MAP - BTP. During mildly (14 +/- 1 (SE) mm Hg) or moderately (37 +/- 3 mm Hg) increased BTP, SNP infusion increased BTP (17 +/- 1 and 44 +/- 3 mm Hg, respectively) (p less than 0.05). During severely increased BTP (70 +/- 4 mm Hg), SNP decreased BTP (53 +/- 4 mm Hg, p less than 0.05). Despite this variable BTP, CCP consistently decreased during SNP infusion. BTP and supratentorial subarachnoid cerebrospinal fluid pressure correlated closely; however, the supratentorial subarachnoid pressure consistently underestimated BTP. These findings suggest that estimation of BTP obtained from subarachnoid screw-type devices may not accurately record the pressure within cerebral tissue and the SBNP should not be administered to patients with known or suspected intracranial hypertension unless an intracranial (either BTP or subarachnoid) pressure is being monitored.
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PMID:Brain tissue pressure measurement during sodium nitroprusside infusion. 746 May 73

Adenosine plays several roles in the kidney mediated by the specific receptors A1, A2, and possibly A3. We studied the localization of adenosine A1 receptor mRNA in rat nephron segments using reverse transcription and polymerase chain reaction (RT-PCR). The nephron segments of male Sprague-Dawley rats (6 to 8 weeks old) were microdissected. Total RNA was prepared by the acid-guanidinium-phenol-chloroform method and used in the following RT-PCR assay. Because the PCR primers spanned no intron, samples reacted in the absence of RT were used as controls for amplification of genomic DNA. The PCR products were size-fractionated by electrophoresis, visualized with ethidium bromide staining, and confirmed by Southern blot analysis. PCR products were detected in all of the nephron segments examined. No signals were detected in samples reacted in the absence of RT. Strong signals were detected in glomeruli, medullary collecting duct, cortical thick ascending limb, and medullary thick ascending limb, while weak signals were found in proximal convoluted and straight tubules. Previously, the presence of A1 receptors has been demonstrated in glomeruli, collecting duct, and thick ascending limb in the rat kidney by autoradiography and binding studies. In addition to these segments, we further detected A1 receptor mRNA in proximal convoluted and straight tubules. Thus, A1 receptor mRNA seems to be broadly expressed along the nephron.
Hypertension 1995 Dec
PMID:Adenosine A1 receptor mRNA in microdissected rat nephron segments. 749 92

8-Bromo-guanosine 3':5'-cyclic monophosphate (8-Br-cGMP), an analogue of cyclic guanosine monophosphate (cGMP), induced a time- and dose-dependent enhancement of interleukin-1-induced nitric oxide production in vascular smooth muscle cells. Human atrial natriuretic polypeptide, which stimulates cGMP accumulation in vascular smooth muscle cells, also enhanced interleukin-1-induced nitric oxide release at a concentration of 100 nmol/L. In contrast, coincubation with 10 mumol/L methylene blue, an inhibitor of soluble guanylate cyclase, inhibited interleukin-1-induced nitric oxide release from vascular smooth muscle cells. Furthermore, coincubation with 8-Br-cGMP also enhanced the interleukin-1-induced increase in inducible nitric oxide synthase messenger RNA in vascular smooth muscle cells. However, the enhancement of nitric oxide production induced by 8-Br-cGMP was significantly prevented by coincubation with neutralizing antibody against tumor necrosis factor-alpha. Furthermore, 8-Br-cGMP enhanced the interleukin-1-induced increase in tumor necrosis factor-alpha messenger RNA level in vascular smooth muscle cells. These findings indicate that cGMP may upregulate inducible nitric oxide synthase gene expression through the stimulation of tumor necrosis factor-alpha production in vascular smooth muscle cells. Thus, there may be a positive feedback mechanism between nitric oxide and the cGMP system in vascular smooth muscle cells.
Hypertension 1995 Apr
PMID:cGMP upregulates nitric oxide synthase expression in vascular smooth muscle cells. 753 12

The factors that predispose to the accelerated organ injury that accompanies the hypertensive syndrome have remained speculative and without a firm experimental basis. Indirect evidence has suggested that a key feature may be related to an enhanced oxygen radical production. The purpose of this study was to refine and use a technique to visualize evidence of spontaneous microvascular oxidative stress in vivo in the spontaneously hypertensive rat (SHR) compared with its normotensive control, the Wistar-Kyoto rat (WKY). We investigated the effects of adrenal glucocorticoids on the microvascular oxidative stress sequence. The mesentery was superfused with hydroethidine, a reduced, nonfluorescent precursor of ethidium bromide. In the presence of oxidative challenge, hydroethidine is transformed intracellularly into the fluorescent compound ethidium bromide, which binds to DNA and can be detected by virtue of its red fluorescence. The fluorescent light emission from freshly exteriorized and otherwise unstimulated mesentery microvessels was recorded by digital microscopy. The number of ethidium bromide-positive nuclei along the arteriolar and venular walls in SHR was found to be significantly increased above the level exhibited by WKY. The elevation in ethidium bromide fluorescence in SHR arterioles could be attenuated by a synthetic glucocorticoid inhibitor and in rats subjected to adrenalectomy. The administration of glucocorticoids after adrenalectomy by injection of dexamethasone restored the oxidative reaction in SHR arterioles. Treatment with dimethylthiourea and with a xanthine oxidase inhibitor attenuated the superoxide formation. Although a nitric oxide synthase inhibitor (NG-nitro-L-arginine methyl ester) enhanced the ethidium bromide staining in WKY, it did not affect that in SHR.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 May
PMID:In vivo evidence for microvascular oxidative stress in spontaneously hypertensive rats. Hydroethidine microfluorography. 773 20

beta-Adrenergic blocking agents are used for the treatment of angina pectoris, cardiac arrhythmia, hypertension, anxiety attacks, thyrotoxicosis, migraine and glaucoma. Owing to their sedative effect, they are also used as doping agents in sport. All beta-blockers have an alkanol amine side chain terminating in a secondary amino group in their structure. The pKa values vary from 9.2 to 9.8. Because some beta-blockers are hydrophilic and some lipophilic, simultaneous determination is difficult. In this work, a method based on micellar electrokinetic capillary chromatography (MECC) was developed for the separation and determination of beta-blockers in serum. The phosphate buffer 0.08 M (pH 6.7) solution contained 15 mM N-cetyl-N,N,N-trimethylammonium bromide. Nine parent beta-blockers could be separated in a single run and the concentrations determined by internal standard (ephedrine) method. The simple clean-up procedure consisted of enzyme hydrolysis (Helix pomatia), protein precipitation, and filtration through 0.5-microns PTFE membranes. The MECC method exhibited good repeatability and a linear range of 75-300 micrograms/ml. The method was successfully applied after concentration to the determination of propranolol in real samples.
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PMID:Determination of nine beta-blockers in serum by micellar electrokinetic capillary chromatography. 791 2

beta-Adrenergic blocking agents are of therapeutic value in the treatment of migraine and various cardiovascular disorders (angina pectoris, cardiac arrhythmia, hypertension). Owing to their sedative effect, they are also used as doping agents in sport. A characteristic feature of beta-blockers is the alkanolamine side-chain terminating in a secondary amino group. The pKa values vary from 9.2 to 9.8. Because some beta-blockers are hydrophilic and some lipophilic, simultaneous determination is difficult. In this work, a method based on micellar electrokinetic capillary chromatography (MECC) was developed for the separation and determination of beta-blockers. The 0.08 M phosphate buffer (pH 7.0) solution contained 10 mM N-cetyl-N,N,N-trimethylammonium bromide (CTAB). Ten parent beta-blockers in human urine could be separated in a single run and determined quantitatively by the internal standard (2,6-dimethylphenol) method. Neither endogenous compounds in urine nor caffeine and its metabolites interfered with the analysis. The clean-up procedure for urine consisted of a simple filtration through 0.5-microns PTFE membranes. The MECC method exhibited good repeatability and a linear range of 25-150 micrograms/ml. The method was applied to determination of oxprenolol in real samples.
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PMID:Determination of ten beta-blockers in urine by micellar electrokinetic capillary chromatography. 809 37

We have recently shown that the spontaneously hypertensive rat (SHR) and the Wistar-Kyoto (WKY) rat differ at a frequency of 1 per 62 bases in their nuclear DNA (Hypertension 1992; 19:425-427). Given the origin of these strains this level of divergence was unexpected. To investigate the origin of this nuclear divergence we have examined mitochondrial DNA. Mitochondrial DNA was isolated from SHR and WKY rats, digested with several restriction enzymes, electrophoresed in 1.0% agarose gels, and the fragments visualized with ethidium bromide staining. This approach allowed us to analyze 220 base pairs of mitochondrial DNA. No differences were detected between SHR and WKY rats. Comparison with the King-Holtzman rat strain produced differences at an average of 1 per 52 base pairs. We also examined several SHR and WKY rats from within our colonies and found no differences suggesting intrastrain homogeneity for mitochondrial DNA phenotypes. These data indicate that the SHR and WKY rat share a recent, common maternal ancestor. This result is consistent with the published origins of the SHR and WKY rat strains. Together with the nuclear divergence results, the data suggest that the original Wistar colony from which SHR and WKY rats were derived was probably highly polymorphic for nuclear genes.
Hypertension 1993 Jun
PMID:Inconsistent divergence of mitochondrial DNA in the spontaneously hypertensive rat. 809 45

In 46 patients with biliary tract and pancreatic disorders, in which a diagnostic ERCP was performed, we used as premedication Propinoxate or hyoscine N-butyl bromide in a randomised, prospective study to demonstrate their effectiveness. This was achieved through the endoscopic evaluation, to determine the number of duodenal contractions observed 5 to 10 minutes after i.v. administration of the drugs, as well as the grade of distensibility of the intestinal folds and the occurrence or not of adverse reactions such as increased heart rate and hypertension. 25 patients received 20 mgs of hyoscine N-butyl bromide and the rest 5 mgs propinoxate, i.v. plus diazepam. 48% of patients in the first group and 42.9% in the second one, experienced optimum contractions (0 to 1) after 5 minutes; while after 10 minutes this difference was not significant (40% vs 38%). The incidence of adverse reactions, mainly increased heart rate, was higher for the first group (Hyoscine). Thirty minutes after there were not adverse reactions. We believe that propinoxate (PLIDAN) and hyoscine N-butylbromide, can be used in the pre-medication when performing ERCP.
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PMID:[A clinical trial comparing propinoxate and hyoscine N-butylbromide in endoscopic retrograde cholangiopancreatography (ERCP)]. 818 80


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