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)

Renal injury-induced by phenol injection activates renal sympathetic afferent pathways, increases norepinephrine release from the posterior hypothalamus, activates renal efferent pathways, and provokes a rapid and persistent hypertension. This study aimed to determine whether phenol injury provoked a redistribution of proximal Na(+) transporters from internal stores to the apical cell surface mediated by sympathetic activation, a response that could contribute to generation or maintenance of hypertension. Anesthetized rats were cannulated for arterial blood pressure tracing and saline infusion and then 50 microl 10% phenol or saline was injected into one renal cortex (n = 7 each). Fifty minutes after injection, kidneys were removed and renal cortex membranes from injected kidneys were fractionated on sorbitol gradients and pooled into three windows (WI-WIII) that contained enriched apical brush border (WI); mixed apical, intermicrovillar cleft and dense apical tubules (WII); and intracellular membranes (WIII). Na(+) transporter distributions were determined by immunoblot and expressed as percentage of total in gradient. Acute phenol injury increased blood pressure 20-30 mmHg and led to redistribution of Na(+)/H(+) exchanger type 3 (NHE3) out of WIII (from 22.79 +/- 4.75 to 10.79 +/- 2.01% of total) to WI (13.07 +/- 1.97 to 27.15 +/- 4.08%), Na(+)-P(i) cotransporter 2 out of WII (68.72 +/- 1.95 to 59.76 +/- 2.21%) into WI (9.5 +/- 1.62 to 18.7 +/- 1.45%), and a similar realignment of dipeptidyl-peptidase IV immunoreactivity and alkaline phosphatase activity to WI. Renal denervation before phenol injection prevented the NHE3 redistribution. By confocal microscopy, NHE3 localized to the brush border after phenol injection. The results indicate that phenol injury provokes redistribution of Na(+) transporters from intermicrovillar cleft/intracellular membrane pools to apical membranes associated with sympathetic nervous system activation, which may contribute to phenol injury-induced hypertension.
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PMID:Responses of proximal tubule sodium transporters to acute injury-induced hypertension. 1238 25

The aim of the study was to investigate influence of polymorphism of angiotensin-converting enzyme (ACE) gene on peculiarities of clinical process of such cardiovascular pathology as hypertrophic cardiomyopathy, coronary arterial disease and arterial hypertension. The polymorphism of ACE gene was studied in 98 patients: 38 with hypertrophic cardiomyopathy, 35 with coronary arterial disease and 25 with arterial hypertension. Nuclear DNA was extracted from blood leukocytes by phenol-chloroform method. Genotypes of ACE gene were determined by polymeraze chain reaction, followed with electrophoresis in agarose gel. It has been established, that I/D polymorphism of ACE gene has important modificative significance in clinical process at the mentioned diseases.
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PMID:[Polymorphism of the angiotensin-converting enzyme gene in cardiovascular pathology]. 1244 45

Renal cortical phenol injection provokes acute sympathetic nervous system-dependent hypertension and a shift of proximal tubule Na(+)/H(+) exchanger isoform 3 (NHE3) and Na(+)-P(i) cotransporter type 2 (NaPi2) to apical microvilli. This study aimed to determine whether proximal tubule (PT) Na(+) transporter redistribution persists chronically and whether the pool sizes of renal Na(+) transporters are altered. At 5 wk after a 50-microl 10% phenol injection, blood pressure is elevated: 154 +/- 8 vs. 113 +/- 11 mmHg after saline injection. Cortical membranes were fractionated into three "windows" enriched in apical brush border (WI), mixed apical and intermicrovillar cleft (WII), and intracellular membranes (WIII). NHE3 relative distribution in these windows, assessed by immunoblots and expressed as %total, remained shifted to apical from intracellular membranes (WI: 25.3 +/- 3 in phenol vs.12.7 +/- 3% in saline and WIII: 9.1 +/- 1.3 in phenol vs. 18.9 +/- 3% in saline). NaPi2 and dipeptidyl-peptidase IV also remained shifted to WI, and alkaline phosphatase activity increased 100.9 +/- 29.7 (WI) and 51.4 +/- 17.5% (WII) in phenol-injected membranes. Na(+) transporter total abundance [NHE3, NaPi2, thiazide-sensitive Na-Cl cotransporter, bumetanide-sensitive Na-K-2Cl cotransporter, Na-K-ATPase alpha(1)- and beta(1)-subunits, and epithelial Na(+) channel (ENaC) alpha- and beta-subunits] was profiled by immunoblotting. Only cortical NHE3 abundance was altered, decreasing to 0.56 +/- 0.06. The results demonstrate that phenol injury provokes a persistant shift of PT NHE3 and NaPi2 to the apical microvilli, along with a 44% decrease in total NHE3, evidence for an escape mechanism that would counteract the redistribution of a larger fraction of NHE3 to the apical surface by normalizing the total amount of NHE3 in apical membranes.
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PMID:Chronic renal injury-induced hypertension alters renal NHE3 distribution and abundance. 1255 35

Aim of the study was to elucidate relationship between complex effect on organism of unfavorable ecological factors of high altitudes and course of ischemic heart disease (IHD) and hypertensive disease in Surgut (Khanty-Mansi Autonomous District). Five year medico-ecological monitoring established direct relation between dynamics of average monthly hospital admissions of patients with IHD and hypertension, level of atmospheric pressure and concentration of phenol in the air. Complex of nature conservation measures resulted in decreases of frequency of hospitalizations as well as cardiovascular morbidity with temporary loss of working capacity.
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PMID:[Medico-ecological monitoring of cardiovascular diseases in the urbanized north]. 1289 Dec 87

Increasing evidence indicates that afferent impulses from injured kidney may activate areas of the brain involved in the noradrenergic regulation of blood pressure and largely contribute to the development and maintenance of hypertension associated with renal diseases. A new model of hypertension developed in our laboratory by an intrarenal injection of phenol has largely substantiated this hypothesis. Our studies also provide evidence that complex interactions exist between interleukin (IL)-1Beta and nitric oxide in the regulation of central sympathetic nervous system (SNS) activity and blood pressure. Following renal injury with phenol, the abundance of IL-1Beta and neuronal isoform of nitric oxide synthase (nNOS) in the brain decreased, and this may mediate the rise in SNS activity. Finally, our studies provide evidence that locally produced angiotensin II in the brain may ultimately mediate the downregulation of IL-1Beta and nNOS and result in increased SNS activity and hypertension in the phenol-renal-injury model.
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PMID:A new model of neurogenic hypertension caused by renal injury: pathophysiology and therapeutic implications. 1458 11

Previous investigations have demonstrated that capsaicin-sensitive sensory nerves are involved in the development of hypertension in some rat models of hypertension. To determine the role played by calcitonin gene-related peptide (CGRP; the predominant neurotransmitter in capsaicin-sensitive sensory nerves) in a rat model of neurogenic hypertension, in which hypertension was induced by injecting 50 microl of 10% phenol in the lower pole of the left kidney, systolic blood pressure (SBP) was monitored by the tail-cuff method throughout the experiment. Fifteen days after injection of phenol, mean arterial pressure (MAP), concentrations of CGRP in the plasma, the expression of CGRP mRNA in dorsal root ganglia (DRG) and CGRP content in laminae I and II of the spinal cord were measured. SBP was significantly increased 5 days after the intrarenal injection of phenol (164+/-7 mm Hg, p<0.01). At the end of experiment, blood pressure (BP) was significantly elevated in the phenol-injected rats compared with the controls (SBP: 187+/-6 vs. 122+/-4 mm Hg, p<0.01; MAP: 157.56+/-3.02 vs. 103.80+/-2.04 mm Hg, p<0.01). Treatment with capsaicin, which selectively depletes neurotransmitters from the capsaicin-sensitive nerves, failed to enhance the development of hypertensive responses to the intrarenal injection of phenol. Intravenous administration of CGRP(8-37), the specific CGRP receptor antagonist, also failed to increase the already elevated MAP. The expression of CGRP mRNA (both alpha- and beta-CGRP isoforms), the content of CGRP in laminae I and II of the dorsal horn of the spinal cord and the concentration of CGRP in the plasma was decreased in the rats treated with phenol. These results suggest that CGRP does not play a counterregulatory role in the phenol-induced hypertensive rats, and support the hypothesis that reduction of CGRP (alpha and beta isoforms) could contribute to a blood pressure elevation in this setting.
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PMID:Role of calcitonin gene-related peptide in the phenol-induced neurogenic hypertension in rats. 1512 Apr 75

Spontaneously hypertensive rats (SHR) exhibit impairment across several cognitive domains such as attention, short-term memory and spatial reference memory. These cognitive deficits have been variously attributed to disrupted dopaminergic, cholinergic and adenosinergic neurotransmitter function. However, social memory in SHR has not been investigated. In the present study, we therefore evaluated whether SHR exhibit altered short-term social memory abilities compared to normotensive Wistar rats (WIS) through two experimental paradigms (social recognition and habituation-dishabituation tests). We also compared the performance of SHR and WIS rats in the object recognition test. SHR exhibited significantly impaired performance in both models of social memory, but not in the object recognition test, demonstrating a selective deficit in the ability to recognize a juvenile rat after a short period of time. The administration of acute doses of the non-selective adenosine receptor antagonist caffeine (3.0 or 10.0 mg/kg, i.p.) and the adenosine A2A receptor antagonist 4-(2-[7-amino-2-[2-furyl][1,2,4]triazolo-[2,3-a][1,3,5]triazin-5-yl-amino]ethyl) phenol (ZM241385, 0.5 or 1.0 mg/kg, i.p.) but not the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 1.0 or 3.0 mg/kg, i.p.) reversed this social memory impairment in SHR, but these treatments did not alter the hypertension state. These results demonstrate an impairment of short-term social memory in SHR and the involvement of the adenosine A2A receptors in this alteration.
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PMID:Blockade of adenosine A2A receptors reverses short-term social memory impairments in spontaneously hypertensive rats. 1581 83

Spontaneously hypertensive rats (SHRs) are often used as a model of attention deficit hyperactivity disorder (ADHD) and to investigate the effects of hypertension on cognitive function. Further, they appear to have reduced numbers of central nicotinic acetylcholine receptors (nAChRs) and, therefore, may be useful to model certain aspects of Alzheimer's disease (AD) and other forms of dementia given that a decrease in nAChRs is thought to contribute to cognitive decline in these disorders. In the present study, based on reports that chronic nicotine exposure increases nAChRs in several mammalian models, we tested the hypothesis that repeated exposures to a relatively low dose of the alkaloid would ameliorate the receptor deficits in SHR. Thus, young-adult SHRs and age-matched Wistar-Kyoto (WKY) control rats were treated with either saline or nicotine twice a day for 14 days (total daily dose = 0.7 mg/kg nicotine base) and then sacrificed. Quantitative receptor autoradiography with [125I]-IPH, an epibatidine analog, revealed: (1) that high-affinity nAChRs were higher in saline-treated WKY (control) rats compared to saline-treated SHRs in 18 of the 19 brain region measured, although statistically different only in the mediodorsal thalamic nuclei, (2) that nicotine significantly increased nAChR binding in WKY rats in six brain areas including cortical regions and the anterior thalamic nucleus, (3) that there were no cases where nicotine significantly increased nAChR binding in SHRs. These results indicate that subjects deficient in nAChRs may be less sensitive to nAChR upregulation with nicotine than normal subjects and require higher doses or longer periods of exposure.
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PMID:Effect of repeated nicotine exposure on high-affinity nicotinic acetylcholine receptor density in spontaneously hypertensive rats. 1591 Nov 41

Capsaicin-sensitive sensory nerves participate in the regulation of cardiovascular functions both in the normal state and the pathophysiology of hypertension through the actions of potent vasodilator neuropeptides, including calcitonin gene-related peptide (CGRP). CGRP, a very potent vasodilator, is the predominant neurotransmitter in capsaicin-sensitive sensory nerves, and plays an important role in the initiation, progression and maintenance of hypertension via: (1) the alterations in its synthesis and release and/or in vascular sensitivity response to it; (2) interactions with pro-hypertensive systems, including renin-angiotensin-aldosterone system, sympathetic nervous system and endothelin system; and (3) anti-hypertrophy and anti-proliferation of vascular smooth muscle cells. The decrease in CGRP synthesis and release contributes to the elevated blood pressure, as shown in the spontaneously hypertensive rats, alpha-CGRP knockout mice, Dahl-salt or phenol-induced hypertensive rats. In contrast, the increase in CGRP levels or the enhancement of vascular sensitivity response to CGRP plays a beneficial compensatory depressor role in the development of hypertension, as shown in deoxycorticosterone-salt, sub-total nephrectomy-salt, N(omega)-nitro-L-arginine methyl ester or two-kidney, one-clip models of hypertension in rats. We found that rutaecarpine causes a sustained depressor action by stimulation of CGRP synthesis and release via activation of vanilloid receptor subtype 1 (VR1) in hypertensive rats, which reveals the therapeutic implications of VR1 agonists for treatment of hypertension.
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PMID:Calcitonin gene-related peptide and hypertension. 1611 10

Injection of 50 microl 10% phenol into rat renal cortex activates renal sympathetic nerve activity which provokes acute hypertension that persists for weeks. We have previously shown with membrane fractionation that phenol injury caused a redistribution of the main proximal tubule (PT) apical transporter NHE3 (Na+/H+ exchanger isoform 3) to low density membranes enriched in apical microvilli. The aim of this study was to determine whether phenol injury increases PT apical Na+/H+ exchanger (NHE) activity. NHE activity was measured in vivo as the initial rate of change in intracellular pH (dpH(i)/dt) during luminal Na+ removal in PT preloaded with the pH-sensitive fluorescence dye BCECF. Injection of 50 microl 10% phenol increased blood pressure from 113 +/- 5.2 to 130 +/- 4.6 mmHg without changing glomerular filtration rate or urine output. NHE activity increased 2.6-fold by 70 min after phenol injury. The increase of NHE activity was accompanied with an increase of tubular reabsorption. Total NHE activity/NHE3 protein in cortical brush-border membrane (BBM) vesicles, measured by acridine orange quench and immunoblot, respectively, was unchanged by phenol injury. In conclusion, acute phenol injury provokes coincident increases in PT apical NHE activity, redistribution of NHE3 into low density apical membranes, and hypertension. The increase in NHE activity may contribute to the lack of pressure-diuresis and the maintenance of chronic hypertension in this model.
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PMID:Phenol injury-induced hypertension stimulates proximal tubule Na+/H+ exchanger activity. 1639 Aug 65


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