dc.creatorKrieger, MH
dc.creatorMoreira, ED
dc.creatorOliveira, EM
dc.creatorOliveira, VLL
dc.creatorKrieger, EM
dc.creatorKrieger, JE
dc.date2006
dc.dateMAY-JUN
dc.date2014-11-20T03:39:27Z
dc.date2015-11-26T17:13:27Z
dc.date2014-11-20T03:39:27Z
dc.date2015-11-26T17:13:27Z
dc.date.accessioned2018-03-29T00:01:49Z
dc.date.available2018-03-29T00:01:49Z
dc.identifierClinical And Experimental Pharmacology And Physiology. Blackwell Publishing, v. 33, n. 41795, n. 471, n. 476, 2006.
dc.identifier0305-1870
dc.identifierWOS:000237420800009
dc.identifier10.1111/j.1440-1681.2006.04389.x
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/62542
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/62542
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/62542
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1281574
dc.description1. Blood pressure (BP) and heart rate (HR) increase 6 and 24 h after sinoaortic baroreceptor denervation (SAD), whereas plasma renin activity (PRA) and renal renin mRNA levels remain unchanged. We postulated that a simultaneous rise in BP could offset the expected activation of renin associated with an increased renal sympathetic discharge secondary to SAD. 2. To test this hypothesis, the increase in BP associated with the onset of SAD was prevented by a continuous infusion of sodium nitroprusside (SNP; 30 mg/kg per h). Changes were measured in five groups of conscious adult male Wistar rats: (i) sham; (ii) SAD; (iii) SAD rats in which the BP was prevented from increasing by infusion of SNP; (iv) sham rats in which the BP was increased by 30% by infusion of phenylephrine (PE; 1.5-2.0 mL/h); and (v) SNP + PE for 3 h by infusion as above. 3. As expected, BP and heart rate (HR) increased significantly following SAD compared with sham rats (152 +/- 4 vs 116 +/- 3 mmHg, respectively, for BP and 503 +/- 6 vs 345 +/- 13 b.p.m., respectively for HR; n = 5; P < 0.05) but remained unchanged when SNP was infused for 3 h (106 +/- 1 mmHg and 455 +/- 9 b.p.m., respectively; n = 5; P < 0.05). 4. Similarly, BP and HR increased with PE infusion compared with PE + SNP (138 +/- 9.9 vs 113 +/- 2.3 mmHg for BP, respectively, and 325 +/- 9 vs 423 +/- 18 b.p.m. for HR, respectively; n = 5; P < 0.05). 5. Plasma renin activity remained unchanged in SAD compared with sham rats (1.67 +/- 0.35 vs 1.05 +/- 0.17 ng angiotensin (Ang) I/mL per h), but increased significantly when hypertension was prevented (5.86 +/- 0.77 ng AngI/mL per h; n = 5; P < 0.05). Renin mRNA levels in the kidneys were unchanged in all groups. 6. These results show that an elevation in BP appears to offset increased renal sympathetic discharge with no change in PRA.
dc.description33
dc.description41795
dc.description471
dc.description476
dc.languageen
dc.publisherBlackwell Publishing
dc.publisherOxford
dc.publisherInglaterra
dc.relationClinical And Experimental Pharmacology And Physiology
dc.relationClin. Exp. Pharmacol. Physiol.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectneurogenic hypertension
dc.subjectplasma renin activity
dc.subjectrenin mRNA
dc.subjectsympathetic hyperactivity
dc.subjectNeurogenic Hypertension
dc.subjectMessenger-rna
dc.subjectNitric-oxide
dc.subjectSecretion
dc.subjectGene
dc.subjectNerves
dc.subjectCells
dc.subjectTranscription
dc.subjectStimulation
dc.subjectProrenin
dc.titleDissociation of blood pressure and sympathetic activation of renin release in sinoaortic-denervated rats
dc.typeArtículos de revistas


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