Linked Life Data

16293681

Source:http://linkedlifedata.com/resource/pubmed/id/16293681

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-3-15
pubmed:abstractText
Nonselective inhibition of nitric oxide (NO) synthase (NOS) augments myogenic autoregulation, an action that implies enhancement of pressure-induced constriction and dilatation. This pattern is not explained solely by interaction with a vasoconstrictor pathway. To test involvement of the Rho-Rho kinase pathway in modulation of autoregulation by NO, the selective Rho kinase inhibitor Y-27632 and/or the NOS inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME) were infused into the left renal artery of anesthetized rats. Y-27632 and l-NAME were also infused into isolated, perfused hydronephrotic kidneys to assess myogenic autoregulation over a wide range of perfusion pressure. In vivo, l-NAME reduced renal vascular conductance and augmented myogenic autoregulation, as shown by increased slope of gain reduction and associated phase peak in the pressure-flow transfer function. Y-27632 (10 mumol/l) strongly dilated the renal vasculature and profoundly inhibited autoregulation in the absence or presence of l-NAME in vivo and in vitro. Afferent arteriolar constriction induced by 30 mmol/l KCl was reversed (-92 +/- 3%) by Y-27632. Phenylephrine caused strong renal vasoconstriction but did not affect autoregulation. Inhibition of neuronal NOS by N(5)-(1-imino-3-butenyl)-l-ornithine (l-VNIO) did not cause significant vasoconstriction but did augment myogenic autoregulation. Thus vasoconstriction is neither necessary (l-VNIO) nor sufficient (phenylephrine) to explain the augmented myogenic autoregulation induced by l-NAME. The effect of l-VNIO implicates tubuloglomerular feedback (TGF) and neuronal NOS at the macula densa in regulation of the myogenic mechanism. This conclusion was confirmed by the demonstration that systemic furosemide removed the TGF signature from the pressure-flow transfer function and significantly inhibited myogenic autoregulation. In the presence of furosemide, augmentation of myogenic autoregulation by l-NAME was significantly reduced. These results provide a potential mechanism to explain interaction between myogenic and TGF-mediated autoregulation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0363-6119
pubmed:author
pubmed:issnType
Print
pubmed:volume
290
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R982-91
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16293681-Amides, pubmed-meshheading:16293681-Animals, pubmed-meshheading:16293681-Drug Synergism, pubmed-meshheading:16293681-Enzyme Inhibitors, pubmed-meshheading:16293681-Feedback, Physiological, pubmed-meshheading:16293681-Kidney, pubmed-meshheading:16293681-Kidney Tubules, pubmed-meshheading:16293681-Male, pubmed-meshheading:16293681-NG-Nitroarginine Methyl Ester, pubmed-meshheading:16293681-Nitric Oxide, pubmed-meshheading:16293681-Nitric Oxide Synthase, pubmed-meshheading:16293681-Ornithine, pubmed-meshheading:16293681-Perfusion, pubmed-meshheading:16293681-Pyridines, pubmed-meshheading:16293681-Rats, pubmed-meshheading:16293681-Rats, Sprague-Dawley, pubmed-meshheading:16293681-Rats, Wistar, pubmed-meshheading:16293681-Renal Circulation, pubmed-meshheading:16293681-Vasoconstriction
pubmed:year
2006
pubmed:articleTitle
Tubuloglomerular feedback-dependent modulation of renal myogenic autoregulation by nitric oxide.
pubmed:affiliation
Biology Department, Concordia University, Montreal, QB, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't