Linked Life Data

9931148

Source:http://linkedlifedata.com/resource/pubmed/id/9931148

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1 Pt 2
pubmed:dateCreated
1999-2-26
pubmed:abstractText
This study was designed to determine the influence of neuronal nitric oxide synthase (nNOS) in tubular flow-dependent regulation of afferent arteriolar diameter in hypertensive Sprague-Dawley rats that received 60 ng/min angiotensin II (Ang II) subcutaneously for 13 days. Systolic blood pressure of control and Ang II-infused rats averaged 122+/-2 (n=23) and 194+/-2 mm Hg (n=24). Afferent arteriolar responses to the nNOS inhibitor S-methyl-L-thiocitrulline (L-SMTC; 0.1 to 10 micromol/L) and the nonselective NOS inhibitor Nomega-nitro-L-arginine (L-NNA; 1 to 100 micromol/L) were assessed in vitro using the blood-perfused juxtamedullary nephron preparation. At a perfusion pressure of 160 mm Hg, afferent arteriolar diameters from control and Ang II-infused rats averaged 18.7+/-1.1 microm (n=8) and 18.1+/-1.1 microm (n=9), respectively, and decreased by 19. 9+/-1.5% and 11.8+/-1.1%, respectively, in response to 10 micromol/L L-SMTC. The L-SMTC-induced afferent arteriolar constriction was significantly greater in control than in Ang II-infused rats. In contrast, 100 micromol/L L-NNA constricted afferent arterioles similarly in both control (n=8) and Ang II-infused (n=7) rats. After transection of the loops of Henle to interrupt flow to the macula densa, the vasoconstrictor responses to L-SMTC but not to L-NNA were reversed. Increasing distal volume delivery by addition of 10 mmol/L acetazolamide to the blood perfusate significantly enhanced the afferent arteriolar constrictor responses to 10 micromol/L L-SMTC (34.5+/-4.8%, n=7) in normotensive rats. In contrast, in Ang II-infused rats, acetazolamide treatment did not enhance the responses to L-SMTC (n=8). These results indicate that chronic Ang II infusion reduces the ability of nNOS-derived nitric oxide to counteract the afferent arteriolar response to increased distal tubular flow.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0194-911X
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
462-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9931148-Acetazolamide, pubmed-meshheading:9931148-Angiotensin II, pubmed-meshheading:9931148-Animals, pubmed-meshheading:9931148-Arterioles, pubmed-meshheading:9931148-Blood Pressure, pubmed-meshheading:9931148-Citrulline, pubmed-meshheading:9931148-Enzyme Inhibitors, pubmed-meshheading:9931148-Hypertension, pubmed-meshheading:9931148-Juxtaglomerular Apparatus, pubmed-meshheading:9931148-Kidney Medulla, pubmed-meshheading:9931148-Male, pubmed-meshheading:9931148-Microscopy, Video, pubmed-meshheading:9931148-Muscle, Smooth, Vascular, pubmed-meshheading:9931148-Nephrons, pubmed-meshheading:9931148-Nitric Oxide Synthase, pubmed-meshheading:9931148-Nitric Oxide Synthase Type I, pubmed-meshheading:9931148-Nitroarginine, pubmed-meshheading:9931148-Rats, pubmed-meshheading:9931148-Rats, Sprague-Dawley, pubmed-meshheading:9931148-Thiourea, pubmed-meshheading:9931148-Vasoconstriction, pubmed-meshheading:9931148-Vasodilation
pubmed:year
1999
pubmed:articleTitle
Neuronal nitric oxide synthase-dependent afferent arteriolar function in angiotensin II-induced hypertension.
pubmed:affiliation
Department of Physiology, Tulane University School of Medicine, New Orleans, LA 70112-2699, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't