Endothelial NO and prostanoid involvement in newborn  and juvenile pig pial arteriolar vasomotor responses

Specific cerebrovascular dilatory responses in newborn piglets are entirely prostanoid dependent, but require both nitric oxide (NO) and prostanoids in juveniles. We examined endothelial dependency and mechanisms of NO- and prostanoid-mediated cerebrovascular responses in anesthetized newborn and juvenile pigs implanted with closed cranial windows. Light/dye endothelial injury inhibited newborn and juvenile hypercapnic and bradykinin (BK) responses and inhibited dilation to acetylcholine in juveniles. Iloprost and NO act permissively in restoring light/dye inhibited newborn and juvenile responses, respectively. Differences in sensitivity to iloprost and sodium nitroprusside were not observed. Juvenile (not newborn) hypercapnic and BK cerebrovascular responses were sensitive to soluble guanylyl cyclase inhibition. Pial arteriolar diameter and cortical production of prostacyclin, cAMP, and cGMP in response to BK were measured under control conditions, after treatment with indomethacin and/or N ω-nitro-l-arginine methyl ester (l-NAME). Indomethacin inhibited BK responses in newborns. Juvenile responses were inhibited by l-NAME, and mildly by indomethacin. Cortical 6-keto-PGF1α, cAMP, and cGMP increased in response to BK in both age groups. Newborn cerebrovascular responses are largely NO independent, but NO becomes more important with maturation.

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Maturational changes in the regulation of pulmonary vascular tone by nitric oxide in neonatal rats

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00235.2006 ◽

2007 ◽

Vol 293 (5) ◽

pp. L1261-L1270 ◽

Cited By ~ 14

Author(s):

Louis G. Chicoine ◽

Michael L. Paffett ◽

Mark R. Girton ◽

Matthew J. Metropoulus ◽

Mandar S. Joshi ◽

...

Keyword(s):

Nitric Oxide ◽

Guanylyl Cyclase ◽

Vascular Tone ◽

Age Groups ◽

Soluble Guanylyl Cyclase ◽

No Production ◽

Sprague Dawley ◽

No Donor ◽

Early Postnatal Development ◽

Old Rats

Nitric oxide (NO) is an important regulator of vasomotor tone in the pulmonary circulation. We tested the hypothesis that the role NO plays in regulating vascular tone changes during early postnatal development. Isolated, perfused lungs from 7- and 14-day-old Sprague-Dawley rats were studied. Baseline total pulmonary vascular resistance (PVR) was not different between age groups. The addition of KCl to the perfusate caused a concentration-dependent increase in PVR that did not differ between age groups. However, the nitric oxide synthase (NOS) inhibitor Nω-nitro-l-arginine augmented the K+-induced increase in PVR in both groups, and the effect was greater in lungs from 14-day-old rats vs. 7-day-old rats. Lung levels of total endothelial, inducible, and neuronal NOS proteins were not different between groups; however, the production rate of exhaled NO was greater in lungs from 14-day-old rats compared with those of 7-day-old rats. Vasodilation to 0.1 μM of the NO donor spermine NONOate was greater in 14-day lungs than in 7-day lungs, and lung levels of both soluble guanylyl cyclase and cGMP were greater at 14 days than at 7 days. Vasodilation to 100 μM of the cGMP analog 8-(4-chlorophenylthio)guanosine-3′,5′-cyclic monophosphate was greater in 7-day lungs than in 14-day lungs. Our results demonstrate that the pulmonary vascular bed depends more on NO production to modulate vascular tone at 14 days than at 7 days of age. The observed differences in NO sensitivity may be due to maturational increases in soluble guanylyl cyclase protein levels.

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The inhibitory effect of sodium nitroprusside on HIF-1 activation is not dependent on nitric oxide-soluble guanylyl cyclase pathway

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2004.09.064 ◽

2004 ◽

Vol 324 (1) ◽

pp. 417-423 ◽

Cited By ~ 21

Author(s):

Satoshi Takabuchi ◽

Kiichi Hirota ◽

Kenichiro Nishi ◽

Seiko Oda ◽

Tomoyuki Oda ◽

...

Keyword(s):

Nitric Oxide ◽

Sodium Nitroprusside ◽

Guanylyl Cyclase ◽

Soluble Guanylyl Cyclase ◽

Inhibitory Effect

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Gene Expression of Brain Nitric Oxide Synthase and Soluble Guanylyl Cyclase in Hypothalamus and Medulla of Two-Kidney, One Clip Hypertensive Rats

Hypertension ◽

10.1161/01.hyp.26.1.171 ◽

1995 ◽

Vol 26 (1) ◽

pp. 171-176 ◽

Cited By ~ 34

Author(s):

Teresa L. Krukoff ◽

Frank Gehlen ◽

Detlev Ganten ◽

Jürgen Wagner

Keyword(s):

Gene Expression ◽

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Guanylyl Cyclase ◽

Soluble Guanylyl Cyclase ◽

Hypertensive Rats ◽

Oxide Synthase ◽

Brain Nitric Oxide

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Cyclic Guanosine Monophosphate Modulates Locomotor Acceleration Induced by Nitric Oxide but not Serotonin in Clione limacina Central Pattern Generator Swim Interneurons

Integrative Organismal Biology ◽

10.1093/iob/obaa045 ◽

2020 ◽

Author(s):

Thomas J Pirtle ◽

Richard A Satterlie

Keyword(s):

Nitric Oxide ◽

Central Pattern Generator ◽

Guanylyl Cyclase ◽

Signal Transduction Pathway ◽

Soluble Guanylyl Cyclase ◽

Cyclic Guanosine Monophosphate ◽

Pattern Generator ◽

Guanosine Monophosphate ◽

Cellular Changes ◽

Clione Limacina

Abstract Typically, the marine mollusk, Clione limacina, exhibits a slow, hovering locomotor gait to maintain its position in the water column. However, the animal exhibits behaviorally relevant locomotor swim acceleration during escape response and feeding behavior. Both nitric oxide and serotonin mediate this behavioral swim acceleration. In this study, we examine the role that the second messenger, cGMP, plays in mediating nitric oxide and serotonin-induced swim acceleration. We observed that the application of an analog of cGMP or an activator of soluble guanylyl cyclase increased fictive locomotor speed recorded from Pd-7 interneurons of the animal’s locomotor central pattern generator. Moreover, inhibition of soluble guanylyl cyclase decreased fictive locomotor speed. These results suggest that basal levels of cGMP are important for slow swimming and that increased production of cGMP mediates swim acceleration in Clione. Because nitric oxide has its effect through cGMP signaling and because we show herein that cGMP produces cellular changes in Clione swim interneurons that are consistent with cellular changes produced by serotonin application, we hypothesize that both nitric oxide and serotonin function via a common signal transduction pathway that involves cGMP. Our results show that cGMP mediates nitric oxide-induced but not serotonin-induced swim acceleration in Clione.

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