Role of Prostacyclin and Nitric Oxide in Regulation of Basal Microvascular Hydraulic Permeability in Cat Skeletal Muscle

Möller, Alma D.; Grände, Per‐Olof

doi:10.1159/000025648

Cited by 21 publications

(31 citation statements)

References 28 publications

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“…26 -30 Although the role of NO in the renal microvascular permeability has not yet been examined, studies conducted in other vascular beds suggest that peritubular capillary permeability may be influenced by alterations in intrarenal NO and thus could influence RIHP. 26,27,29,30 Thus, one possible mechanism by which increased NO could increase RIHP is by decreasing the filtration coefficient. 27,30 It was reported, however, that hydraulic conductivity in frog mesenteric capillaries was increased by luminal exposure of a NO donor agent, sodium nitroprusside, and decreased by superfusion with a NO inhibitor agent.…”

Section: Renal Responses To Reductions In Rap Before and During No Symentioning

confidence: 99%

“…26,27,29,30 Thus, one possible mechanism by which increased NO could increase RIHP is by decreasing the filtration coefficient. 27,30 It was reported, however, that hydraulic conductivity in frog mesenteric capillaries was increased by luminal exposure of a NO donor agent, sodium nitroprusside, and decreased by superfusion with a NO inhibitor agent. 31,32 These findings indicate that NO can elicit changes in RIHP by altering the filtration coefficient (K f ) of the peritubular capillary membrane, but the available data indicate that such changes are opposite to those required.…”

Section: Renal Responses To Reductions In Rap Before and During No Symentioning

confidence: 99%

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Nitric Oxide Dependency of Arterial Pressure–Induced Changes in Renal Interstitial Hydrostatic Pressure in Dogs

Majid

Said

Omoro

et al. 2001

Circulation Research

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Abstract-A direct relationship between renal arterial pressure (RAP) and renal interstitial hydrostatic pressure (RIHP) has been shown under conditions of efficient renal blood flow autoregulation. Experiments were performed in six anesthetized dogs to evaluate whether these RIHP responses to changes in RAP were modified during nitric oxide (NO) inhibition with nitro-L-arginine (NLA) or after administration of NO donor agents. A microtip catheter transducer was placed underneath the renal capsule to measure RIHP. Stepwise reductions in RAP (140 to 80 mm Hg) during control conditions resulted in decreases in RIHP from its basal value of 4.7Ϯ1.1 mm Hg with a slope of 0.04Ϯ0.026 mm Hg ⅐ mm Hg Ϫ1 along with decreases in urinary nitrate/nitrite excretion rate (U NOx V). Renal cortical and medullary blood flows, measured by laser-Doppler flowmetry, exhibited high autoregulatory efficiency over this RAP range. The changes in RIHP during alterations in RAP were positively correlated (rϭ0.743; PϽ0.001) with the changes in U NOx V but not with cortical or medullary blood flow. NLA infusion decreased RIHP to 1.9Ϯ0.5 mm Hg and also reduced U NOx V from 1.8Ϯ0.2 to 0.9Ϯ0.01 nmol ⅐ min Ϫ1 ⅐ g Ϫ1 . Infusion of NO donors restored RIHP (4.3Ϯ0.9 mm Hg) andDuring NLA infusion, the RIHP responses to reductions in RAP were markedly attenuated and were not restored even during constant-rate infusion of NO donors. The results suggest that changes in RIHP in response to alterations in RAP are associated with changes in intrarenal NO, suggesting a direct effect of NO to regulate RIHP. Key Words: renal regional blood flow Ⅲ laser-Doppler flowmetry Ⅲ nitrate/nitrite excretion P revious studies in dogs and rats have shown that changes in renal arterial pressure (RAP), within the autoregulatory range, are associated with changes in renal interstitial hydrostatic pressure (RIHP), and it has been suggested that these changes in RIHP contribute to the control of tubular reabsorptive function via alterations in the renal interstitial environment. [1][2][3][4][5] The mechanism responsible for RAP-induced changes in RIHP has remained difficult to explain, because renal blood flow (RBF) and peritubular capillary pressure are efficiently autoregulated during alterations in RAP over a wide range. 6 -8 Findings in volume-expanded rats that the renal medullary blood flow (MBF) is more sensitive to changes in RAP than the cortical blood flow (CBF) 9 have led to the suggestion that impaired autoregulatory efficiency of MBF may be linked to the changes in RIHP. 1,10 However, direct associations between changes in RIHP and changes in regional blood flows in the kidney during alterations in RAP have not been established. In addition, studies in dogs as well as in euvolumic rats have failed to demonstrate reduced autoregulatory efficiency of MBF. 6,9,11,12 Inhibition of nitric oxide (NO) synthesis in rats was shown to decrease RIHP and attenuate RIHP responses to changes in renal perfusion pressure. 3 Moreover, selective inhibition of NO in the rat renal med...

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Section: Renal Responses To Reductions In Rap Before and During No Symentioning

confidence: 99%

Section: Renal Responses To Reductions In Rap Before and During No Symentioning

confidence: 99%

Nitric Oxide Dependency of Arterial Pressure–Induced Changes in Renal Interstitial Hydrostatic Pressure in Dogs

Majid

Said

Omoro

et al. 2001

Circulation Research

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“…This relative decrease in PGI 2 levels would lead to decreased vasodilation, increased leukocyte adhesion and platelet aggregation, and thus an impaired microcirculation. Beneficial effects of PGI 2 in experimental models of traumatic brain injury and microvascular permeability have been reported (Moller and Grande, 1997, 1999a, 1999bBentzer et al, 1999Bentzer et al, , 2001aBentzer et al, , 2001b. In a study of experimental brain trauma, cerebral cortical blood flow and cortical lesion volume were studied in mice with and without the prostacylin receptor gene (IP þ=þ and IP…”

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confidence: 99%

Prostacyclin Treatment in Severe Traumatic Brain Injury: A Microdialysis and Outcome Study

Olivecrona

Rodling-Wahlström

Naredi

et al. 2009

Journal of Neurotrauma

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Prostacyclin (PGI 2 ) is a potent vasodilator, inhibitor of leukocyte adhesion, and platelet aggregation. In trauma the balance between PGI 2 and thromboxane A 2 (TXA 2 ) is shifted towards TXA 2 . Externally provided PGI 2 would, from a theoretical and experimental point of view, improve the microcirculation in injured brain tissue. This study is a prospective consecutive double-blinded randomized study on the effect of PGI 2 versus placebo in severe traumatic brain injury (sTBI). All patients with sTBI were eligible. Inclusion criteria: verified sTBI, Glasgow Coma Score (GCS) at intubation and sedation of 8, age 15-70 years, a first-recorded cerebral perfusion pressure (CPP) of !10 mm Hg, and arrival within 24 h of trauma. All subjects received an intracranial pressure (ICP) measuring device, bilateral intracerebral microdialysis catheters, and a microdialysis catheter in the abdominal subcutaneous adipose tissue. Subjects were treated according to an ICP-targeted therapy based on the Lund concept. 48 patients (mean age of 35.5 years and a median GCS of 6 [3-8]) were included. We found no significant effect of prostacyclin (epoprostenol, Flolan) on either the lactate-pyruvate ratio (L=P) at 24 h or the brain glucose levels. There was no significant difference in clinical outcome between the two groups. The median Glasgow Outcome Score (GOS) at 3 months was 4, and mortality was 12.5%. The favorable outcome (GOS 4-5) was 52%. The initial L=P did not prognosticate for outcome. Thus our results indicate that there is no effect of PGI 2 at a dose of 0.5 ng=kg=min on brain L=P, brain glucose levels, or outcome at 3 months.

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“…To ensure reproducibility, CFC measurements were always performed at a constant arterial pressure and at a constant vascular resistance to eliminate possible blood volume capacitance effects in the volume registration. The transvascular pressure increase is also highly reproducible since it is independent of variation in post-precapillary resistance [4, 21]. …”

Section: Methodsmentioning

confidence: 99%

“…Recently, it was shown that prostacyclin at doses with effects compatible with the endogenous production reduces microvascular hydraulic permeability (conductivity) in vivo. This means that prostacyclin may be involved in the regulation of fluid exchange across the capillary membrane [3, 4]. The cellular mechanisms through which prostacyclin influences capillary permeability, however, are still unclear.…”

Section: Introductionmentioning

confidence: 99%

Prostacyclin Reduces Microvascular Fluid Conductivity in Cat Skeletal Muscle through Opening of ATP-Dependent Potassium Channels

1999

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Prostacyclin is suggested to reduce microvascular permeability, but the cellular mechanisms mediating this response in the microvascular endothelial cells are still unknown. Considering that prostacyclin relaxes vascular smooth muscle cells via opening of ATP-dependent potassium channels, and opening of ATP-dependent potassium channels in the endothelial cells is suggested to influence microvascular permeability, this study was designed to test (1) if ATP-dependent potassium channels are involved in the regulation of microvascular hydraulic permeability, (2) if the permeability-reducing effect of prostacyclin is mediated through opening of ATP-dependent potassium channels, and (3) if cAMP is involved in this process. An autoperfused cat calf hindlimb was used as experimental model, and microvascular hydraulic permeability (conductivity) was estimated by a capillary filtration coefficient (CFC) technique. The potassium channel opener PCO-400 (0.5 μg·min^–1 per 100 g muscle, intra-arterially), prostacyclin (1 ng·min^–1 per kg body weight, intravenously) and the cAMP analogue dibutyryl-cAMP (24 μg·min^–1 per 100 g muscle, intra-arterially), decreased CFC to 77, 72 and 69% compared to control, respectively (p < 0.01). The decrease in CFC obtained by these substances was completely restituted after the start of a simultaneous infusion of the ATP-dependent potassium channel blocker glibenclamide (6 μg·min^–1 per 100 g muscle, intra-arterially; p < 0.01). Infusion of glibenclamide alone increased CFC to 107% of control (p < 0.05). In conclusion, the ATP-dependent potassium channels contribute to the regulation of microvascular hydraulic conductivity, and the prostacyclin permeability-reducing effect may act through this mechanism via increase in intracellular cAMP.

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Role of Prostacyclin and Nitric Oxide in Regulation of Basal Microvascular Hydraulic Permeability in Cat Skeletal Muscle

Cited by 21 publications

References 28 publications

Nitric Oxide Dependency of Arterial Pressure–Induced Changes in Renal Interstitial Hydrostatic Pressure in Dogs

Nitric Oxide Dependency of Arterial Pressure–Induced Changes in Renal Interstitial Hydrostatic Pressure in Dogs

Prostacyclin Treatment in Severe Traumatic Brain Injury: A Microdialysis and Outcome Study

Prostacyclin Reduces Microvascular Fluid Conductivity in Cat Skeletal Muscle through Opening of ATP-Dependent Potassium Channels

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