Effects of hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume

Rd, Manning

doi:10.1152/ajprenal.1987.252.1.f91

Cited by 13 publications

(12 citation statements)

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“…These values are very close to those measured in control dogs in another experiment in our laboratory and indicate that L-NAME did not impair renal function significantly. 19 Fig 8 shows the short-term effects of L-arginine on the arterial pressure response to acetylcholine, and this measurement was taken 15 minutes after the 30-minute L-arginine infusion was completed. During the control period, L-arginine caused no significant enhancement of the acetylcholine depressor effect.…”

Section: Fig 6 Bar Graphs Show Effects Of Intravenous Infusion Of Nimentioning

confidence: 99%

Cardiovascular responses to long-term blockade of nitric oxide synthesis.

Manning

Mizelle

et al. 1993

Hypertension

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The goal of this study was to determine if there is a basal release of nitric oxide that affects long-term arterial pressure regulation in dogs. Studies were conducted over a 23-day period in eight conscious dogs with indwelling catheters. Nitric oxide synthesis was blocked by continuous intravenous infusion of nitro-L-arginine-methyl ester at 37.1 nmol/kg per minute for 11 days. Arterial pressure increased to 120±4% of control on the first day, decreased for a few days, and then increased to a maximum value of 122±6% of control on day 7. Bradycardia was sustained throughout the entire nitro-arginine period. Blockade of nitric oxide synthesis was evidenced by attenuated pressure and flow responses to systemic acetylcholine infusion. The pressor response to phenylephrine was increased for only 1 day, and the hypotensive effects of nitroprusside were enhanced. Also, the variability of arterial pressure was significantly increased during nitro-arginine. Sodium and water balances were positive the first day of nitro-arginine infusion but were unchanged for the entire nitro-arginine period. In conclusion, the data suggest that blockade of the basal release of nitric oxide in dogs causes an increase in the long-term level of arterial pressure without any sustained sodium or water retention. (Hypertension 1993;22:40-48) KEY WORDS • endothelium • vasodilation • arginine • nitric oxide • hypertension, essential I n 1980 Furchgott and Zawadzki 1 found that acetyl-choline-induced relaxation of vascular strips or rings was dependent on the presence of an intact endothelium. A substance released from the endothe-lium, later known as endothelium-derived relaxing factor (EDRF), was primarily responsible for this relaxation. Furchgott 2 later suggested that EDRF was nitric oxide (NO), and Ignarro et al 3 speculated that EDRF might be NO or a related compound. Other investigators have confirmed that NO is an integral part of EDRF, and specific NO synthesis inhibitors have been successfully developed. 4 The two major inhibitors of NO production are JV G-monomethyl L-arginine (L-NMMA) and Af G-nitro-L-arginine-methyl ester (L-NAME), and they both act by competitive inhibition of NO synthase. This inhibition prevents the conversion of L-arginine to NO. Of these two inhibitors, L-NAME is much more potent and causes acute vasoconstriction in a number of vascular beds, whereas D-NAME does not. 5 Most experiments on NO synthesis blockade have been performed in vitro on vascular rings. However, more recently, administration of NO synthesis blockers resulted in acute increases in arterial pressure in rats, 6 ' 7 guinea pigs, 8 and rabbits. 9 In addition, studies by Gar-diner et al 5 and Baylis et al 10 showed that administration of L-NAME for several hours to conscious rats resulted in increases in arterial pressure. More recently, several longer experiments have been performed in which NOson, MS 39216-4505 (Dr Manning). synthesis inhibitors were administered to rats orally for periods lasting between 9 hours and 6 months, and mean arter...

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Section: Fig 6 Bar Graphs Show Effects Of Intravenous Infusion Of Nimentioning

confidence: 99%

Cardiovascular responses to long-term blockade of nitric oxide synthesis.

Manning

Mizelle

et al. 1993

Hypertension

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“…17] would appear to lie in the time scale of the experiments. Manning [11] re duced the plasma concentration over 27 days, and FF reached a maximum value 5 days into the experiment and thereafter declined. Joles et al [17] carried out their study 80 h after completing 12 days of repeated plasmaphere sis accompanied bv a low-protein diet.…”

Section: Discussionmentioning

confidence: 91%

“…Of necessity, there are homeostatic variations in many physiological parameters in response to experimentally induced chang es. The results obtained by Manning [11] may have been due, in part, to changes in intraca pillary hydrostatic pressure when MAP and ERPF decreased during the experiment. We have no information on BP changes found by Joles et al [17], and changes in renal haemo dynamics may have been quite different from those in our study.…”

Section: Discussionmentioning

confidence: 92%

Acute Lowering of Plasma Oncotic Pressure Increases Filtration Fraction and Sodium Excretion in Conscious Sheep

Fleming

Dallemagne²,

Endre³

et al. 1992

Kidney Blood Press Res

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We examined the effect of acutely lowering the colloid osmotic pressure by removing plasma (36.2 ± 3.1 ml/kg) and replacing it with Hartmann’s solution (93.0 ± 8.2 ml/kg) in 6 conscious merino sheep. The colloid osmotic pressure was reduced significantly (p < 0.05) from 20.3 ± 0.9 to 8.5 ± 2.5 mm Hg 0 h after plasmapheresis and to 15.2 ± 0.8 mm Hg 20 h after treatment. The filtration fraction increased from 0.16 ± 0.02 to 0.27 ± 0.02 at 0 h (p < 0.05 vs. control) and to 0.20 ± 0.02 at 20 h after treatment (p < 0.05 vs. control). At 0 h after plasmapheresis there was an increase in both sodium excretion from 187 ± 69 to 459 ± 82 µmol · min^-1(p < 0.05) and in fractional sodium excretion from 1.6 ± 0.4 to 4.4 ± 1.0% (p < 0.05). The results are consistent with the hypothesis that acute alteration of Starling forces produce clinically significant effects on both glomerular filtration and tubular reabsorption.

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“…The volume of distribution of sodium iothalamate, an index of extracellular fluid volume, was determined using the technique of Sapirstein et al 14 Renal vascular resistance (RVR), filtration fraction, and the fractional excretion of sodium were calculated using standard techniques. 10 Plasma renin activity and plasma concentrations of aldosterone and cortisol were determined by radioimmunoassay. Plasma and urine sodium and potassium concentrations were determined by flame photometry.…”

Section: Experimental Methods and Instrumentationmentioning

confidence: 99%

“…Using aseptic techniques and anesthesia with thiopental sodium (Pentothal, 25 mg/kg i.v., Abbott, North Chicago) and methoxyflurane (Penthrane, Abbott), we implanted catheters in the aorta and inferior vena cava through the femoral artery and vein as previously described. 10 An intrarenal artery catheter was also implanted using the technique of Herd and Barger, 11 except that the intravascular portion of the catheter was Silastic. The contralateral kidney was then surgically removed.…”

Section: Animal Preparation and Experimental Protocolmentioning

confidence: 99%

Role of nitric oxide in long-term angiotensin II-induced renal vasoconstriction.

Manning

Mizelle

et al. 1993

Hypertension

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In vitro studies have indicated that nitric oxide may play ah important role in modulating the renal vascular actions of angiotensin II (Ang II). However, the physiological importance of this interaction in the long-term regulation of renal hemodynamics is unknown. Therefore, the goal of this study was to determine if long-term Ang II-induced renal vasoconstriction was potentiated by nitric oxide synthesis inhibition. The intrarenal effects of Ang II were examined in eight unilaterally nephrectomized, conscious dogs before and after systemic inhibition of nitric oxide synthesis. Ang II infusion into the renal artery at 0.5 ng/kg per minute resulted in decreases in renal plasma flow of 15% and 9% after 3 and 5 days, respectively. During this time, glomerular filtration rate decreased 12% after 3 days of angiotensin but was not significantly changed after 5 days. After 4 days of recovery from Ang II, nitric oxide synthesis was inhibited with intravenous iV G -nitro-L-arginine-methyi ester (L-NAME) at 10 Mg/kg per minute for 5 days, and this caused a significant decrease in renal plasma flow but no change in glomerular filtration rate. Infusion of Ang II into L-NAME-pretreated dogs for an additional 5 days further decreased renal plasma flow and glomerular filtration 14% and 11%, respectively. However, the effects of Ang II and L-NAME on renal plasma flow were only additive on days 3 and 5 of this period, and the effects on glomerular filtration were additive on day 3 but were potentiated on day 5. Neither iothalamate space, plasma renin activity, plasma aldosterone concentration, nor plasma cortisol concentration was changed during the experiment, and a marked decrease in the acetylcholine depressor response during L-NAME indicated significant nitric oxide synthesis inhibition. In conclusion, long-term inhibition of nitric oxide synthesis did not potentiate the Ang II-induced reduction in renal plasma flow, but by the end of the angiotensin and nitric oxide inhibition periods, the effects of angiotensin on glomerular filtration were potentiated. (Hypertension 1993^1:949-955) KEY WORDS • endothelium • endothelium-derived relaxing factor • arginine • glomerular filtration rate E ndothelium-derived relaxing factor has been recently identified as nitric oxide (NO) or a related compound. 12 Acute blockade of NO synthesis has resulted in increases in arterial pressure in anesthetized 3 and conscious 4 animals, suggesting that there is a basal release of NO.In addition to its effects on basal vascular resistance, several recent studies have indicated that NO may acutely counteract the constrictor effects of several pressor systems. Previous studies have shown that removal of the vascular endothelium enhances the acute vasoconstrictor effects of angiotensin II (Ang II) 5 and phenylephrine 6 in isolated vascular rings and arginine vasopressin in the perfused mesenteric vascular bed of the rat.7 NO has also been suggested to counteract the effects of vasoconstrictors in the renal circulation. Ito et al 8 found that the ...

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Effects of hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume

Cited by 13 publications

References 0 publications

Cardiovascular responses to long-term blockade of nitric oxide synthesis.

Cardiovascular responses to long-term blockade of nitric oxide synthesis.

Acute Lowering of Plasma Oncotic Pressure Increases Filtration Fraction and Sodium Excretion in Conscious Sheep

Role of nitric oxide in long-term angiotensin II-induced renal vasoconstriction.

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