Platelet-activating factor and solute transport processes in the kidney

2003 ◽  
Vol 284 (2) ◽  
pp. F274-F281 ◽  
Author(s):  
Rajash K. Handa ◽  
Jack W. Strandhoy ◽  
Carlos E. Giammattei ◽  
Shelly E. Handa
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Proximal Tubule ◽  
Sodium Transport ◽  
Platelet Activating Factor ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Arterial Blood ◽  
Oxide Synthase ◽  
Cytochrome P 450

We examined the hemodynamic and tubular transport mechanisms by which platelet-activating factor (PAF) regulates salt and water excretion. In anesthetized, renally denervated male Wistar rats, with raised systemic blood pressure and renal arterial blood pressure maintained at normal levels, intrarenal PAF infusion at 2.5 ng · min−1 · kg−1resulted in a small fall in systemic blood pressure (no change in renal arterial blood pressure) and an increase in renal blood flow and urinary water, sodium, and potassium excretion rates. The PAF-induced changes in cardiovascular and renal hemodynamic function were abolished and renal excretory function greatly attenuated by treating rats with a nitric oxide synthase inhibitor. To determine whether a tubular site of action was involved in the natriuretic effect of PAF, cortical proximal tubules were enzymatically dissociated from male Wistar rat kidneys, and oxygen consumption rates (Qo 2) were used as an integrated index of transcellular sodium transport. PAF at 1 nM maximally inhibited Qo 2 in both untreated and nystatin-stimulated (sodium entry into renal cell is not rate limiting) proximal tubules by ∼20%. Blockade of PAF receptors or Na+-K+-ATPase pump activity with BN-52021 or ouabain, respectively, abolished the effect of PAF on nystatin-stimulated proximal tubule Qo 2. Inhibition of nitric oxide synthase or guanylate cyclase systems did not alter PAF-mediated inhibition of nystatin-stimulated proximal tubule Qo 2, whereas phospholipase A2 or cytochrome- P-450 monooxygenase inhibition resulted in a 40–60% reduction. These findings suggest that stimulation of PAF receptors on the proximal tubule decreases transcellular sodium transport by activating phospholipase A2 and the cytochrome- P-450 monooxygenase pathways that lead to the inhibition of an ouabain-sensitive component of the basolateral Na+-K+-ATPase pump. Thus PAF can activate both an arachidonate pathway-mediated suppression of proximal tubule sodium transport and a nitric oxide pathway-mediated dilatory action on renal hemodynamics that likely contributes to the natriuresis and diuresis observed in vivo.

Volume expansion natriuresis during servo control of systemic blood pressure in conscious dogs

2000 ◽  
Vol 278 (1) ◽  
pp. R19-R27 ◽  
Author(s):  
Jens Lundbæk Andersen ◽  
Lars Juel Andersen ◽  
Niels C. F. Sandgaard ◽  
Peter Bie
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
High Pressure ◽  
Volume Expansion ◽  
Systemic Blood Pressure ◽  
Servo Control ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Systemic Blood ◽  
Arterial Blood

.—The importance of arterial blood pressure (BP) and ANG II for the renal natriuretic response (NaEx) to volume expansion (3.5% body wt) was investigated during converting enzyme blockade (enalaprilate, 2 mg/kg). In separate experiments, BP was clamped either 30 mmHg above or a few millimeters mercury below baseline by servo-controlled infusion of ANG II or sodium nitroprusside, respectively, so that volume expansion did not change BP. Enalapril decreased BP by 8 mmHg. Without clamping, volume expansion returned BP to that of preenalapril control and increased NaEx 10-fold (40 ± 10 to 377 ± 69 μmol/min). During high pressure clamping (133 ± 2 mmHg), peak NaEx after volume expansion was 6% of control experiments. During low pressure clamping, NaEx was 68% of control experiments (45 ± 15 to 256 ± 64 μmol/min). The results show that 1) in absence of ANG II, volume expansion elicited pronounced natriuresis without increases in BP beyond baseline, 2) in the presence of hypertensive amounts of ANG II, the volume expansion-induced natriuresis was almost eliminated, and 3) nitroprusside prevented the increase in BP but not sodium excretion during volume expansion. ANG II appears to dominate the control of NaEx; however, when absent, volume expansion may still induce marked natriuresis even at constant BP, possibly via nitric oxide-mediated mechanisms.

Effects of systemic arterial blood pressure on the contractile force of a human hand muscle

2000 ◽  
Vol 88 (4) ◽  
pp. 1390-1396 ◽  
Author(s):  
Julie R. Wright ◽  
D. I. McCloskey ◽  
Richard C. Fitzpatrick
Keyword(s):  
Blood Pressure ◽  
Muscular Activity ◽  
Systemic Blood Pressure ◽  
Muscle Performance ◽  
Knee Extensors ◽  
Human Hand ◽  
Physiological Changes ◽  
Force Output ◽  
Systemic Blood ◽  
Arterial Blood

The effect of physiological changes in systemic blood pressure on the force output of working abductor pollicis (AP) muscle was studied in six normal subjects. Supramaximal tetanic stimulation at the ulnar nerve produced repeated isometric contractions at 1-s intervals. Force output declined gradually with time. During the train of contractions, subjects voluntarily contracted the knee extensors for 1 min; this raised systemic blood pressure by 29%. Force output from AP rose in parallel with blood pressure so that 18% of the contraction force lost through fatigue was recovered for each 10% increase in blood pressure. When blood pressure in the hand was kept constant despite the increased systemic pressure, force output did not rise. The results show that muscle performance is strongly affected by physiological changes in central blood pressure and suggest that sensory input concerning the adequacy of muscle performance exerts a feedback control over the increase in systemic blood pressure during muscular activity.

scholarly journals Effect of Nitric Oxide Blockade by NG-Nitro-l-Arginine on Cerebral Blood Flow Response to Changes in Carbon Dioxide Tension

1992 ◽  
Vol 12 (6) ◽  
pp. 947-953 ◽  
Author(s):  
Qiong Wang ◽  
Olaf B. Paulson ◽  
Niels A. Lassen
Keyword(s):  
Nitric Oxide ◽  
Carbon Dioxide ◽  
Blood Pressure ◽  
Control Level ◽  
Inhibitory Effect ◽  
Carbon Dioxide Tension ◽  
Extracellular Acidosis ◽  
Flow Response ◽  
Arterial Blood ◽  
Oxide Synthase

The importance of nitric oxide (NO) for CBF variations associated with arterial carbon dioxide changes was investigated in halothane-anesthetized rats by using an inhibitor of nitric oxide synthase, NG-nitro-l-arginine (NOLAG). CBF was measured by intracarotid injection of 133Xe. In normocapnia, intracarotid infusion of 1.5, or 7.5, or 30 mg/kg NOLAG induced a dose-dependent increase of arterial blood pressure and a decrease of normocapnic CBF from 85 ± 10 to 78 ± 6, 64 ± 5, and 52 ± 5 ml 100g−1 min−1, respectively. This effect lasted for at least 2 h. Raising Paco2 from a control level of 40 to 68 mm Hg increased CBF to 230 ± 27 ml 100g−1 min−1, corresponding to a percentage CBF response (CO2 reactivity) of 3.7 ± 0.6%/mm Hg Paco2 in saline-treated rats. NOLAG attenuated this reactivity by 32, 49, and 51% at the three-dose levels. Hypercapnia combined with angiotensin to raise blood pressure to the same level as the highest dose of NOLAG did not affect the CBF response to hypercapnia. l-Arginine significantly prevented the effect of NOLAG on normocapnic CBF as well as blood pressure and also abolished its inhibitory effect on hypercapnic CBF. d-Arginine had no such effect. Decreasing Paco2 to 20 mm Hg reduced control CBF to 46 ± 3 ml 100g−1 min−1 with no further reduction after NOLAG. Furthermore, NOLAG did not change the percentage CBF response to an extracellular acidosis induced by acetazolamide (50 mg/kg). The results suggest that NO or a closely related compound is involved in the regulation of CBF in normocapnia and even more so in hypercapnia.

scholarly journals Association of endothelial nitric oxide synthase (eNOS) gene polymorphisms and physical fitness levels with plasma nitrite concentrations and arterial blood pressure values in older adults

PLoS ONE ◽  
2018 ◽  
Vol 13 (10) ◽  
pp. e0206254
Author(s):  
Roberta Fernanda da Silva ◽  
Átila Alexandre Trapé ◽  
Thaís Amanda Reia ◽  
Riccardo Lacchini ◽  
Gustavo Henrique Oliveira-Paula ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Older Adults ◽  
Endothelial Nitric Oxide Synthase ◽  
Gene Polymorphisms ◽  
Enos Gene ◽  
Arterial Blood ◽  
Plasma Nitrite ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Blunted respiratory responses to hypoxia in mutant mice deficient in nitric oxide synthase-3

2000 ◽  
Vol 88 (4) ◽  
pp. 1496-1508 ◽  
Author(s):  
David D. Kline ◽  
Tianen Yang ◽  
Daniel R. D. Premkumar ◽  
Agnes J. Thomas ◽  
Nanduri R. Prabhakar
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Blood Gases ◽  
Mutant Mice ◽  
No Production ◽  
Experimental Conditions ◽  
Arterial Blood ◽  
Oxide Synthase ◽  
Respiratory Responses

In the present study, the role of nitric oxide (NO) generated by endothelial nitric oxide synthase (NOS-3) in the control of respiration during hypoxia and hypercapnia was assessed using mutant mice deficient in NOS-3. Experiments were performed on awake and anesthetized mutant and wild-type (WT) control mice. Respiratory responses to 100, 21, and 12% O2and 3 and 5% CO2-balance O2were analyzed. In awake animals, respiration was monitored by body plethysmography along with O2consumption (V˙o2) and CO2production (V˙co2). In anesthetized, spontaneously breathing mice, integrated efferent phrenic nerve activity was monitored as an index of neural respiration along with arterial blood pressure and blood gases. Under both experimental conditions, WT mice responded with greater increases in respiration during 12% O2than mutant mice. Respiratory responses to hyperoxic hypercapnia were comparable between both groups of mice. Arterial blood gases, changes in blood pressure,V˙o2, andV˙co2during hypoxia were comparable between both groups of mice. Respiratory responses to cyanide and brief hyperoxia were attenuated in mutant compared with WT mice, indicating reduced peripheral chemoreceptor sensitivity. cGMP levels in the brain stem during 12% O2, taken as an index of NO production, were greater in mutant compared with WT mice. These observations demonstrate that NOS-3 mutant mice exhibit selective blunting of the respiratory responses to hypoxia but not to hypercapnia, which in part is due to reduced peripheral chemosensitivity. These results support the idea that NO generated by NOS-3 is an important physiological modulator of respiration during hypoxia.

Does nitric oxide synthesis really contribute to systemic blood pressure control?

1995 ◽  
Vol 13 (6) ◽  
pp. 709 ◽  
Author(s):  
Marielle M. E. Krekels ◽  
Frank C. Huvers ◽  
Peter W. de Leeuw ◽  
Nicolaas C. Schaper
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Pressure Control ◽  
Pressure Control ◽  
Systemic Blood Pressure ◽  
Nitric Oxide Synthesis ◽  
Systemic Blood
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