Dietary Zn Deficiency Does Not Influence Systemic Blood Pressure and Vascular Nitric Oxide Signaling in Normotensive Rats

2003 ◽  
Vol 91 (2) ◽  
pp. 157-172 ◽  
Author(s):  
Masamichi Sato ◽  
Nobutaka Kurihara ◽  
Kazuaki Moridaira ◽  
Hironosuke Sakamoto ◽  
Jun'ichi Tamura ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Systemic Blood Pressure ◽  
Zn Deficiency ◽  
Systemic Blood ◽  
Nitric Oxide Signaling

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

scholarly journals Alterations of systemic blood pressure, serum levels of endothelin and nitric oxide under erythropoietin treatment in hemodialysis patients.

1998 ◽  
Vol 31 (5) ◽  
pp. 945-951 ◽  
Author(s):  
Noriaki Shimada ◽  
Shiori Osada ◽  
Isao Ebihara ◽  
Masayasu Mizoguchi ◽  
Shinji Saka ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Serum Levels ◽  
Systemic Blood Pressure ◽  
Hemodialysis Patients ◽  
Systemic Blood ◽  
Erythropoietin Treatment

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

1995 ◽  
Vol 13 (10) ◽  
pp. 1221
Author(s):  
Marielle M.E. Krekels ◽  
Frank C. Huvers ◽  
Peter W. de Leeuw ◽  
Nicolaa C. Schaper
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Pressure Control ◽  
Pressure Control ◽  
Systemic Blood Pressure ◽  
Nitric Oxide Synthesis ◽  
Systemic Blood

scholarly journals The effects of unripe grape extract on systemic blood pressure, nitric oxide production, and response to angiotensin II administration

2013 ◽  
Vol 5 (2) ◽  
pp. 60 ◽  
Author(s):  
Mehdi Nematbakhsh ◽  
Fatemeh Eshraghi ◽  
Zahra Pezeshki ◽  
Behzad Zolfaghari ◽  
Tahereh Safari ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Systemic Blood Pressure ◽  
Nitric Oxide Production ◽  
Systemic Blood ◽  
Grape Extract ◽  
Oxide Production

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.

scholarly journals Effects of inhibition of nitric oxide synthesis and of hypercapnia on blood pressure and brain blood flow in the turtle.

1997 ◽  
Vol 200 (4) ◽  
pp. 815-820
Author(s):  
V Söderström ◽  
G E Nilsson ◽  
P L Lutz
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Systemic Blood Pressure ◽  
Mammalian Brain ◽  
Compensatory Mechanisms ◽  
Systemic Blood ◽  
Additional Increase ◽  
Systemic Injection ◽  
Nos Inhibitor

In the mammalian brain, nitric oxide (NO) is responsible for a vasodilatory tonus as well as the elevation of cerebral blood flow (CBF) induced by hypercapnia. There have been few comparative studies of cerebral vasoregulation in lower vertebrates. Using epi-illumination microscopy in vivo to observe CBF velocity on the brain surface (cerebral cortex), we show that turtles (Trachemys scripta) exposed to hypercapnia (inspired PCO2 = 4.9 kPa) displayed a 62% increase in CBF velocity, while systemic blood pressure remains constant. Exposing turtles to a PCO2 of 14.9 kPa caused an additional increase in CBF velocity, to 104% above control values, as well as a 30% increase in systemic blood pressure. The elevated CBF velocity during hypercapnia could not be blocked by a systemic injection of the NO synthase (NOS) inhibitor NG-nitro-L-arginine (L-NA). However, L-NA injection caused a temporary stop in CBF as well as a persistent increase in systemic blood pressure, suggesting that there is a NO tonus that is attenuated by the NOS inhibitor and that CBF is strongly dependent on this tonus, although compensatory mechanisms exist. Thus, although the cerebrovascular reaction to hypercapnia appeared to be NO-independent, the results suggest that there is a NO-dependent vasodilatory tonus affecting both cerebral and systemic blood circulation in this species.

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