Mechanism of natriuresis during intrarenal infusion of prostaglandins

1984 ◽  
Vol 247 (3) ◽  
pp. F475-F479 ◽  
Author(s):  
J. A. Haas ◽  
T. G. Hammond ◽  
J. P. Granger ◽  
E. H. Blaine ◽  
F. G. Knox
Keyword(s):  
Blood Flow ◽  
Hydrostatic Pressure ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Prostaglandin Analogue ◽  
Similar Increase ◽  
Interstitial Pressure

Intrarenal infusion of the natural prostaglandin PGE2 increases renal blood flow, renal interstitial hydrostatic pressure, and urinary sodium excretion. A newly synthesized prostaglandin analogue, 4-3-[3-[2-(1-hydroxycyclohexyl)- ethyl]-4-oxo-2-thiazolidinyl]propyl benzoic acid, increases renal blood flow without increasing sodium excretion. To investigate the role of renal interstitial hydrostatic pressure in this dissociation, comparisons were made between PGE2 and the prostaglandin analogue. Intrarenal infusion of PGE2 increased renal blood flow, renal interstitial hydrostatic pressure, and urinary sodium excretion. Following a similar increase in renal blood flow with intrarenal infusion of prostaglandin analogue, renal interstitial hydrostatic pressure and urinary sodium excretion were not changed. To determine whether increases in urinary sodium excretion due to PGE2 infusion are causally related to the increase in renal interstitial hydrostatic pressure rather than to the increase in renal blood flow, responses to PGE2 were obtained in the absence of increases in interstitial pressure. When renal interstitial hydrostatic pressure was held constant, urinary sodium excretion did not change although there was a marked increase in renal blood flow. We conclude that increased renal interstitial hydrostatic pressure is necessary to produce an increase in urinary sodium excretion with prostaglandin-mediated renal vasodilation.

Role of renal alpha-adrenoceptors mediating renin secretion

1982 ◽  
Vol 242 (6) ◽  
pp. F620-F626 ◽  
Author(s):  
J. L. Osborn ◽  
G. F. DiBona ◽  
M. D. Thames
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Renin Secretion ◽  
Renal Nerve ◽  
Alpha Adrenoceptors ◽  
Alpha Adrenoceptor

The increase in renin secretion resulting from low-frequency renal nerve stimulation (0.5 Hz) occurs in the absence of changes in urinary sodium excretion or renal blood flow and is apparently derived from a direct effect of renal sympathetic nerves on juxtaglomerular granular cells. We sought to determine the role of renal alpha-adrenoceptors in this neurally evoked renin secretion. The neurally evoked renin secretion was unaffected by renal alpha-adrenoceptor blockade with phentolamine or prazosin; however, two dose levels of phenoxybenzamine equally inhibited the renin secretion. The renal vasoconstrictor response to graded renal nerve stimulation was similarly diminished by phentolamine, prazosin, and the higher phenoxybenzamine dose, whereas the lower phenoxybenzamine dose was significantly less effective. Renal alpha-adrenoceptor stimulation with methoxamine infusion at doses that were just subthreshold for altering renal blood flow and urinary sodium excretion or at doses that just reduced urinary sodium excretion also did not change renin secretion. Higher doses of methoxamine that decreased both renal blood flow and sodium excretion increased renin secretion. Based on the inability of phentolamine and prazosin to prevent neurally mediated renin secretion and on the dose-response relationship between methoxamine and changes in renin secretion, renal blood flow, and urinary sodium excretion, we conclude that renal alpha-adrenoceptors do not mediate renin secretion elicited by direct neural activation of the juxtaglomerular granular cells. The data suggest that phenoxybenzamine inhibits neurally mediated renin secretion by a mechanism other than renal alpha-adrenoceptor blockade.

scholarly journals Vascular Type 1A Angiotensin II Receptors Control BP by Regulating Renal Blood Flow and Urinary Sodium Excretion

2015 ◽  
Vol 26 (12) ◽  
pp. 2953-2962 ◽  
Author(s):  
Matthew A. Sparks ◽  
Johannes Stegbauer ◽  
Daian Chen ◽  
Jose A. Gomez ◽  
Robert C. Griffiths ◽  
...  
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Angiotensin Ii Receptors ◽  
Vascular Type

Effect of secretin on renal blood flow, interstitial pressure, and sodium excretion

1977 ◽  
Vol 232 (2) ◽  
pp. F147-F151 ◽  
Author(s):  
G. R. Marchand ◽  
C. E. Ott ◽  
F. C. Lang ◽  
R. F. Greger ◽  
F. G. Knox
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Similar Increase ◽  
Interstitial Pressure ◽  
Polyethylene Matrix ◽  
The Relationship

Most renal vasodilators are natriuretic. However, secretin increases renal blood flow (RBF) markedly but produces only a very slight increase in sodium excretion (UNaV). To investigate this observation further, the relationship between vasodilatation, interstitial pressure (IP), and UNaV was studied in dogs. Intrarenal infusion of secretin increased RBF (delta=107+/-19 ml/min). The IP, as measured from chronically implanted polyethylene matrix capsules, was not significantly changed (delta=-0.3+/-0.5 mmHg). UNaV was slightly, although significantly, increased (delta=19+/-4 mueq/min). Following a similar increase in RBF with an intrarenal infusion of acetylcholine (ACh), IP and UNaV increased markedly (delta=8.2+/-0.8 mmHg and 174+/-23 mueq/min, respectively). Neither secretin nor ACh) altered glomerular filtration rate or blood pressure. Both secretin and ACh produced comparable increases in peritubule capillary(delta=5+/-1 and 7.5+/-1.4 mmHg, respectively) and free-flow tubule pressure (delta=7+/-2 and 9.5+/-1.4 mmHg, respectively). In summary, the usual relationship between vasodilatation and IP was dissociated during secretin infusion, whereas the relationship between IP and natriuresis was not dissociated.

Role of atrial natriuretic peptide in volume-expansion natriuresis

1986 ◽  
Vol 251 (2) ◽  
pp. R310-R313 ◽  
Author(s):  
T. R. Schwab ◽  
B. S. Edwards ◽  
D. M. Heublein ◽  
J. C. Burnett
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urinary Sodium ◽  
Right Atrial ◽  
Fractional Excretion Of Sodium

Studies were performed to investigate the role of circulating atrial natriuretic peptide (ANP) in acute volume-expansion natriuresis. Sham-operated (SHAM, n = 6) and right atrial appendectomized (ATRX, n = 12) anesthetized rats underwent acute volume expansion with isoncotic albumin. After equilibration and control periods, volume expansion increased urine flow rate, urinary sodium excretion, fractional excretion of sodium, and circulating ANP. Absolute increases in urine flow rate (delta 46 +/- 4 SHAM; delta 25 +/- 5 microliter/min ATRX), urinary sodium excretion (delta 9.48 +/- 1.01 SHAM; delta 4.77 +/- 1.03 mueq/min ATRX), fractional excretion of sodium (delta 3.16 +/- 0.53 SHAM; delta 1.65 +/- 0.32% ATRX), and ANP (delta 303.3 +/- 35.9 SHAM; delta 156.6 +/- 26.0 pg/ml ATRX) were significantly reduced by right atrial appendectomy. No significant differences in mean arterial pressure, central venous pressure, or glomerular filtration rate during volume expansion were observed between groups. These studies support the hypothesis that right atrial appendectomy in the rat attenuates acute volume expansion-induced increases in circulating ANP and urinary sodium excretion and that the natriuresis of acute volume expansion is mediated in part by an increase in circulating ANP.

Acetylcholine-induced vasodilation without natriuresis during control of interstitial pressure

1982 ◽  
Vol 243 (4) ◽  
pp. F325-F329 ◽  
Author(s):  
D. A. Hartupee ◽  
J. C. Burnett ◽  
J. I. Mertz ◽  
F. G. Knox
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Interstitial Pressure ◽  
Aortic Clamping ◽  
Fractional Sodium Excretion ◽  
Flow Experiments

Increased renal blood flow and increased renal interstitial pressure have been proposed as mechanisms for the natriuresis caused by vasodilation with acetylcholine. We tested the hypothesis that the natriuresis due to acetylcholine is associated with the increase in interstitial pressure rather than with the increase in blood flow. Experiments were performed in decapsulated kidneys that, along with partial aortic clamping, allowed dissociation of the increases in renal interstitial pressure and blood flow. At the beginning of intrarenal acetylcholine infusion (2 micrograms . kg-1 . min-1), the aorta was clamped so that a vasodilation occurred without an increase in interstitial pressure. A response to acetylcholine was also obtained when interstitial pressure was allowed to increase. During this response, renal blood flow, interstitial pressure, and fractional sodium excretion increased. During control of interstitial pressure, renal blood flow increased, but fractional sodium excretion did not change. Thus, when interstitial pressure was controlled, the acetylcholine-induced vasodilation did not result in an increase in fractional sodium excretion. These results demonstrate that an increase in renal interstitial pressure is required for the natriuresis associated with acetylcholine-induced vasodilation.

Prostaglandin blockade blunts the natriuresis of elevated renal interstitial hydrostatic pressure

1988 ◽  
Vol 254 (4) ◽  
pp. F507-F511 ◽  
Author(s):  
D. Pawlowska ◽  
J. A. Haas ◽  
J. P. Granger ◽  
J. C. Romero ◽  
F. G. Knox
Keyword(s):  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Left Kidney ◽  
Urinary Sodium Excretion ◽  
Prostaglandin Synthesis ◽  
Urinary Sodium ◽  
Fractional Sodium Excretion ◽  
Interstitial Volume ◽  
Inhibition Of Prostaglandin Synthesis

Previous studies have shown that renal interstitial volume expansion (RIVE) increases renal interstitial hydrostatic pressure and urinary sodium excretion. In the present study we investigated whether blockade of prostaglandin synthesis inhibits the increase in fractional sodium excretion induced by RIVE. Expansion of the renal interstitial volume was achieved by injecting 50 microliters of 2.5% albumin solution into a polyethylene matrix chronically implanted in the left kidney. Fractional sodium excretion (FENa), renal interstitial hydrostatic pressure (PI), and urinary prostaglandin excretion (UPGE2) were measured before and after RIVE in eight control, seven meclofenamate-treated, and eight indomethacin-treated rats. RIVE in the control animals resulted in significant increases in PI (delta + 4.2 +/- 0.8 mmHg), in FENa (delta + 1.02 +/- 0.27%), and in UPGE2 (% delta + 150 +/- 38%) without significant changes in glomerular filtration rate. Inhibition of prostaglandin synthesis with meclofenamate or indomethacin attenuated the natriuretic response and blocked the increase in UPGE2 associated with RIVE. In summary, direct increases in renal interstitial hydrostatic pressure increase UPGE2 and urinary sodium excretion. This natriuretic response is markedly diminished by inhibition of prostaglandin synthesis. These studies suggest that prostaglandin synthesis may have an important role in mediating the natriuretic effect of increased renal interstitial hydrostatic pressure during renal interstitial volume expansion.

Activation of histamine H3 receptors inhibits renal noradrenergic neurotransmission in anesthetized dogs

2001 ◽  
Vol 280 (5) ◽  
pp. R1450-R1456 ◽  
Author(s):  
Tomoyuki Yamasaki ◽  
Isao Tamai ◽  
Yasuo Matsumura
Keyword(s):  
Receptor Antagonist ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urinary Sodium ◽  
Renal Nerve ◽  
Anesthetized Dogs ◽  
Induced Changes ◽  
Antidiuretic Action

To investigate the possible involvement of histamine H3 receptors in renal noradrenergic neurotransmission, effects of (R)alpha-methylhistamine (R-HA), a selective H3-receptor agonist, and thioperamide (Thiop), a selective H3-receptor antagonist, on renal nerve stimulation (RNS)-induced changes in renal function and norepinephrine (NE) overflow in anesthetized dogs were examined. RNS (0.5–2.0 Hz) produced significant decreases in urine flow and urinary sodium excretion and increases in NE overflow rate (NEOR), without affecting renal hemodynamics. When R-HA (1 μg · kg−1 · min−1) was infused intravenously, mean arterial pressure and heart rate were significantly decreased, and there was a tendency to reduce basal values of urine flow and urinary sodium excretion. During R-HA infusion, RNS-induced antidiuretic action and increases in NEOR were markedly attenuated. Thiop infusion (5 μg · kg−1 · min−1) did not affect basal hemodynamic and excretory parameters. Thiop infusion caused RNS-induced antidiuretic action and increases in NEOR similar to the basal condition. When R-HA was administered concomitantly with Thiop infusion, R-HA failed to attenuate the RNS-induced antidiuretic action and increases in NEOR. However, in the presence of pyrilamine (a selective H1-receptor antagonist) or cimetidine (a selective H2-receptor antagonist) infusion, R-HA attenuated the RNS-induced actions, similarly to the case without these antagonists. Thus functional histamine H3 receptors, possibly located on renal noradrenergic nerve endings, may play the role of inhibitory modulators of renal noradrenergic neurotransmission.

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