Atriopeptins: correlation between renal vasodilation and natriuresis

1985 ◽  
Vol 249 (1) ◽  
pp. F49-F53 ◽  
Author(s):  
K. Wakitani ◽  
B. R. Cole ◽  
D. M. Geller ◽  
M. G. Currie ◽  
S. P. Adams ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Rank Order ◽  
Urine Volume ◽  
Systemic Blood Pressure ◽  
Functional Changes ◽  
Positive Linear Correlation ◽  
Diuretic Agents

The effect of atrial peptides on renal function was studied in intact anesthetized dogs. A quantitative comparison of bolus intra-arterial injections demonstrated a rank order potency as renal vasodilators and natriuretic/diuretic agents as follows: ser-leu-arg-arg-atriopeptiin III (SLRR-APIII) greater than high molecular weight artrial peptide greater than or equal to atriopeptin (AP)III = APII much greater than API (essentially inactive). A sustained infusion of APIII was employed in order to study the temporal and quantitative correlation of the renal functional changes induced by the atrial peptide. Both intra-arterial and intravenous administration of the peptide produced concentration-dependent increases in renal blood flow, urine volume, sodium excretion, and osmotic clearance. Infusion of APIII into the renal artery did not alter systemic blood pressure or heart rate. Intravenous infusions of APIII required 10 times higher doses to induce the changes in renal vascular resistance and electrolyte excretion, and a fall in blood pressure and tachycardia resulted. The natriuretic-diuretic effect of the atriopeptins appears to be closely associated with renal vasodilation, exhibiting a positive linear correlation between the peptide-induced changes in sodium excretion and changes in renal blood flow.

Excessive Zinc Intake Increases Systemic Blood Pressure and Reduces Renal Blood Flow via Kidney Angiotensin II in Rats

2012 ◽  
Vol 150 (1-3) ◽  
pp. 285-290 ◽  
Author(s):  
Miyoko Kasai ◽  
Takashi Miyazaki ◽  
Tsuneo Takenaka ◽  
Hiroyuki Yanagisawa ◽  
Hiromichi Suzuki
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Zinc Intake

scholarly journals Impact of the NO-Sensitive Guanylyl Cyclase 1 and 2 on Renal Blood Flow and Systemic Blood Pressure in Mice

2018 ◽  
Vol 19 (4) ◽  
pp. 967 ◽  
Author(s):  
Evanthia Mergia ◽  
Manuel Thieme ◽  
Henning Hoch ◽  
Georgios Daniil ◽  
Lydia Hering ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Guanylyl Cyclase ◽  
Systemic Blood Pressure ◽  
Systemic Blood

Contralateral Natriuresis During Reduced Renal Artery Perfusion Pressure in "Renin-Depleted" Dogs

1972 ◽  
Vol 50 (3) ◽  
pp. 215-227
Author(s):  
L. J. Belleau ◽  
D. Mailhot
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Systemic Blood Pressure ◽  
Renal Perfusion ◽  
Systemic Blood ◽  
Renal Perfusion Pressure

The mechanism of contralateral natriuresis subsequent to reduction of renal perfusion pressure was studied. In control dogs a drop in the renal perfusion pressure caused a very significant increase in the arterial and renal venous plasma renin activity, as well as a significant contralateral natriuresis. Systemic blood pressure increased along with contralateral intrarenal resistance. Glomerular filtration rate and renal blood flow did not change in the opposite kidney.In "renin-depleted" dogs a comparable drop in the renal perfusion pressure failed to stimulate renal venous and arterial plasma renin activity. Contralateral natriuresis increased significantly as well as the systemic blood pressure. In the absence of renin, intrarenal resistance of the opposite kidney did not change. Contralateral glomerular filtration rate and renal blood flow remained unchanged.During reduction of renal perfusion pressure, the most significant findings were: (1) absence of renin release despite the stimulation in renin-depleted dogs, (2) increase in contralateral resistance explained by the renin–angiotensin system, (3) systemic blood pressure increment despite renin release inhibition, and (4) the renin–angiotensin system not directly responsible for the contralateral natriuresis following a reduction in the renal perfusion pressure.Contralateral natriuresis cannot be explained by changes in glomerular filtration, renal blood flow, or intrarenal resistance. It is suggested that the rise in blood pressure or another factor, possibly neural or humoral, could explain the contralateral natriuresis.

Effect of a kinin antagonist on renal function and haemodynamics during alterations in sodium balance in conscious normotensive rats

1990 ◽  
Vol 78 (2) ◽  
pp. 165-168 ◽  
Author(s):  
Paolo Madeddu ◽  
Nicola Glorioso ◽  
Aldo Soro ◽  
Paolo Manunta ◽  
Chiara Troffa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Urinary Sodium Excretion

1. To evaluate whether sodium intake can modulate the action of endogenous kinins on renal function and haemodynamics, a receptor antagonist of bradykinin was infused in conscious normotensive rats maintained on either a normal or a low sodium diet. 2. The antagonist inhibited the hypotensive effect of exogenously administered bradykinin. It did not change the vasodepressor effect of acetylcholine, dopamine or prostaglandin E2. 3. The antagonist did not affect mean blood pressure, glomerular filtration rate, renal blood flow or urinary sodium excretion, in rats on sodium restriction. It did not change mean blood pressure, glomerular filtration rate or urinary sodium excretion, but decreased renal blood flow, in rats on a normal sodium intake. 4. The kallikrein–kinin system has a role in the regulation of renal blood flow in rats on a normal sodium diet.

Contribution of renal prostaglandins to the natriuretic action of bradykinin in the dog

1979 ◽  
Vol 237 (3) ◽  
pp. F182-F187
Author(s):  
M. C. Blasingham ◽  
A. Nasjletti
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Prostaglandin Synthetase ◽  
Renal Functions ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Stimulation Of

To study the effects of stimulation of renal prostaglandin biosynthesis by bradykinin, we assessed the changes in renal functions induced by intrarenal infusion of bradykinin (10 ng . min-1 . kg-1) in the dog anesthetized with pentobarbital before and during inhibition of prostaglandin synthesis by sodium meclofenamate (5 mg/kg). Before meclofenamate administration, bradykinin augmented the urinary output of a "PGE"-like substance from 1.00 +/- 0.25 to 3.88 +/- 1.09 ng/min (P less than 0.05) and increased renal blood flow by 65 +/- 9 ml/min (P less than 0.001), urine flow by 0.55 +/- 0.23 ml/min (P less than 0.05), and sodium excretion by 64.8 +/- 18.0 mueq/min (P less than 0.01). Administration of meclofenamate did not affect the bradykinin-induced increase in renal blood flow and urine volume, but suppressed the evoked output of "PGE" and reduced the associated natriuresis, i.e., sodium excretion increased by only 11.1 +/- 4.8 mueq/min (P greater than 0.05). In contrast, meclofenamate did not affect the natriuresis effected by an equidilator dose of PGE2 (5 ng . min-1 . kg-1) infused intrarenally. These observations suggest that a product of prostaglandin synthetase produced by the kidney during intrarenal infusion of bradykinin contributes to the natriuretic action of the peptide.

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.

Autoregulation of renal blood flow in two-kidney, one-clip hypertensive rats

1986 ◽  
Vol 251 (2) ◽  
pp. F245-F250 ◽  
Author(s):  
B. M. Iversen ◽  
K. J. Heyeraas ◽  
I. Sekse ◽  
K. J. Andersen ◽  
J. Ofstad
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Complete Loss ◽  
Hypertensive Rats ◽  
Functional Changes ◽  
Pressure Limit ◽  
Renal Vascular

Renal blood flow (RBF) autoregulation was examined in the clipped and nonclipped kidneys in two groups of two-kidney, one-clip (2K-1C) hypertensive rats 10 wk after clipping. The arterial pressure distal to the clip and the renin secretion rate (RSR) were also examined. The blood pressure (BP) was 149 +/- 4 and 162 +/- 6 mmHg in the two hypertensive groups vs. 114 +/- 3 mmHg in the controls (P less than 0.02). The RBF (in ml X min-1 X kidney-1) was 4.27 +/- 0.41 in the nonclipped and 2.18 +/- 0.23 in the clipped kidneys (P less than 0.001). The pressure distal to the clip was 104 +/- 7 mmHg. The renal vascular resistance (RVR) (in mmHg X ml-1 X min-1 X g-1) was 25.0 +/- 1.4 in the control kidneys vs. 58.4 +/- 4.5 in the nonclipped (P less than 0.001) and 39.9 +/- 6.6 in the clipped kidneys (P less than 0.01). The RBF autoregulation was well preserved in the nonclipped kidneys but reset to a higher lower pressure limit of autoregulation of 106 +/- 4 mmHg, which was significantly higher than in the normotensive controls (84 +/- 6 mmHg) (P less than 0.01). In the clipped kidneys there was complete loss of RBF autoregulation. RSR decreased with reduction of the perfusion pressure in the clipped kidneys. The increased RVR might have been due to a combination of structural and functional changes in both kidneys.

Renal effect of meclofenamate in presence and absence of superfusion bioassay

1976 ◽  
Vol 230 (3) ◽  
pp. 711-714 ◽  
Author(s):  
S Satoh ◽  
BG Zimmerman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Prostaglandin E ◽  
Renal Effect ◽  
Systemic Blood ◽  
Renal Vascular

Systemic blood pressure (SBP), renal blood flow (RBF), renal vascular resistance (RVR), and arterial and renal venous prostaglandin E (PGE) concentrations were determined in pentobarbital-anesthetized dogs.The effect of sodium meclofenamate infused into the renal artery was compared under two sets of conditions. In experiments carried out under control conditions, SBP, RBF, and RVR were stable and meclofenamate caused only a slight decrease in RBF (5.4%) and increase in RVR.

Relationship between arterial baroreflex, cardiopulmonary vagal reflex and renal natriuretic response to saline in conscious rabbits

1998 ◽  
Vol 95 (6) ◽  
pp. 693-699 ◽  
Author(s):  
Nadine MAYBAUM ◽  
Elena GORODETSKY ◽  
Marta WEINSTOCK
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Baroreflex Sensitivity ◽  
Saline Infusion ◽  
Vagal Afferents ◽  
Arterial Baroreflex ◽  
Cardiopulmonary Baroreceptors ◽  
Arterial Baroreflex Sensitivity

1. We have previously shown that normotensive rabbits with a genetic impairment in arterial baroreflex sensitivity showed a delayed sodium excretion and failed to increase their renal blood flow in response to a saline infusion that did not alter blood pressure. These renal haemodynamic and excretory abnormalities were abolished by renal denervation. The present study determined the sensitivity of the cardiopulmonary baroreceptors and the renal response to a mild saline infusion in normotensive rabbits varying widely in their arterial baroreflex sensitivity. 2. Sensitivity of cardiopulmonary baroreceptors was assessed from the slope of the relationship of the change in both blood pressure and heart rate and the dose of phenylbiguanide, a stimulator of vagal afferents. 3. The change in renal blood flow and lithium and sodium excretion was measured in response to saline, infused at a rate of 0.11 ml·min-1·kg-1 into the ear vein. Urine was collected via a urethral catheter and renal blood flow was measured by para-aminohippurate clearance. 4. A significant correlation was found between the magnitude of the gain of the cardiac arterial baroreflex and the sensitivity of the cardiopulmonary baroreceptor response to phenylbiguanide. The latter was significantly correlated to renal blood flow and lithium clearance 60–90 min after the start of the saline infusion. 5. It was also found that in some normotensive rabbits there was a blunting of cardiovascular regulation as indicated by a reduced sensitivity of cardiopulmonary and arterial baroreceptors. This may explain their abnormal haemodynamic and natriuretic response to salt.

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