Postnatal kidney maturation regulates renal artery myogenic constriction

2014 ◽  
Vol 0 (0) ◽  
Author(s):  
Hitesh Soni ◽  
Randal K. Buddington ◽  
Adebowale Adebiyi

AbstractIntravascular pressure-induced vasoconstriction (myogenic constriction) is central to renal blood flow autoregulation. At term, kidney maturation is functionally incomplete. Premature neonates are at risk of kidney dysfunction. However, it is unclear whether renal artery myogenic constriction is altered after preterm birth. Here, we compared renal artery myogenic constriction in full-term and preterm pigs during the first week of life.We investigated myogenic constriction in small interlobular arteries isolated from the kidneys of pigs delivered at term and at 91% of term (with and without 96 h of neonatal intensive care).Cross-sectional area, media/lumen ratio, and luminal diameter measured under passive conditions were similar in arteries from full-term and preterm pig kidneys. An acute elevation in intravascular pressure from 20 to 100 mm Hg increased arterial wall tension and induced steady-state constriction of the arteries. However, arteries isolated from newly born preterm pigs (within 24 h) developed greater myogenic tone and lower active wall tension compared with arteries from full-term and 4-day-old preterm neonates. Pressure-induced elevation in intracellular CaMyogenic constriction is elevated in newly born preterm pigs. Our data also suggests that postnatal kidney maturation may modulate renal blood flow autoregulation.

1978 ◽  
Vol 235 (4) ◽  
pp. F286-F290 ◽  
Author(s):  
W. S. Spielman ◽  
H. Osswald

In contrast to the postocclusive hyperemia of brain, heart, and skeletal muscle, the hemodynamic response of the kidney following renal artery occlusion is highly variable in that both hyperemia and ischemia have been reported. The present study evaluates the factors influencing the renal response to complete renal artery occlusion (5-60 s) in the anesthetized cat. Marked postocclusive vasoconstriction could only be domonstrated in meclofenamate-treated (10 mg/kg) cats. The delta% renal blood flow (RBF) (30-s occlusion) was 16 +/- 4 in controls and 54 +/- 4 after meclofenamate (n= 10; P less than 0.001). Chronic denervation of the kidney, alpha-adrenergic receptor blockade, or infusion of [Sar1, Ile8]angiotensin II(2 microgram/min per kg) did not affect the postocclusive reduction of RBF, indicating that the vasoconstriction was independent of renal nerves, catecholamines, and circulating angiotesin II. Adenosine injected into the renal artery of five cats caused a dose-dependent transient fall of RBF. A dose of 100 nmol adenosine reduced RBF by 44 +/- 6% whereas after meclofenamate only 1 nmol produced the same degree of vasoconstriction. In summary, this study demonstrates a marked potentiation of the postocclusive vasoconstrictor response and the vasoconstrictive action of adenosine by meclofenamate in the anesthetized animal. No evidence was obtained to support a role for the sympathetic nervous system or circulating angiotensin II in mediating the postocclusive vasoconstriction.


2020 ◽  
Vol 13 (3) ◽  
pp. 281-285
Author(s):  
Takumi Kawase ◽  
Yosuke Inoue ◽  
Jiro Matsuo ◽  
Atsushi Omura ◽  
Yoshimasa Seike ◽  
...  

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Eisei Yamamoto ◽  
Hitoshi Takano ◽  
Hiroyuki Tajima ◽  
Jun Tanabe ◽  
Hidekazu Kawanaka ◽  
...  

Background: Renal artery stenosis (RAS) often plays an important role not only in malignant hypertension but also in sudden development of heart failure (HF) so called ‘flash pulmonary edema’ or chronic HF refractory to medical treatment. One of the possible mechanisms whereby RAS affects these unique conditions of HF is suppression of LV compliance through the complex interaction between neurohormonal systems originating from the reduction of renal blood flow. Renal artery angioplasty is expected to be an effective treatment for restoring renal blood flow in patients with RAS. The aim of the present study was whether the angioplasty can improve the impaired neurohormonal systems and diastolic cardiac function in patients with RAS. Methods: A prospective analysis was performed in 18 HF patients with RAS (age: 72±6, 3 females, NYHA I/II/III: 5/9/4) who underwent renal artery angioplasty between 2005 and 2007. Four patients with significant bilateral RAS and 3 patients with unilateral RAS in the vessel supplying a functional solitary kidney were included. We monitored the changes of biochemical and neurohormonal markers and blood pressure. Cardiac function was evaluated by tissue Doppler echocardiogram before and 3 months after the procedure. Results: Technical success was achieved in all interventions. The results are shown in table . Systolic arterial blood pressure significantly decreased by renal angioplasty. B-type natriuretic peptide (BNP) was significantly reduced 3 months after the angioplasty, whereas the change of sCr or angiotensinII was not statistically significant. Myocardial early diastolic velocity (Em), a parameter of diastolic LV function, was significantly improved compared with that measured before the procedure. Conclusions: In patients with either overt or latent HF possessing RAS, renal artery angioplasty not only decreases arterial blood pressure but also improves diastolic cardiac function in parallel with the reduction of BNP level.


Author(s):  
N.-H. Holstein-Rathlou ◽  
K. H. Chon ◽  
D. J. Marsh ◽  
V. Z. Marmarelis

1979 ◽  
Vol 236 (3) ◽  
pp. H427-H433
Author(s):  
J. A. Oliver ◽  
R. R. Sciacca ◽  
P. J. Cannon

To determine whether the prostaglandin endoperoxides PGG2 and PGH2 have direct effects in the kidney, PGG2 and PGH2 were administered into the renal artery of anesthetized dogs and their effects were compared to those of PGE2. Like PGE2, PGG2 and PGH2 induced a dose-related renal vasodilation. A 50% increase in the renal blood flow was observed with 0.05 microgram/kg body wt of PGE2 and with four- and sixfold higher doses of PGH2 and PGG2, respectively. Infusion of all three compounds at doses inducing a 50% increase in the renal blood flow resulted in 1) increases in blood flow to all cortical areas, with the greatest increase occurring in the juxtamedullary area, 2) diuresis with no change in the glomerular filtration rate, and 3) natriuresis and kaliuresis. In vitro incubation of PGH2, a maneuver known to result in its conversion to other prostaglandins, had no influence on its renal effects. The data indicate that PGH2 and PGG2 are biologically active when infused into the renal artery of the anesthetized dog and suggest that the endoperoxides exert their effects after bioconversion to other prostaglandins.


1964 ◽  
Vol 207 (1) ◽  
pp. 123-127 ◽  
Author(s):  
Victor E. Nahmod ◽  
Alfredo Lanari

In order to study the mechanism of autoregulation of renal blood flow, 36 mongrel dogs were connected in parabiosis according to the Brull method. The following determinations were made: a) flow/pressure curves in innervated and denervated kidneys and b) acetylcholine and arterenol infusion in innervated kidneys. The critical closing pressure and the "run-off" index were also determined in all cases. The results of these experiments show the existence of renal blood flow autoregulation in innervated, denervated, and arterenol-infused kidneys, and the abolition of the autoregulatory mechanism in the acetylcholine-infused kidneys. The run-off index showed a better correlation with renal resistance than with critical closing pressure.


1964 ◽  
Vol 206 (4) ◽  
pp. 707-713 ◽  
Author(s):  
J. P. Gilmore

Experiments have been undertaken to determine the role which tissue pressure plays in renal blood flow autoregulation. The following results have been obtained: 1) During occlusion of the ureter of the dog undergoing mannitol diuresis renal blood flow changes little, or increases, while tissue and ureteral pressures may increase up to 70 and 100 mm Hg, respectively. 2) Rapid sustained increases in ureteral pressure are associated with a rapid initial decline in renal blood flow followed by a gradual return to or near the control value; during these blood flow changes the elevated needle and ureteral pressures are constant. 3) During ureteral occlusion vasodilator drugs have little effect on renal blood flow. 4) The decapsulated kidney autoregulates. These data indicate that renal blood flow autoregulation cannot be explained on the basis of the tissue pressure hypothesis, but rather give further support to the myogenic theory.


1983 ◽  
Vol 245 (3) ◽  
pp. F408-F415 ◽  
Author(s):  
L. Rosivall ◽  
D. F. Rinder ◽  
J. Champion ◽  
M. C. Khosla ◽  
L. G. Navar ◽  
...  

Intrarenal conversion of angiotensin I (ANG I) to angiotensin II (ANG II) under conditions of normal and reduced renal blood flow (RBF) elicited by constriction of the renal artery was examined in pentobarbital-anesthetized dogs. In eight animals, tracer doses of 125I-ANG I (5-12 pmol) were injected into the renal artery and 125I-ANG I, 125I-ANG II, and 125I-labeled metabolites were measured in renal venous effluent by high-voltage paper electrophoresis. The mean conversion of ANG I to ANG II during a single passage through the kidney was 21.8 +/- 2.1% at control RBF. When RBF was decreased by 25 and 53%, percent ANG I conversion was not altered significantly. In six dogs percent conversion of 125I-[Sar1, Ile5]ANG I, an ANG I analogue refractory to hydrolysis by aminopeptidases, was 18.1 +/- 1.7% at control RBF and did not change significantly when the RBF was reduced by 55%. Although there were severalfold increases in renal renin secretion rate and net ANG I generation rate during reduced RBF, net renal ANG II formation rate did not change significantly. These data indicate that there is substantial conversion of ANG I in a single passage through the dog kidney and that intrarenal ANG I conversion is independent of RBF even under conditions in which renin secretion rate and ANG I generation rate are increased severalfold.


2007 ◽  
Vol 190 (4) ◽  
pp. 329-338 ◽  
Author(s):  
M. P. Koeners ◽  
S. Racasan ◽  
H. A. Koomans ◽  
J. A. Joles ◽  
B. Braam

Sign in / Sign up

Export Citation Format

Share Document