scholarly journals Effect of angiotensin II-induced changes in perfusion flow rate on chlorothiazide transport in the isolated perfused rat kidney

1992 ◽  
Vol 20 (2) ◽  
pp. 195-207 ◽  
Author(s):  
David E. Smith ◽  
Stephanie Guillard ◽  
Carlos A. Rodriguez
1991 ◽  
Vol 4 (4_Pt_2) ◽  
pp. 303S-308S ◽  
Author(s):  
Beatriz M.A. Fontoura ◽  
Daniel R. Nussenzveig ◽  
Pieter B.M.W.M. Timmermans ◽  
Thomas Maack

2015 ◽  
Vol 308 (10) ◽  
pp. F1178-F1187 ◽  
Author(s):  
Rocio Bautista-Pérez ◽  
Leonardo del Valle-Mondragón ◽  
Agustina Cano-Martínez ◽  
Oscar Pérez-Méndez ◽  
Bruno Escalante ◽  
...  

The possibility that angiotensin II (ANG II) exerts its effects through the activation of neutral sphingomyelinase (nSMase) has not been tested in kidneys. The results of the present study provide evidence for the activity and expression of nSMase in rat kidneys. In isolated perfused rat kidney, ANG II-induced renal vasoconstriction was inhibited by GW4869, an inhibitor of nSMase. We used nSMase for investigating the signal transduction downstream of ceramide. nSMase constricted the renal vasculature. An inhibitor of ceramidase (CDase), N-oleoylethanolamine (OEA), enhanced either ANG II- or nSMase-induced renal vasoconstriction. To demonstrate the interaction between the nSMase and cytosolic phospholipase A2 (cPLA2) signal transduction pathways, we evaluated the response to nSMase in the presence and absence of inhibitors of arachidonic acid (AA) metabolism: arachidonyl trifluoromethyl ketone (AACOCF3), an inhibitor of cPLA2; 5,8,11,14-eicosatetraynoic acid (ETYA), an inhibitor of all AA pathways; indomethacin, an inhibitor of cyclooxygenase (COX); furegrelate, a thromboxane A2 (TxA2)-synthase inhibitor; and SQ29548 , a TxA2-receptor antagonist. In these experiments, the nSMase-induced renal vasoconstriction decreased. ANG II or nSMase was associated with an increase in the release of thromboxane B2 (TxB2) in the renal perfusate of isolated perfused rat kidney. In addition, the coexpression of the ceramide with cPLA2, was found in the smooth muscle layer of intrarenal vessels. Our results suggest that ANG II stimulates ceramide formation via the activation of nSMase; thus ceramide may indirectly regulate vasoactive processes that modulate the activity of cPLA2 and the release of TxA2.


1991 ◽  
Vol 25 (3) ◽  
pp. 195-204 ◽  
Author(s):  
Takano Takehito ◽  
Nakata Kazuyo ◽  
Kawakami Tsuyoshi ◽  
Miyazaki Yoshifumi ◽  
Murakami Masataka ◽  
...  

1979 ◽  
Vol 2 (1) ◽  
pp. 1-11
Author(s):  
Richard Solomon ◽  
Patricio Silva ◽  
Franklin H. Epstein

Author(s):  
Tohru Ogihara ◽  
Therese Dupin ◽  
Haruyuki Nakane ◽  
Yoko Nakane ◽  
Takao Saruta ◽  
...  

1987 ◽  
Vol 43 (6) ◽  
pp. 795-799 ◽  
Author(s):  
David R. Luke ◽  
Bertram L. Kasiske ◽  
Gary R. Matzke ◽  
Walid M. Awni ◽  
William F. Keane

1992 ◽  
Vol 83 (4) ◽  
pp. 477-482 ◽  
Author(s):  
N. Krivoy ◽  
H. Schlüter ◽  
M. Karas ◽  
W. Zidek

1. Human plasma was incubated with tissue kallikrein from porcine pancreas, dialysed to obtain a fraction with a molecular mass < 10 kDa and further purified by reverse-phase chromatography. 2. Vasopressor activity in the fractions obtained was tested in the isolated perfused rat kidney. 3. In one fraction a strong vasopressor action was found, which was blocked by saralasin and by an angiotensin II antibody. 4. Aprotinin inhibited the formation of vasopressor substances by tissue kallikrein. 5. U.v.-laser desorption/ionization mass spectrometry revealed a molecular mass of 1046 Da in the purified active fraction. 6. It is concluded that tissue kallikrein forms not only kinins, but also angiotensin II, from human plasma under physiological conditions.


1990 ◽  
Vol 126 (3) ◽  
pp. 403-408 ◽  
Author(s):  
A. G. Ellis ◽  
W. R. Adam ◽  
T. J. Martin

ABSTRACT The isolated perfused rat kidney was used to study the effects of amino-terminal fragments of human parathyroid hormone, hPTH(1–34), bovine parathyroid hormone, bPTH(1–84) and of PTH-related proteins, PTHrP(1–34), PTHrP(1–84), PTHrP(1–108) and PTHrP(1–141) on urinary bicarbonate excretion. PTHrP(1–34) (7 nmol/l), bPTH(1–84) (5·5 nmol/l) and hPTH(1–34) (7 nmol/l) had similar effects in increasing bicarbonate excretion with respect to the control. At lower concentrations (0·7 nmol/l) all PTHrP components, but not hPTH(1–34) or bPTH(1–84) increased bicarbonate excretion significantly. Infusions of PTHrP(1–108) and PTHrP(1–141) at 0·7 nmol/l, while associated with a rise in urinary bicarbonate concentration and excretion during the early stages of perfusion, produced a sharp decline in bicarbonate concentration and excretion in the latter part of perfusion. The different peptides produced no significant differences in glomerular filtration rate, fractional excretion of sodium or urine volume. The absence of substantial differences between the effects of hPTH(1–34) and PTHrP(1–34) are as noted in previous studies. The differences between PTHrP(1–108)/PTHrP(1–141) and PTHrP(1–34) demonstrated here are consistent with (1) the clinical manifestations of acidosis in hyperparathyroidism and alkalosis in humoral hypercalcaemia of malignancy, and (2) an independent action of a component of PTHrP beyond amino acids 1–34. Journal of Endocrinology (1990) 126, 403–408


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