scholarly journals Renal vein plasma renin activity in patients with unilateral renovascular hypertension.

1988 ◽  
Vol 52 (5) ◽  
pp. 431-436 ◽  
Author(s):  
Ko SATO ◽  
KEISHI ABE ◽  
MASAHIDE SEINO ◽  
MINORU YASUJIMA ◽  
YUTAKA IMAI ◽  
...  
1986 ◽  
Vol 75 (6) ◽  
pp. 728-732
Author(s):  
Ko SATO ◽  
Keishi ABE ◽  
Masahide SEINO ◽  
Minoru YASUJIMA ◽  
Yutaka IMAI ◽  
...  

1981 ◽  
Vol 240 (4) ◽  
pp. H533-H538
Author(s):  
J. R. Dietz ◽  
J. O. Davis ◽  
J. M. DeForrest ◽  
R. H. Freeman ◽  
S. F. Echtenkamp ◽  
...  

This study examines the role that prostaglandins play in both the developmental and chronic phases of renovascular hypertension. Two 5-mg/kg doses of indomethacin were given to conscious dogs with renal denervation and receiving propranolol during the acute and chronic phases of one-kidney (1-KHT) and the acute phase of two-kidney (2-KHT) renovascular hypertension. Indomethacin produced striking reductions in plasma renin activity from the high level observed during the acute phase of both 1-KHT and 2-KHT. However, plasma renin activity failed to return to normal, and the hypertensive level of pressure decreased only slightly. In the chronic 1-KHT dogs, indomethacin did not lower plasma renin activity or mean arterial blood pressure unless plasma renin activity was elevated above the normal level. Also, indomethacin failed to alter renal function during the acute phase of 1-KHT but effective renal plasma flow fell during chronic 1-KHT. These results suggest that, in the dog, renal prostaglandins are involved in the pathogenesis of both acute 1-KHT and 2-KHT, whereas the role of renal prostaglandins in the regulation of arterial pressure appears to be negligible in chronic 1-KHT except during superimposed sodium depletion or severe hypertension. The data indicate that prostaglandins are involved in renovascular hypertension in the dog only under conditions where plasma renin activity is elevated. It is suggested that the release of renin after renal artery constriction is mediated by the vascular receptor that is at least partially independent of renal prostaglandin synthesis.


2003 ◽  
Vol 284 (3) ◽  
pp. F498-F502 ◽  
Author(s):  
Andrea Hartner ◽  
Nada Cordasic ◽  
Margarete Goppelt-Struebe ◽  
Roland Veelken ◽  
Karl F. Hilgers

Upregulation of the inducible cyclooxygenase (COX-2) in the macula densa accompanies the activation of the juxtaglomerular apparatus in many high-renin conditions. The functional role of COX-2 in these disease states is poorly understood. We tested whether COX-2 is required to increase renin in renovascular hypertension. Rats with established two-kidney, one-clip (2K1C) hypertension were treated for 2 wk with two different inhibitors of COX-2, NS-398 and rofecoxib, respectively. Hypertension in 2K1C rats was not affected or slightly enhanced by COX-2 inhibition, as measured intra-arterially in conscious animals. The increase in plasma renin activity was also unchanged by both rofecoxib and NS-398. The number of glomeruli with a renin-positive juxtaglomerular apparatus was elevated in clipped kidneys and decreased in contralateral kidneys of 2K1C rats. This pattern was unaltered by COX-2 inhibition. To test the effects of COX-2 blockade on a primarily macula densa-mediated stimulus, we studied salt depletion for comparison. A low-salt diet induced a significant increase in plasma renin activity, which was partially inhibited by treatment with NS-398. We conclude that inhibition of COX-2 in established renovascular hypertension does not affect renin synthesis or release. Thus either COX-2 is not necessary for the macula densa mechanism or the macula densa is not important for maintaining high renin in renovascular hypertension.


1982 ◽  
Vol 54 (4) ◽  
pp. 348-353 ◽  
Author(s):  
D. ARMANINI ◽  
F. FALLO ◽  
G. OPOCHER ◽  
M. BOSCARO ◽  
C. SCARONI ◽  
...  

1972 ◽  
Vol 36 (6) ◽  
pp. 617-621 ◽  
Author(s):  
YUKIO MIURA ◽  
TATSUO SATO ◽  
KEISHI ABE ◽  
IWAO ONO ◽  
KAORU YOSHINAGA

The Lancet ◽  
1980 ◽  
Vol 316 (8199) ◽  
pp. 821-824 ◽  
Author(s):  
GunnarH. Anderson ◽  
Patricia Randall ◽  
Jay Springer ◽  
DavidH.P. Streeten ◽  
Nancy Blakeman

1974 ◽  
Vol 48 (s2) ◽  
pp. 287s-290s ◽  
Author(s):  
U. Werner ◽  
H. Günnewig ◽  
K. D. Bock

1. The relations between the changes in plasma renin activity (PRA) and urinary catecholamine excretion (UCA) or plasma noradrenaline concentration have been investigated (a) in patients with benign primary hypertension, with renovascular hypertension and with idiopathic asympatheticotonic hypotension (ASH), and (b) during orthostasis and after administration of frusemide, of the β-blocking agent tenormin, of clonidine and of dihydralazine. 2. In primary hypertension noradrenaline and mean arterial pressure (Pm) showed a close positive correlation. 3. The mean values of both PRA and UCA were higher in renovascular hypertension than in primary hypertension and extremely low in ASH. The overlap of individual values between the patient groups was markedly reduced by using the quotient PRA/UCA. There was a statistically significant positive correlation between PRA and UCA in primary hypertension and in renovascular hypertension, with a different slope of the regression lines. 4. The increase of PRA and of noradrenaline during orthostasis was closely correlated. Frusemide and β-receptor blockade changed the slope of the regression line by additional stimulation or inhibition respectively of PRA. 5. Clonidine decreased, and dihydralazine increased both PRA and noradrenaline concentration. These changes again showed a significant positive correlation. The fall of mean arterial pressure produced by clonidine was correlated with the decrease of PRA and of noradrenaline concentration.


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