scholarly journals Role of Renocortical Cyclooxygenase-2 for Renal Vascular Resistance and Macula Densa Control of Renin Secretion

2001 ◽  
Vol 12 (5) ◽  
pp. 867-874
Author(s):  
HAYO CASTROP ◽  
FRANK SCHWEDA ◽  
KARL SCHUMACHER ◽  
KONRAD WOLF ◽  
ARMIN KURTZ
Keyword(s):  
Vascular Resistance ◽  
Macula Densa ◽  
Renal Vascular Resistance ◽  
Renin Secretion ◽  
Expression Level ◽  
Flow Rates ◽  
Low Salt ◽  
Cox 2 ◽  
Renal Vascular

Abstract. This study aimed to assess the role of cyclooxygenase-2 (COX-2)-derived prostanoids for the macula densa control of renal afferent arteriolar resistance and for renin secretion. For this purpose, studied were the effects of blocking macula densa salt transport by the loop diuretic bumetanide (100 μM) on renal perfusate flow and on renin secretion in isolated perfused rats, in which renocortical COX-2 expression was prestimulated in vivo by treatment with the angiotensin-converting enzyme inhibitor ramipril, with low-salt diet, or with a combination of both. These maneuvers stimulated COX-2 expression in an order of ramipril + low salt ≫ low salt > ramipril > controls. Flow rates through isolated kidneys at a constant pressure of 100 mmHg were dependent on the pretreatment regimen, in the way that they went in parallel with COX-2 expression. The COX-2 inhibitor NS-398 (10 μM) lowered flow rates depending on the COX-2 expression level and was most pronounced therefore after pretreatment with low salt + ramipril. NS-398 did not change the increase of flow in response to bumetanide but attenuated the stimulation of renin secretion in response to bumetanide in a manner depending on the expression level of COX-2. These findings suggest that in states of increased renocortical expression of COX-2, overall renal vascular resistance and the macula densa control of renin secretion become dependent on COX-2—derived prostanoids.

Functional role of sodium-calcium exchange in the regulation of renal vascular resistance

2001 ◽  
Vol 280 (1) ◽  
pp. F155-F161 ◽  
Author(s):  
Frank Schweda ◽  
Helga Seebauer ◽  
Bernhard K. Krämer ◽  
Armin Kurtz
Keyword(s):  
Calcium Channels ◽  
Vascular Resistance ◽  
Functional Role ◽  
Channel Blocker ◽  
Sodium Concentration ◽  
Renal Vascular Resistance ◽  
Partial Replacement ◽  
Chloride Channel Blocker ◽  
Renal Vascular

Our study aimed to assess a possible functional role of the Na+/Ca2+ exchanger in the regulation of renal vascular resistance (RVR). Therefore, we investigated the effects of an inhibition of the Na+/Ca2+ exchanger either by lowering the extracellular sodium concentration ([Na+]e) or, pharmacologically on RVR, by using isolated perfused rat kidneys. Graded decreases in [Na+]e led to dose-dependent increases in RVR to 4.3-fold (35 mM Na+). This vasoconstriction was markedly attenuated by lowering the extracellular calcium concentration, by the L-type calcium channel blocker amlodipine or by the chloride channel blocker niflumic acid. Further lowering of [Na+]e to 7 mM led to an increase in RVR to 7.5-fold. In this setting, amlodipine did not influence the magnitude but did influence the velocity of vasoconstriction. Pharmacological blockade of the Na+/Ca2+ exchanger with KB-R7943, benzamil, or nickel resulted in significant vasoconstriction (RVR 2.5-, 1.8-, and 4.2-fold of control, respectively). Our data suggest a functional role of the Na+/Ca2+ exchanger in the renal vascular bed. In conditions of partial replacement of [Na+]e, vasoconstriction is dependent on chloride and L-type calcium channels. A total replacement of [Na+]e leads to a vasoconstriction that is nearly independent of L-type calcium channels. This might be due to an active calcium transport into the cell by the Na+/Ca2+ exchanger.

Renal protection by a dual ETA/ETB endothelin antagonist, L-754,142, after aortic cross-clamping in the dog.

1997 ◽  
Vol 8 (7) ◽  
pp. 1061-1071 ◽  
Author(s):  
S M Krause ◽  
T F Walsh ◽  
W J Greenlee ◽  
R Ranaei ◽  
D L Williams ◽  
...  
Keyword(s):  
Renal Insufficiency ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Sodium Reabsorption ◽  
High Dose ◽  
Renal Protection ◽  
Suprarenal Aorta ◽  
Renal Vascular ◽  
Endothelin Antagonist

Renal insufficiency is a significant complication that occurs after surgical procedures, requiring cross-clamping of the aorta. The mechanism for this renal dysfunction is currently not known, but studies suggest a potential role of endothelin in mediating the insufficiency. Accordingly, the role of endothelin was assessed using the nonpeptidyl, dual ETA/ETB endothelin antagonist L-754,142 in a model of renal insufficiency in the anesthetized dog induced by cross-clamping the suprarenal aorta for 60 min, followed by 2 h of reperfusion. In vehicle-treated animals (saline, n = 8) after 2 h of reperfusion, plasma [ET-1] increased 66% and renal blood flow (RBF) was reduced by 38% compared with baseline. This decline was associated with an 84% increase in renal vascular resistance and a 54% reduction in GFR (baseline, 46 +/- 5 ml/min; 21 +/- 3 ml/min at 2 h; P < 0.01) and sodium reabsorption (baseline, 6.7 +/- 0.7 microEq/min; 3.0 +/- 0.5 microEq/min at 2 h, P < 0.01). After baseline measurements, pretreatment with L-754,142 at 0.3 mg/kg bolus + 0.1 mg/kg per h continuous infusion (low dose; n = 8) or 3.0 mg/kg bolus + 1 mg/kg per h infusion (high dose; n = 8) initiated 45 min before aortic cross-clamp led to a dose-dependent normalization of RBF and renal vascular resistance within 2 h of cross-clamp removal. GFR was also improved and returned to within 75% of baseline (P < 0.01 versus vehicle) by 2 h of reperfusion with L-754,142 (baseline, 55 +/- 5 ml/min; 42 +/- 5 ml/min at 2 h with the high dose). The improvement of GFR with L-754,142 treatment was associated with a preservation of sodium reabsorption compared with vehicle-treated animals. This study supports a role of endothelin in the pathogenesis of renal insufficiency after aortic cross-clamping and demonstrates that pretreatment with the dual ETA/ETB endothelin antagonist L-754,142 preserves RBF and sodium reabsorption, leading to a significant improvement in GFR.

Increased Renal Vascular Resistance In Zinc-Deficient Rats: Role Of Nitric Oxide and Superoxide

2002 ◽  
Vol 29 (12) ◽  
pp. 1096-1104 ◽  
Author(s):  
Nobutaka Kurihara ◽  
Hiroyuki Yanagisawa ◽  
Masamichi Sato ◽  
Chang-Kuen Tien ◽  
Osamu Wada
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Renal Vascular

Stimulation of renin secretion by alpha-adrenoceptor agonists

1983 ◽  
Vol 244 (1) ◽  
pp. E37-E44 ◽  
Author(s):  
M. L. Blair
Keyword(s):  
Vascular Resistance ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Renin Secretion ◽  
Alpha Adrenoceptors ◽  
Alpha Adrenoceptor ◽  
Phenylephrine Infusion ◽  
Renal Vascular ◽  
Stimulation Of

This study was designed to determine whether stimulation of intrarenal alpha-adrenoceptors can increase renin secretion rate (RSR) in the absence of increased renal vascular resistance and to identify the accompanying changes in renal function. Experiments were performed in pentobarbital-anesthetized dogs in which renal perfusion pressure was maintained at approximately 90 mmHg and the infused kidney was acutely denervated. Renal artery infusion of the alpha-adrenoceptor agonist methoxamine (0.5 microgram X kg-1 X min-1 for 30 min) increased RSR from 160 +/- 95 to 1,376 +/- 385 ng ANG I/min (P = 0.01) but did not decrease renal blood flow (RBF); the same dose infused intravenously had no effect on RSR or RBF. Intra-arterial phenylephrine infusion (0.5 microgram X kg-1 X min-1 for 9 min) increased RSR by 500 +/- 157 ng ANG I/min (P less than 0.01) and decreased both inulin clearance (Cin) and urinary sodium excretion (UNaV) by 25% but did not affect RBF. At a lower concentration of phenylephrine (0.2 microgram X kg-1 X min-1 for 9 min), RSR increased by 318 +/- 103 ng ANG I/min (P less than 0.01) and RBF, Cin, and UNaV did not change. The increase in RSR was completely blocked by prazosin but was unaffected by propranolol. In summary, renin secretion can be stimulated by activation of intrarenal alpha-adrenoceptors even in the absence of increased renal vascular resistance.

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