A renal vasodilator effect of angiotensin II revealed by dual thromboxane inhibition

1994 ◽  
Vol 72 (6) ◽  
pp. 632-636 ◽  
Author(s):  
Al-Hassan Badahman ◽  
Thomas W. Wilson
Keyword(s):  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Sprague Dawley ◽  
Synthesis Inhibition ◽  
Renal Vasoconstriction ◽  
Sprague Dawley Rats ◽  
Renal Vascular ◽  
Arachidonate Release ◽  
Stimulation Of

Angiotensin II (AII) stimulates arachidonate release from renal endothelial and other ceils. Arachidonate is then metabolized by cyclooxygenase to prostaglandin (PG) H2, then PGI2 and thromboxane A2 (TXA2). PGH2 and TXA2 activate the same receptor and should augment AII-mediated vasoconstriction, whereas PGI2 is a vasodilator. We had previously shown that inhibiting TXA2 synthesis with furegrelate (FRG) redirects PGH2 metabolism toward PGI2, causing renal vasodilation. Because TXA2 synthesis inhibition may be incomplete and unmetabolized PGH2 may cause vasoconstriction, we reasoned that adding a PGH2/TXA2 receptor antagonist (BMS 180,290, formerly SQ 29548 (SQ)) to furegrelate should cause further renal vasodilation in the presence of AII Eight groups of 10 Sprague–Dawley rats received 120-min intravenous infusions of vehicle, FRG (2 mg∙kg−1 plus 2 mg∙kg−1∙h−1), SQ (2 mg∙kg−1 plus 2 mg∙kg−1∙h−1), FRG plus SQ, AII (10 ng∙kg−1∙min−1), AII plus FRG, AII plus SQ, or AII plus FRG plus SQ. Mean arterial pressure (MAP), p-[14C]aminohippurate clearance (CPAH), and [3H]insulin clearance were averaged for each rat for the final 90 min in three clearance periods. MAP did not change with any treatment. Estimating renal vascular resistance as MAP/CPAH confirmed a renal vasoconstrictor effect of this dose of AII: 58.1 ± 6.3 vs. 47.3 ± 6.8 (arbitrary units) with the vehicle (p < 0.05). FRG, SQ, or their combination did not affect renal vascular resistance, but adding FRG or SQ to AII prevented AII-mediated renal vasoconstriction. Adding both to AII caused net renal vasodilation to 24.8 ± 2.6 (p < 0.05 vs. vehicle). Inulin clearance changed in the same direction in all groups, but the changes were less marked. We conclude that stimulation of renal arachidonate release by AII combined with TXA2 synthesis inhibition and receptor antagonism results in vasodilation. This renal effect could be due to increased and unopposed renal vasodilator PG (principally PGI2) action.Key words: renal hemodynamics, angiotensin II, prostaglandins, thromboxane.

Myogenic contribution to agonist-induced renal vasoconstriction during normoxia and hypoxia

1997 ◽  
Vol 272 (4) ◽  
pp. H1945-H1951 ◽  
Author(s):  
M. R. Eichinger ◽  
J. M. Resta ◽  
B. R. Walker
Keyword(s):  
Renal Artery ◽  
Vascular Resistance ◽  
Acute Hypoxia ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Left Renal Artery ◽  
Sprague Dawley ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Renal Vascular

Acute hypoxia attenuates agonist-induced constrictor and pressor responses in conscious rats, and a recent report suggests that hypoxia may also diminish myogenic reactivity in isolated, perfused rat kidneys. Thus we hypothesized that the diminished responsiveness to pressor agents during hypoxia is caused by an impairment of myogenic reactivity. Male Sprague-Dawley rats were instrumented with a pulsed Doppler flow probe on the left renal artery, an aortic vascular occluder cuff immediately above the left renal artery to control renal perfusion pressure, and catheters were inserted to measure systemic arterial blood pressure and renal arterial pressure (RAP) and for administration of agents. Animals were studied under normoxic or acute hypoxic (fractional concentration of O2 in inspired gials = 0.12) conditions and were administered phenylephrine, arginine vasopressin, or angiotensin II. To determine the myogenic (pressure-dependent) component of agonist-induced vasoconstriction, renal vascular resistance was calculated during agonist infusion with RAP uncontrolled and with RAP controlled to preinfusion levels. Significant myogenic components of agonist-induced renal vasoconstriction were evident with all pressor agents used. However, hypoxia did not attenuate agonist-induced, pressure-dependent increases in renal vascular resistance. We conclude that the reduced vasoreactivity associated with acute hypoxia is not caused by diminished myogenic reactivity.

Glycerol-Induced Acute Renal Failure in Brattleboro Rats with Hypothalamic Diabetes Insipidus

1979 ◽  
Vol 56 (2) ◽  
pp. 133-138 ◽  
Author(s):  
A. Konrads ◽  
K. G. Hofbauer ◽  
K. Bauereiss ◽  
J. Möhring ◽  
F. Gross
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Diabetes Insipidus ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Renal Vascular

1. During the development of glycerol-induced acute renal failure in Sprague-Dawley rats, plasma concentrations of vasopressin rise and probably induce an increase in blood pressure. 2. In the present studies the role of vasopressin in acute renal failure was further analysed by experiments in Brattleboro rats homozygous for hereditary hypothalamic diabetes insipidus which were injected intramuscularly with 10 ml of glycerol/kg (61 mmol/l). 3. After the injection of glycerol plasma osmolality increased transiently and packed cell volume was elevated. The rats became anuric and plasma urea concentrations rose progressively. Plasma renin concentration increased significantly within 2 h. Plasma renin substrate concentration rose progressively and had almost doubled by 8 h. 4. In contrast with previous observations in Sprague-Dawley rats, blood pressure did not rise in rats with diabetes insipidus after the injection of glycerol. 5. When 2 h after the injection of glycerol kidneys were taken from rats with diabetes insipidus and perfused with an electrolyte solution in a single-pass system for 1 h, renal vascular resistance was 30% higher than in control kidneys 10 min after the start of the perfusion and remained elevated thereafter. In similar experiments with kidneys from Sprague-Dawley rats with acute renal failure, renal vascular resistance was increased fivefold immediately after the start of the perfusion, but decreased subsequently. 6. These data support the idea that in glycerol-induced acute renal failure of Sprague-Dawley rats an increased release of vasopressin is responsible for the elevation of blood pressure and suggest that this hormone also participates in renal vasoconstriction. However, a rise of plasma vasopressin concentrations alone cannot fully explain the increase in renal vascular resistance and the development of acute renal failure.

Area postrema stimulation induces differential renal hemodynamics with two anesthetics

1992 ◽  
Vol 262 (2) ◽  
pp. R289-R294 ◽  
Author(s):  
D. K. Hartle ◽  
A. S. Soliman
Keyword(s):  
Vascular Resistance ◽  
Area Postrema ◽  
Renal Vascular Resistance ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Pentobarbital Sodium ◽  
Percent Change ◽  
Anesthetized Rats ◽  
Sprague Dawley Rats ◽  
Renal Vascular

The effect of area postrema stimulation (APS) on blood pressure, renal blood flow (RBF), and renal vascular resistance was compared in urethan-anesthetized and pentobarbital sodium-anesthetized Sprague-Dawley rats. Mean arterial pressure (MAP) increased in a frequency-dependent manner during APS in both urethan- and pentobarbital-anesthetized rats. Although no significant differences occurred in the maximum percent change in MAP between groups, marked differences occurred in RBF and calculated renal vascular resistance (RVR) changes. In urethan-anesthetized rats, RBF and MAP increased during APS, but RVR did not change. In contrast, APS significantly decreased RBF (-26.5 +/- 1.9%) while increasing RVR (+99.4 +/- 11.4%) in pentobarbital-anesthetized rats. The increase in RVR in the pentobarbital-anesthetized group during APS was eliminated by prior ganglionic blockade. It was concluded that the anesthetic agent employed can significantly alter the degree to which APS can activate renal vasomotion in the rat.

scholarly journals L-arginine does not prevent the renal effects of endothelin in humans.

1995 ◽  
Vol 5 (7) ◽  
pp. 1508-1516
Author(s):  
J A Bijlsma ◽  
A J Rabelink ◽  
K A Kaasjager ◽  
H A Koomans
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Sodium Excretion ◽  
Renal Vascular Resistance ◽  
Nitric Oxide Production ◽  
Renal Effects ◽  
Renal Vasoconstriction ◽  
Oxide Production ◽  
Renal Vascular ◽  
Stimulation Of

The infusion of endothelin to obtain plasma levels as present in sodium-retaining conditions such as heart failure and hepatorenal syndrome has been shown to cause sodium retention and renal vasoconstriction. Whether these renal effects of endothelin could be modulated by the stimulation of nitric oxide production by the infusion of L-arginine was examined. Therefore, the renal and endocrine effects of the systemic administration of endothelin (2.5 ng/kg per minute for 90 min), L-arginine (5 mg/kg per minute for 90 min), or the combination of endothelin and L-arginine were studied in healthy subjects under clearance conditions. During endothelin infusion, plasma endothelin levels rose from 3.0 +/- 0.2 to 14.1 +/- 2.4 pmol/L (P < 0.01). Mean arterial pressure increased by 7 mm Hg (P < 0.01). The effects on renal function were disproportionately large: renal vascular resistance increased from 77.5 +/- 3.2 to 124.1 +/- 6.7 mm Hg/min per liter (P < 0.01), and sodium excretion fell from 178 +/- 30 to 83 +/- 11 mumol/min (P < 0.01). Endothelin had no effect on urinary nitrite excretion. L-Arginine caused a fall in blood pressure of 5 mm Hg (P < 0.01) and decreased renal vascular resistance by 12% (P < 0.05). Sodium excretion increased twofold. This was associated with an increase in urinary nitrite excretion from 112 +/- 36 to 465 +/- 190 nmol/min (P < 0.01), suggesting stimulation of renal nitric oxide production. During the combination of endothelin and L-arginine, urinary nitrite excretion increased similarly.(ABSTRACT TRUNCATED AT 250 WORDS)

Vasoconstrictor and vasodilator sites within anteroventral third ventricle region

1987 ◽  
Vol 253 (6) ◽  
pp. R827-R831 ◽  
Author(s):  
M. L. Mangiapane ◽  
M. J. Brody
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Third Ventricle ◽  
Renal Vascular Resistance ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Tungsten Microelectrode ◽  
Renal Vascular ◽  
Stimulation Of

Previous studies have shown that electrical stimulation of the rat anteroventral third ventricle (AV3V) region produces a characteristic pattern of hemodynamic effects, i.e., renal and mesenteric vasoconstriction, and hindquarters vasodilation. In the present study, we localized the vasoconstrictor and vasodilator effects to specific subregions of the AV3V. In urethan-anesthetized rats prepared with arterial catheters and pulsed Doppler flow probes, we assessed the effects of electrical stimulation of four nuclei within AV3V on mean arterial pressure and renal, mesenteric, and hindquarters resistance. These nuclei were the organum vasculosum lamina terminalis (OVLT), ventral nucleus medianus (median preoptic nucleus), anterior (precommissural) nucleus medianus (median preoptic nucleus), and periventricular preoptic nuclei. Stimulation was carried out by use of a tungsten microelectrode. Stimulation of the OVLT consistently provoked stimulus-locked increases in arterial pressure coupled with increases in mesenteric and renal vascular resistance. Ganglionic blockade with chlorisondamine prevented these responses, demonstrating that they were mediated neurogenically. Stimulation of the three remaining nuclei produced decreases in arterial pressure, hindquarters vasodilation, and little change in mesenteric and renal vascular resistance. No changes in heart rate were observed with stimulation of any of the four nuclei. These results suggest that the vasoconstrictor and pressor functions of the AV3V region are localized in or near the OVLT region, whereas the remaining nuclei of the AV3V region mediate vasodilator and depressor responses.

scholarly journals Basal and stimulated nitric oxide in control of kidney function in the aging rat

1997 ◽  
Vol 272 (6) ◽  
pp. R1747-R1753 ◽  
Author(s):  
C. Hill ◽  
A. M. Lateef ◽  
K. Engels ◽  
L. Samsell ◽  
C. Baylis
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Renal Vascular Resistance ◽  
Oxidation Products ◽  
No Oxidation ◽  
No Production ◽  
Sprague Dawley ◽  
Vasoconstrictor Response ◽  
Renal Vascular

To investigate the activity of nitric oxide (NO) in control of renal hemodynamics during aging, studies were conducted on conscious Sprague-Dawley rats aged 3-5 mo (young, Y) and 18-22 mo (old, O). Blood pressure (BP) and renal vascular resistance (RVR) were higher in O vs. Y in control, and acute systemic NO synthesis inhibition (NOSI) increased BP and RVR, with an enhanced renal vasoconstrictor response in O. Infusion of the NO substrate L-arginine produced similar, selective renal vasodilation in both groups. The endothelium-dependent vasodilator acetylcholine caused similar falls in BP and RVR, whereas sodium nitroprusside produced an exaggerated depressor response in O vs. Y without falls in RVR in either age group. Urinary excretion of the stable NO oxidation products (NOx) decreased with age, suggesting a decline in the overall somatic NO production. In conclusion, basal tonically produced NO has a more pronounced role in maintenance of renal perfusion in aging, whereas L-arginine- and agonist-stimulated renal vasodilation is not impaired with age. NO production from some source may be reduced with aging, as indicated by falls in 24-h NOX excretion, although the similarity in pressor response and enhanced renal vasoconstrictor response to NOSI suggests that the role of NO in control of total peripheral and renal vascular resistance is maintained.

Renal vasodilatation after inhibition of renin or converting enzyme in marmoset

1986 ◽  
Vol 251 (5) ◽  
pp. H897-H902
Author(s):  
D. Neisius ◽  
J. M. Wood ◽  
K. G. Hofbauer
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Enzyme Inhibitor ◽  
Renal Vascular Resistance ◽  
Converting Enzyme ◽  
Renin Inhibition ◽  
Renal Vascular

The relative importance of angiotensin II for the renal vasodilatory response after converting-enzyme inhibition was evaluated by a comparison of the effects of converting-enzyme and renin inhibition on renal vascular resistance. Renal, mesenteric, and hindquarter blood flows were measured with chronically implanted ultrasonic-pulsed Doppler flow probes in conscious, mildly volume-depleted marmosets after administration of a converting-enzyme inhibitor (enalaprilat, 2 mg/kg iv), a synthetic renin inhibitor (CGP 29,287, 1 mg/kg iv), or a renin-inhibitory monoclonal antibody (R-3-36-16, 0.1 mg/kg iv). Enalaprilat reduced blood pressure (-16 +/- 4 mmHg, n = 6) and induced a selective increase in renal blood flow (27 +/- 8%, n = 6). CGP 29,287 and R-3-36-16 induced comparable reductions in blood pressure (-16 +/- 4 mmHg, n = 6 and -20 +/- 4 mmHg, n = 5, respectively) and selective increases in renal blood flow (36 +/- 12%, n = 6 and 34 +/- 16%, n = 4, respectively). The decrease in renal vascular resistance was of similar magnitude for all of the inhibitors (enalaprilat -28 +/- 3%, CGP 29,287 -32 +/- 6%; and R-3-36-16 -33 +/- 7%). These results indicate that the renal vasodilatation induced after converting-enzyme or renin inhibition is mainly due to decreased formation of angiotensin II.

Mechanism of prostaglandin E2-induced increase of proximal sodium reabsorption in the rat

1990 ◽  
Vol 258 (1) ◽  
pp. R82-R86 ◽  
Author(s):  
Y. Kinoshita ◽  
F. G. Knox
Keyword(s):  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Rat Kidney ◽  
Sodium Reabsorption ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Convoluted Tubules ◽  
Stimulation Of ◽  
Interstitial Infusion

Prostaglandin E2, when infused directly into the renal interstitium, enhances sodium reabsorption by the superficial proximal convoluted tubules of anesthetized Sprague-Dawley rats. The present study was designed to investigate the role of angiotensin II in the prostaglandin E2-induced stimulation of proximal sodium reabsorption. Micropuncture at the superficial late proximal tubule demonstrated a significant increase in the fractional reabsorption of sodium from 39.9 +/- 2.3% in control conditions to 51.8 +/- 3.0% (n = 9, P less than 0.01) during the renal interstitial infusion of prostaglandin E2. The stimulatory effect of prostaglandin E2 on proximal sodium reabsorption was markedly attenuated by pretreatment with saralasin. During intravenous saralasin infusion, prostaglandin E2 did not significantly change the fractional reabsorption of sodium from 42.2 +/- 5.8 to 45.4 +/- 6.0% (n = 7, NS). In summary, the stimulatory effect of renal interstitial infusion of prostaglandin E2 on proximal sodium reabsorption was attenuated by pretreatment with saralasin. Therefore renal interstitial infusion of prostaglandin E2 may enhance proximal sodium reabsorption, at least in part, through stimulation of angiotensin II production in the rat kidney.

Acetylcholine chloride and renal hemodynamics during postnatal maturation in conscious lambs

1999 ◽  
Vol 87 (4) ◽  
pp. 1296-1300 ◽  
Author(s):  
Alp Sener ◽  
Francine G. Smith
Keyword(s):  
Renal Artery ◽  
Vascular Resistance ◽  
Renal Hemodynamics ◽  
Renal Vascular Resistance ◽  
Postnatal Maturation ◽  
Renal Vasoconstriction ◽  
Acetylcholine Chloride ◽  
Renal Vascular ◽  
Dose Dependent ◽  
Conscious Animals

To test the hypothesis that acetylcholine-induced relaxation of the renal artery decreases with postnatal age, we measured parameters of renal hemodynamics before and for 35 s after aortic suprarenal injection of acetylcholine in conscious, chronically instrumented lambs aged ∼1 wk ( n = 5) and ∼6 wk ( n = 5). Acetylcholine was administered in one of five doses ranging from 0 to 10 mg/kg body wt; doses were administered randomly, in the same volume. There were significant age- and dose-dependent changes in renal vascular resistance after acetylcholine administration, such that the response was greater in 1-wk-old lambs. After the highest dose tested, renal vascular resistance decreased by 13.6 ± 7.3 (SD) mmHg ⋅ ml−1 ⋅ min ⋅ g kidney wt in 1-wk-old lambs and by 9.1 ± 3.2 mmHg ⋅ ml−1 ⋅ min ⋅ g kidney wt in 6-wk-old lambs at 35 s. We also observed a transient renal vasoconstriction before the renal vasodilatation in 6-wk-old lambs but not in 1-wk-old animals. These data provide the first age- and dose-dependent effects of exogenous administration of acetylcholine on renal hemodynamics during maturation in conscious animals.

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