Inhibition by Bradykinin of the Vascular Effects of Pressor Hormones in the Canine Kidney: Relationship to Prostaglandins

1980 ◽  
Vol 59 (s6) ◽  
pp. 145s-148s ◽  
Author(s):  
H. Sušić ◽  
A. Nasjletti ◽  
K. U. Malik
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Vascular Reactivity ◽  
Sodium Pentobarbital ◽  
Vascular Effects ◽  
Arterial Infusion ◽  
Renal Vasoconstriction ◽  
Renal Vascular ◽  
Canine Kidney

1. Renal arterial injection of bolus doses of angiotensin II or noradrenaline, (0.06, 0.12 and 0.25 μg) caused renal vasoconstriction and decreased blood flow to the kidney in a dose-related manner in dogs anaesthetized by sodium pentobarbital. 2. The effect of angiotensin II and noradrenaline in lowering renal blood flow was reduced during renal arterial infusion of either bradykinin (10 ng min−1 kg−1) or prostaglandin E2 (4 ng min−1 kg−1). 3. Pretreatment of the dogs with an inhibitor of prostaglandin synthesis, sodium meclofenamate (5 mg/kg), blunted the inhibitory action of bradykinin, but not that of prostaglandin E2, on renal vascular reactivity to angiotensin II and noradrenaline. 4. These results indicate that bradykinin reduces the renal vasoconstriction induced by angiotensin II and noradrenaline in the dog by a mechanism dependent upon synthesis of prostaglandins.

Cyclosporine augments renal but not systemic vascular reactivity

1990 ◽  
Vol 258 (1) ◽  
pp. F211-F217
Author(s):  
M. D. Garr ◽  
M. S. Paller
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Arginine Vasopressin ◽  
Vascular Reactivity ◽  
Pressor Response ◽  
Sprague Dawley ◽  
Renal Vasoconstriction ◽  
Vascular Responsiveness ◽  
Renal Vascular

Renal vasoconstriction and hypertension are major side effects of cyclosporine. We tested the acute effects of cyclosporine on renal and systemic vascular reactivity to norepinephrine, angiotensin II, and arginine vasopressin. Renal vascular reactivity was tested in anesthetized Sprague-Dawley rats with denervated kidneys. Renal blood flow was measured with an electromagnetic flow probe in response to graded intra-arterial infusions of vasoconstrictors before and after intravenous administration of cyclosporine. Cyclosporine augmented the decrease in renal blood flow and the increase in renal vascular resistance produced by intrarenal norepinephrine, angiotensin II, and arginine vasopressin. In these studies, systemic blood pressure did not change and cyclosporine caused no direct change in basal renal blood flow. In contrast, in conscious animals, cyclosporine did not increase the pressor response to intravenous norepinephrine or to angiotensin II. Rather, cyclosporine caused enhanced baroreflex slowing of heart rate and a decrease in the pressor response to both norepinephrine and angiotensin II. Even when the baroreceptor reflex was blocked by pentolinium, the pressor response to norepinephrine in cyclosporine-treated animals was diminished compared with vehicle-treated animals. Therefore, although cyclosporine augmented renal vasoconstriction in response to norepinephrine, angiotensin II, and arginine vasopressin, it did not acutely increase the systemic vascular response to these agents. Enhanced renal vascular responsiveness is an additional mechanism for cyclosporine-mediated renal vasoconstriction. Lack of enhanced peripheral vascular responsiveness suggests that hypertension is not likely to be due to direct effects on the systemic vasculature and is more likely to be a consequence of renal functional impairment.

Effect of prostaglandin synthetase inhibitors on renal blood flow in the rat

1976 ◽  
Vol 231 (5) ◽  
pp. 1541-1545 ◽  
Author(s):  
WF Finn ◽  
WJ Arendshorst
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Small Diameter ◽  
Base Line ◽  
Sodium Pentobarbital ◽  
Prostaglandin Synthetase ◽  
Flow Transducer ◽  
Renal Vascular

Using a small-diameter electromagnetic flow transducer, the effect on the autoregulation of renal blood flow (RBF) of two structurally different prostaglandin synthetase inhibitors, indomethacin, 4 mg/kg BW, and meclofenamate, 5 mg/kg BW, was studied in nondiuretic rats anesthetized with either the oxybarbiturate, sodium pentobarbital, or the thiobarbiturate, Inactin. Regardless of the anesthetic agent, RBF remained relatively constant above a perfusion pressure of 105 mmHg. Treatment with either indomethacin or meclofenamate had no measurable effect on the autoregulatory response. Each agent, however, resulted in an increase in the renal vascular response to exogenous angiotensin II, an effect consistent with prostaglandin synthetase inhibition. Base-line RBF was significantly reduced by indomethacin or meclofenamate only in those animals that had previously received angiotensin. These results support the hypothesis that, in th rat, autoregulation of RBF occurs independently of prostaglandin activity, but that a relationship does exist between the renal vascular actions of angiotensin II and prostaglandins.

Bradykinin effects on adrenergic transmission in the canine kidney: relation to prostaglandins

1981 ◽  
Vol 241 (3) ◽  
pp. R146-R151 ◽  
Author(s):  
H. Susic ◽  
A. Nasjletti ◽  
K. U. Malik
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Inhibitory Effect ◽  
Prostaglandin Synthesis ◽  
Renal Nerve ◽  
Renal Vasoconstriction ◽  
Anesthetized Dogs ◽  
Renal Vascular ◽  
Increased Blood Flow ◽  
Canine Kidney

We studied the action(s) of bradykinin at the renal vascular neuroeffector junction, and its relation to prostaglandin synthesis, by investigating the effect of the peptide on the renal venous output of the neurotransmitter and on the renal vasoconstrictor responses elicited by sympathetic nerve stimulation and by norepinephrine in pentobarbital-anesthetized dogs. Renal arterial infusion of bradykinin at 10 ng . kg-1 . min-1 increased blood flow to the kidney and inhibited the vasoconstrictor effect of renal nerve stimulation (1-8 Hz) and injected norepinephrine (0.06-0.5 micrograms). However, bradykinin did not alter the rise in venous output of norepinephrine elicited by nerve stimulation. Infusion of another vasodilatory peptide, substance P (2 ng . kg-1 . min-1) into the renal artery also increased blood flow to the kidney but failed to alter the vasoconstriction produced by either adrenergic stimulus. Pretreatment of dogs with an inhibitor of prostaglandin synthesis, either sodium meclofenamate or indomethacin (5 mg/kg), abolished the inhibitory effect of the kinin on renal vasoconstriction produced by adrenergic stimuli. These data suggest that bradykinin acts on postjunctional sites to reduce adrenergically induced vasoconstriction in the canine kidney by a mechanism dependent on prostaglandin synthesis.

Renal vascular reactivity to U 46619 and adrenergic agonists in Goldblatt hypertension

1987 ◽  
Vol 253 (6) ◽  
pp. H1523-H1529 ◽  
Author(s):  
B. G. Zimmerman
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Vascular Reactivity ◽  
Adrenergic Agonists ◽  
Contralateral Kidney ◽  
Beta Adrenoceptor ◽  
Arterial Blood ◽  
Arterial Plasma ◽  
Renal Vascular ◽  
Goldblatt Hypertension

Vascular reactivity of the contralateral kidney of conscious Goldblatt hypertensive dogs was studied by eliciting renal blood flow (RBF) responses to intra-arterial infusions of vasoconstrictor and vasodilator agonists in control sessions and at weekly intervals postclipping. Systemic arterial blood pressure (BP) and RBF were monitored during each recording session via an implanted catheter and electromagnetic blood flow probe, respectively. BP was maximally increased within 1 wk and remained elevated for the duration of the study. The relationship between the negative percent change in RBF (-% delta RBF) and the renal arterial plasma concentration of adrenergic agonists, angiotensin II and thromboxane mimetic (U 46619), infused intra-arterially was subjected to regression analysis, and 25 and 50% effective doses (ED25 and ED50, respectively) were calculated. Vascular sensitivity to phenylephrine and norepinephrine increased within a month or more of hypertension. Vascular reactivity to angiotensin II was unchanged. In contrast to the delayed increase in renal vascular reactivity to adrenergic agonists, enhancement of the RBF responses to U 46619 was seen within 1-2 wk. In addition, beta-adrenoceptor-mediated vasodilation appeared suppressed during hypertension. Alteration in the response of the contralateral kidney to both vasoconstrictor and beta-adrenoceptor-mediated vasodilator stimuli may contribute to renal hemodynamic changes in Goldblatt hypertension.

Exaggerated renal vascular reactivity to angiotensin and thromboxane in young genetically hypertensive rats

1990 ◽  
Vol 259 (2) ◽  
pp. F372-F382 ◽  
Author(s):  
C. Chatziantoniou ◽  
F. H. Daniels ◽  
W. J. Arendshorst
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Receptor Agonist ◽  
Vascular Reactivity ◽  
Prostaglandin Synthesis ◽  
Genetic Hypertension ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Renal Vascular

The objective of this study was to test the hypothesis that angiotensin II and thromboxane A2 (TxA2) contribute to the elevated renal vascular resistance observed during the development of genetic hypertension. In 6-wk-old anesthetized spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats, renal blood flow (electromagnetic flowmetry) and carotid arterial pressure were measured during bolus injections of different doses of angiotensin II and U46619 (stable receptor agonist of TxA2) into the renal artery before and during inhibition of prostaglandin synthesis by indomethacin. In all cases, arterial pressure remained unchanged at the pre-injection levels. Under control conditions, angiotensin II reduced renal blood flow in SHR almost twice as much as in WKY. This strain difference was abolished by inhibition of prostaglandin synthesis, suggesting that a deficiency in the action of endogenous vasodilator prostaglandins is responsible for the enhanced response to angiotensin II in SHR. Under control conditions, the TxA2-receptor agonist produced similar reductions of renal blood flow in SHR and WKY. However, after indomethacin, the agonist-induced vasoconstriction was twice as large in SHR as in WKY, suggesting that SHR kidneys have an increased vascular reactivity to TxA2, which is unmasked when indomethacin reduces elevated levels of endogenous TxA2. These findings indicate important strain differences between young SHR and WKY in the renal vascular response to angiotensin II and TxA2 that may contribute to the renal vasoconstriction observed during the development of genetic hypertension.

scholarly journals Mice lacking the ADP ribosyl cyclase CD38 exhibit attenuated renal vasoconstriction to angiotensin II, endothelin-1, and norepinephrine

2009 ◽  
Vol 297 (1) ◽  
pp. F169-F176 ◽  
Author(s):  
Tiffany L. Thai ◽  
William J. Arendshorst
Keyword(s):  
Angiotensin Ii ◽  
Vascular Reactivity ◽  
Pressor Response ◽  
Family Members ◽  
Cell Types ◽  
Ang Ii ◽  
Renal Vasoconstriction ◽  
Endothelin 1 ◽  
Adp Ribosyl Cyclase ◽  
Renal Vascular

ADP ribosyl (ADPR) cyclases comprise a family of ectoenzymes recently shown to influence cytosolic Ca2+concentration in a variety of cell types. At least two ADPR cyclase family members have been identified in mammals: CD38 and CD157. We recently found reduced renal vascular reactivity to angiotensin II (ANG II), endothelin-1 (ET-1), and norepinephrine (NE) in the presence of the broad ADPR cyclase inhibitor nicotinamide. We hypothesized that CD38 mediates effects attributed to ADPR cyclase. We found expression of ADPR cyclases CD38 and CD157 mRNA in spleen, thymus, skin, and preglomerular arterioles of wild-type (WT) animals. Mice lacking CD38 showed decreased CD157 expression in most tissues tested. No difference in systolic or mean arterial pressure was observed between strains in either conscious or anesthetized states, whereas heart rate was reduced 10–20% in CD38−/− animals ( P < 0.05). During anesthesia, CD38−/− mice had reduced basal renal blood flow (RBF) and urine excretion ( P < 0.05). RBF responses to intravenous injection of ANG II, ET-1, and NE were attenuated ∼50% in CD38−/− vs. WT mice ( P < 0.01 for all). The systemic pressor response to ANG II was decreased in the absence of CD38 ( P < 0.01), whereas that to NE was normal ( P > 0.05); ET-1 was administered at a nonpressor dose. Nicotinamide effectively inhibited ANG II-induced renal vasoconstriction in WT mice ( P < 0.001), but had no effect on renal responses to ANG II in CD38−/− mice ( P > 0.5). Overall, our observations indicate the presence of two ADPR cyclase family members in renal preglomerular resistance arterioles and the importance of CD38 participation in acute vascular responses to all three vasoconstrictors in the renal microcirculation.

Vascular reactivity to angiotensin II in the normotensive and hypertensive pregnant ewe

1980 ◽  
Vol 238 (2) ◽  
pp. H209-H213
Author(s):  
S. M. Lieb ◽  
T. Cabalum ◽  
M. Zugaib ◽  
R. Erkkola ◽  
K. Tabsh ◽  
...  
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Vascular Reactivity ◽  
Pressor Response ◽  
Renal Hypertension ◽  
Circulatory Response ◽  
Pregnant Sheep ◽  
Experimental Renal Hypertension ◽  
Pregnant Ewe ◽  
Renal Vascular

The circulatory responses to progressively increasing doses of angiotensin II were studied in the same group of chronically instrumented unanesthetized pregnant sheep during three consecutive periods: a) normotensive with intact kidneys; b) normotensive with unilateral nephrectomy; and c) one-kidney hypertension. The results show that 1) the pressor response to a given dose of angiotensin was significantly greater in the normotensive than in the hypertensive condition; 2) uterine blood flow decreased markedly with the development of hypertension; 3) uterine circulatory response to angiotensin depended on the dosage; the response was less the the hypertensive than in the normotensive condition; 4) renal blood flow decreased and renal vascular resistance increased during angiotensin infusion, but the response was less in the hypertensive than in the normotensive condition; the response of the renal circulation decreased with increasing doses of angiotensin. These observations suggest a generalized vascular refractoriness to exogenous angiotensin II in the pregnant ewe with experimental renal hypertension.

Renal hemodynamics and vascular reactivity in canine DOCA-salt hypertension

1988 ◽  
Vol 255 (4) ◽  
pp. R563-R568
Author(s):  
J. L. Goering ◽  
P. C. Raich ◽  
B. G. Zimmerman
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Vascular Tone ◽  
Vascular Reactivity ◽  
Control Period ◽  
Indwelling Catheter ◽  
Alpha Adrenoceptor ◽  
Arterial Blood ◽  
Salt Hypertension ◽  
Renal Vascular

Because of the potential role that the kidney may play in deoxycorticosterone acetate (DOCA)-salt hypertension, changes in renal blood flow, renal vascular reactivity, and renal adrenergic vascular tone were followed in the conscious instrumented dog. DOCA-salt was administered daily after obtaining control measurements. Systemic mean arterial blood pressure (MAP) was monitored with an indwelling catheter, renal blood flow (RBF) was measured electromagnetically using an implanted blood flow probe, and drugs were administered intrarenal arterially through an indwelling renal artery catheter. During the first week of DOCA-salt administration MAP increased from 106 +/- 3 to 118 +/- 2 mmHg and at week 2 to 123 +/- 2 mmHg (P less than 0.01). RBF increased from 275 +/- 32 to 336 +/- 34 during week 1 (P less than 0.05) and to 324 +/- 29 ml/min during week 2. The log ED50 of norepinephrine administered intra-arterially decreased from 1.66 +/- 0.114 to 1.48 +/- 0.091 and 1.41 +/- 0.067 ng/ml (P less than 0.05), and of angiotensin II from 2.58 +/- 0.072 to 2.31 +/- 0.09 (P less than 0.05) and 2.38 +/- 0.05 pg/ml, during weeks 1 and 2, respectively. There was, however, no increase in adrenergic vascular tone as determined by the change in RBF obtained with the intra-arterial infusion of alpha-adrenoceptor antagonists. These experiments indicate that RBF is not compromised in canine DOCA-salt hypertension, and renal adrenergic tone is no greater in the hypertensive than in the normotensive control period.

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