Disappearance of Angiotensin II and Noradrenaline from the Renal and Femoral Circulations of the Dog

1980 ◽  
Vol 58 (1) ◽  
pp. 29-35 ◽  
Author(s):  
M. J. S. Miller ◽  
G. C. Scroop
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Femoral Artery ◽  
Pressor Response ◽  
Intravenous Route ◽  
Vascular Bed ◽  
Pressor Responses ◽  
Vascular Beds ◽  
Degree Of Extraction ◽  
Renal Vascular

1. The relative ability of the renal and femoral vascular beds to remove infused angiotensin II and noradrenaline was examined in anaesthetized greyhounds. 2. The degree of extraction of infused drug by each vascular bed was expressed as a percentage, calculated by comparing the pressor response to intra-arterial infusion with that obtained when the same dose was administered by the intravenous route. 3. When compared with the same dose given intravenously, the pressor responses after renal artery administration of angiotensin II were reduced by a mean of 77·8 ± 4·1% (mean ± sem, n = 12), whereas those after femoral artery infusions at the same dose were reduced by a mean of only 27·2 ± 4·9%(n = 12). 4. The pattern of extraction seen with noradrenaline infusions administered in a similar manner was the reverse of that with angiotensin II. There was a 28·9 ± 6·8% (n = 7) reduction in pressor responses to renal artery infusions; in contrast, femoral artery infusions of the same dose exhibited a 99·0 ± 1·0% (n = 7) reduction in the pressor responses. 5. Local arterial administration of the angiotensin II competitive antagonist, [Sar1,Ile8]angiotensin II, potentiated the systemic pressor responses to renal artery infusions of angiotensin II, but not those to femoral artery infusions. 6. It is suggested that the marked ability of the renal vascular bed to remove circulating angiotensin II may, in part, involve receptor-binding, although this seems not to be the case in the femoral vascular bed.

Comparative responses to α,β-methylene-ATP in cat pulmonary, mesenteric, and hindquarter vascular beds

2002 ◽  
Vol 93 (4) ◽  
pp. 1287-1295 ◽  
Author(s):  
Trinity J. Bivalacqua ◽  
Hunter C. Champion ◽  
Mrugeshkumar K. Shah ◽  
Bracken J. De Witt ◽  
Edward W. Inscho ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Pyridoxal Phosphate ◽  
Pressor Response ◽  
P2x Receptor ◽  
Disulfonic Acid ◽  
Flow Conditions ◽  
Vascular Bed ◽  
Pressor Responses ◽  
Pressor Activity ◽  
Vascular Beds

Responses to the P2X-purinoceptor agonist α,β-methylene-ATP (α,β-MeATP) were investigated in the pulmonary, hindquarter, and mesenteric vascular beds in the cat. Under constant-flow conditions, injections of α,β-MeATP caused dose-related increases in perfusion pressure in the pulmonary and hindquarter beds and a biphasic response in the mesenteric circulation. In the pulmonary vascular bed, the order of potency was α,β-MeATP > U-46619 > angiotensin II, whereas, in the hindquarters, the order of potency was angiotensin II > U-46619 > α,β-MeATP. The order of potency was similar in the hindquarter and mesenteric beds when the pressor component of the response to α,β-MeATP was compared with responses to angiotensin II and U-46619. The P2X-receptor antagonist pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonic acid attenuated the pressor response to α,β-MeATP in the hindquarter circulation and the pressor component in the mesenteric vascular bed. Pressor responses to α,β-MeATP were not altered by cyclooxygenase, α-adrenergic, or angiotensin AT1 antagonists. These data show that α,β-MeATP has potent pressor activity in the pulmonary circulation, where it was 100-fold more potent than angiotensin II. In contrast, α,β-MeATP had modest pressor activity in the systemic bed, where it was 1,000-fold less potent than angiotensin II. These data suggest that responses to α,β-MeATP are dependent on the vascular bed studied and may be dependent on the density of P2X receptors in the vascular bed.

Regional autoregulatory responses during infusion of vasoconstrictor agents in conscious dogs

1990 ◽  
Vol 259 (4) ◽  
pp. H1270-H1277 ◽  
Author(s):  
L. J. Hellebrekers ◽  
J. F. Liard ◽  
A. L. Laborde ◽  
A. S. Greene ◽  
A. W. Cowley
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Conscious Dogs ◽  
Flow Probe ◽  
Electromagnetic Flow ◽  
Vascular Bed ◽  
Vasoconstrictor Agents ◽  
Electromagnetic Flow Probe ◽  
Vascular Beds ◽  
Renal Vascular

We investigated pressure-dependent autoregulatory responses in mesenteric, iliac, and renal vascular beds of conscious dogs during intravenous infusion of angiotensin II, phenylephrine, or arginine vasopressin at rates which increased arterial pressure by 20-40 mmHg. The arteries supplying these beds were instrumented with an electromagnetic flow probe, a nonoccluding catheter, and an electromagnetic flow probe, a nonoccluding catheter, and an occluder cuff connected with a servo-amplifier, which enabled us to return perfusion pressure to control levels during infusion of the vasoconstrictor agents. We attempted to differentiate between the increase in vascular resistance due to the direct effect of the vasoconstrictor agent and the increase induced by an autoregulatory response induced by elevations of aortic perfusion pressure. We measured a strong degree of autoregulation in the renal vascular bed with a fractional compensation value close to 1. Moderate autoregulation occurred in the mesenteric vascular bed, where the compensation was 0.4-0.5 with angiotensin II and phenylephrine and between 0.74 and 0.94 with vasopressin. No autoregulatory capacity could be demonstrated in the hindlimb. The findings indicate that, under conditions of increased systemic blood pressure, both the renal and the mesenteric vascular beds contribute to the increase in total peripheral resistance by pressure-dependent vasoconstrictor responses.

Angiotensin receptors and pressor hyperresponsiveness in renal prehypertensive rabbits

1986 ◽  
Vol 251 (1) ◽  
pp. H196-H204 ◽  
Author(s):  
D. W. Zeigler ◽  
J. A. Johnson ◽  
D. G. Koivunen ◽  
S. Siripaisarnpipat ◽  
W. L. Fowler ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Pressor Response ◽  
Artery Stenosis ◽  
Angiotensin Receptors ◽  
Ang Ii ◽  
Pressor Responses ◽  
Conscious Rabbits

This study consisted of five different experiments with conscious rabbits. In experiment 1, the angiotensin II (ANG II) antagonist [Sar1-Ala8]ANG II infused iv into one-kidney rabbits with renal artery stenosis (RAS) of 3 days' duration, at a dose that blocked pressor responses to ANG II, did not decrease the exaggerated pressor responses to norepinephrine (NE). In experiment 2, captopril infused iv into one-kidney, 3-day, RAS rabbits blocked pressor hyperresponsiveness to NE, and the concurrent infusion of [Sar1-Ala8]ANG II did not reestablish pressor hyperresponsiveness, indicating that this ANG II analogue had no agonistic action to promote hyperresponsiveness to NE. In experiment 3, infusion of ANG II at a subpressor dose (6.7 pmol . min-1 . kg body wt-1) into normal rabbits resulted in pressor hyperresponsiveness to NE, which was blocked by [Sar1-Ala8]ANG II. Experiment 4 involved infusing [Sar1-Ala8]ANG II or [Sar1-Ile8]ANG II at various doses into 3-day RAS rabbits, to determine their abilities to attenuate the pressor responses to ANG II (100 ng/kg) and the pressor hyper-responses to NE (800 ng . min-1 . kg-1). [Sar1-Ile8]ANG II decreased the ANG II pressor responses at an ID50 dose of 64 +/- 5 (SEM) pmol . min-1 . kg-1 and attenuated the NE pressor hyper-response at an ID50 dose of 65 +/- 5 pmol . min-1 . kg-1; [Sar1-Ala8]ANG II diminished the ANG II pressor response at an ID50 dose of 757 +/- 247 and the NE pressor hyper-response at an ID50 dose of 10,061 +/- 944 pmol . min-1 . kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin III and pressor responsiveness in 3-day renal artery stenosis rabbits

1990 ◽  
Vol 258 (2) ◽  
pp. H540-H548
Author(s):  
J. A. Johnson ◽  
D. E. Dostal ◽  
A. Elsberry-Gonder
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Intravenous Infusion ◽  
Enzyme Inhibitor ◽  
Pressor Response ◽  
Artery Stenosis ◽  
Ang Ii ◽  
Pressor Responses ◽  
Angiotensin Iii

This study examined the ability of [des-Asp1]angiotensin II (angiotensin III, ANG III) to interact with the angiotensin II (ANG II) receptors involved in pressor hyperresponsiveness in one-kidney, 3-day renal artery stenosis (RAS) rabbits. In experiment 1, six 3-day RAS rabbits had significantly larger pressor responses to norepinephrine (NE; 800 ng.min-1.kg body wt-1) than did six 3-day controls. The intravenous infusion of captopril, an angiotensin-converting enzyme inhibitor, diminished the pressor response NE in the RAS rabbits. ANG III at 0.5, 1.0, and 2.0 pmol.min-1.kg-1 iv with captopril resulted in a progressive restoration of pressor hyperresponsiveness to NE in the RAS rabbits, and ANG II at 2.0 pmol.min-1.kg-1 iv produced no further enhancement of the pressor responses to NE. In experiment 2, 12 3-day RAS rabbits had pressor hyperresponsiveness to NE that was alleviated by the infusion of captopril and was restored by the intravenous infusion of ANG III (2 pmol.min-1.kg-1). In six of the these rabbits an additional intravenous infusion of the ANG II antagonist [Sar1,Ile8]ANG II at 300 ng.min-1.kg body wt-1 diminished the pressor hyperresponsiveness to NE; in the other six rabbits the infusion of [Sar1,Ala8] ANG II at 6 micrograms.min-1.kg body wt-1 did not reduce the pressor hyperresponse to NE. In experiment 3, the infusion of ANG III (5 pmol.min-1.kg-1) in six normal rabbits did not alter the pressor responses to NE (400 ng.min-1.kg-1), whereas the infusion of ANG II (5 pmol.min-1.kg-1) resulted in increased pressor responses to NE.(ABSTRACT TRUNCATED AT 250 WORDS)

Metabolic clearance of angiotensin II in pregnant and nonpregnant sheep

1985 ◽  
Vol 249 (1) ◽  
pp. E49-E55 ◽  
Author(s):  
R. P. Naden ◽  
S. Coultrup ◽  
B. S. Arant ◽  
C. R. Rosenfeld
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Metabolic Clearance ◽  
Ang Ii ◽  
Pressor Responses ◽  
Pregnant Sheep ◽  
Vascular Responsiveness ◽  
Arterial Plasma ◽  
In Pregnancy

Reduced vascular responsiveness to infused angiotensin II (ANG II) has been observed during pregnancy. It has been proposed that infusions produce lower circulating concentrations of ANG II in pregnancy, due to an increase in the metabolic clearance rate of ANG II (MCRangii). We have evaluated the MCRangii and the arterial plasma concentrations of ANG II during constant infusions of 1.15 micrograms ANG II/min into chronically instrumented pregnant (n = 6) and nonpregnant (n = 9) sheep. Although the pressor responses were significantly less in the pregnant than in the nonpregnant sheep (17.5 +/- 0.5 vs. 34.9 +/- 3.2 mmHg, P less than 0.001), the values for MCRangii were not different: 56.2 +/- 6.3 ml X min-1 X kg-1 in nonpregnant and 55.9 +/- 4.3 ml X min-1 X kg-1 in pregnant sheep. The steady-state plasma ANG II concentrations during the infusions were slightly less in pregnant than in nonpregnant sheep (388 +/- 36 vs. 454 +/- 36 pg/ml); however, this difference would be responsible for only a 2-mmHg reduction in the pressor response. We conclude that the reduced pressor response to infused ANG II in pregnancy is not due to an increase in MCRangii nor to lower plasma ANG II concentrations.

Pulmonary and systemic vasodilator effects of the newly discovered prostaglandin, PGI2

1978 ◽  
Vol 45 (3) ◽  
pp. 408-413 ◽  
Author(s):  
P. J. Kadowitz ◽  
B. M. Chapnick ◽  
L. P. Feigen ◽  
A. L. Hyman ◽  
P. K. Nelson ◽  
...  
Keyword(s):  
Vena Cava ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Vascular Bed ◽  
Vasodilator Activity ◽  
Pulmonary Arterial ◽  
Vascular Beds ◽  
Renal Vascular ◽  
Dose Dependent

The effects of the newly discovered bicyclic prostaglandin, prostacyclin (PGI2), on the pulmonary and systemic vascular beds were investigated in the anesthetized dog. PGI2 decreased systemic and pulmonary arterial pressures in a dose-related manner when injected into the vena cava in doses of 1--30 microgram. Since left ventricular end-diastolic, left atrial, and right atrial pressures were unchanged, and since cardiac output was increased or unchanged, pulmonary and systemic vascular resistances were decreased. PGI2 was 10 times more potent than prostaglandins E1 or E2 in decreasing aortic pressure when injected intravenously, and the effects of PGI2 on the systemic vascular bed were similar when injected into the vena cava or the left atrium. These data indicate that inactivation of PGI2 is minimal in the lung. The stable prostacyclin metabolite, 6-keto-PGF1alpha, had little hemodynamic effects, suggesting that responses to PGI2 were not due to formation of this metabolite. PGI2 produced dose-dependent increases in blood flow in the mesenteric and renal vascular beds. These data demonstrate that PGI2 has marked vasodilator activity in the pulmonary and systemic vascular beds and suggest that prostacyclin is the only known metabolite of arachidonic acid that dilates the pulmonary and systemic circulations.

Mechanisms of pressor response produced by stimulation of nucleus ambiguus

1990 ◽  
Vol 259 (5) ◽  
pp. R955-R962
Author(s):  
B. H. Machado ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Pressor Responses ◽  
Regional Vascular Resistance ◽  
Parasympathetic Control ◽  
Renal Vascular ◽  
Stimulation Of

We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.

scholarly journals Pressor responses to norepinephrine in rabbits with 3-day and 30-day renal artery stenosis. The role of angiotensin II.

1978 ◽  
Vol 43 (3) ◽  
pp. 437-446 ◽  
Author(s):  
S Ichikawa ◽  
J A Johnson ◽  
W L Fowler ◽  
C G Payne ◽  
K Kurz ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Artery Stenosis ◽  
Pressor Responses

Pressor responses of rats to vasopressin: effect of sodium, angiotensin, and catecholamines

1983 ◽  
Vol 244 (2) ◽  
pp. H253-H258 ◽  
Author(s):  
M. Burnier ◽  
H. R. Brunner
Keyword(s):  
Angiotensin Ii ◽  
Sodium Intake ◽  
Pressor Response ◽  
Response Curves ◽  
Ether Anesthesia ◽  
Spontaneously Hypertensive ◽  
Lysine Vasopressin ◽  
Pressor Responses ◽  
Wistar Kyoto ◽  
The Right

The pressor response to lysine vasopressin was tested in groups of male Wistar, Brattleboro, Wistar-Kyoto, and spontaneously hypertensive rats. Moreover, the influence of sodium intake, angiotensin II, saralasin, captopril, norepinephrine, and isoproterenol on vasopressin pressor responses was evaluated. The right iliac artery and one or both femoral veins of the animals were catheterized under light ether anesthesia. The experiments were carried out following a 2-h stabilization period with the rats awake and semirestrained. Pressor responsiveness was evaluated acutely on the basis of dose-response curves (0.5-4 mU). In the Wistar rats, angiotensin II (10 and 30 ng/min) and isoproterenol (10 ng/min) markedly decreased the response to vasopressin, whereas variations in sodium intake and blood pressure per se did not seem to exert any influence. Norepinephrine (250 ng/min) slightly enhanced the pressor responsiveness to the smaller doses of lysine-vasopressin. Brattleboro rats with congenital diabetes insipidus were less sensitive to vasopressin than the other animals, and neither angiotensin II nor isoproterenol induced any change. In conclusion, the pressor responsiveness to vasopressin can vary considerably depending on several factors. These must be taken into account when evaluating the possible pressor role of vasopressin in experimental and clinical settings.

Altered pressor responses to NE and ANG II during cyclosporin A administration to conscious rats

1990 ◽  
Vol 258 (3) ◽  
pp. H854-H860 ◽  
Author(s):  
S. C. Textor ◽  
L. Smith-Powell ◽  
T. Telles
Keyword(s):  
Angiotensin Ii ◽  
Cyclosporin A ◽  
Dose Response ◽  
Peak Effect ◽  
Relative Resistance ◽  
Pressor Responses ◽  
Induced Hypertension ◽  
Vascular Responsiveness ◽  
Renal Vascular ◽  
Conscious Animals

Vasoconstriction and hypertension have been prominent during cyclosporin A (CSA) administration. To evaluate whether CSA modulates vascular responsiveness to pressor stimuli in the intact organism, CSA was administered via osmotic pump (10 and 20 mg.kg-1.day-1 ip vs. olive oil vehicle) for 2 wk. After 8 days, arterial pressure and dose-response relationships to norepinephrine, angiotensin II, and bradykinin were measured in conscious animals. Despite similar initial pressures, dose-response relationships were markedly attenuated to both norepinephrine and angiotensin II. Maximal responses were not affected, indicating a rightward shift without loss of peak effect. Vasodilation with bradykinin was not diminished. These changes were not evident after an acute CSA infusion at the same dose (10 mg.kg-1.day-1 over 2 h). Treatment with verapamil (0.505 mg/kg over 2 days) lowered basal arterial pressures but did not change the effects of CSA on pressor sensitivity. Despite attenuated pressor responses, renal vascular resistance was elevated and glomerular filtration diminished during CSA administration. These observations indicate that cyclosporin modifies vascular responsiveness to pressor stimuli in the rat and may explain the relative resistance of this species to cyclosporin-induced hypertension.

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