An educational tool to improve understanding of angiotensin II function and the adrenergic system in renal circulation

Arterial rings were prepared from the branchial artery, coeliac artery and ventral aorta of the Japanese dogfish Triakis scyllia and used to determine arterial contraction in a myograph. Noradrenaline caused a dose-dependent contraction (10(-9)-3 x 10(-6) M) that was completely inhibited by pre-treatment with 10(-7) M phentolamine. Homologous dogfish angiotensin II (ANG II) ([Asn1, Pro3, Ile5]-ANG II) also caused dose-dependent contraction (10(-9)-3 x 10(-6) M), but phentolamine had no effect on this response. Administration of dogfish angiotensin I (ANG-I) ([Asn1, Pro3, Ile5, Gln9]-ANG I) resulted in a contraction similar to that produced by ANG II and the effect could be blocked with 10(-7) M captopril. The mammalian ANG II receptor antagonists [Sar1, Ile8]-ANG II and [Sar1, Ala8]-ANG II caused dose-dependent contractions of coeliac artery rings, but were less potent than homologous ANG I and ANG II. These results show that the contractile effect of [Asn1, Pro3, Ile5]-ANG II is not mediated by the alpha-adrenergic system and contractions of arterial rings by noradrenaline and elasmobranch ANG II are mediated by separate vascular receptors. The elasmobranch ANG II vascular receptor may have co-evolved with the unusual structure of this peptide.

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Different Vascular Responses to Subpressor Angiotensin II Administration in the Mesenteric and Renal Circulation of Rats

American Journal of Hypertension ◽

10.1016/0895-7061(95)00398-3 ◽

1996 ◽

Vol 9 (4) ◽

pp. 385-392 ◽

Cited By ~ 7

Author(s):

G Cserep

Keyword(s):

Angiotensin Ii ◽

Renal Circulation ◽

Vascular Responses

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Renal medullary plasma flow rate and reabsorption of salt and water from inner medullary collecting duct

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y87-383 ◽

1987 ◽

Vol 65 (12) ◽

pp. 2415-2421 ◽

Cited By ~ 9

Author(s):

W. A. Cupples ◽

H. Sonnenberg

Keyword(s):

Blood Flow ◽

Sodium Chloride ◽

Angiotensin Ii ◽

Flow Rate ◽

Plasma Flow ◽

Collecting Duct ◽

Urine Osmolality ◽

Renal Circulation ◽

Inner Medullary Collecting Duct ◽

Medullary Collecting Duct

It has been proposed that medullary washout secondary to increased blood flow will limit maximal urine osmolality and reabsorption of salt and water from the inner medullary collecting duct. We have tested this prediction. The function of the inner medullary collecting duct was examined by microcatheterization. Acetylcholine was infused directly into the renal circulation, captopril was infused intravenously, and angiotensin II was infused into the renal circulation in rats which also received captopril. Medullary plasma flow rate, measured by dye–dilution in parallel experiments, was not significantly increased by acetylcholine; it was increased 30% (p < 0.02) by systemic infusion of captopril, and was returned to control by angiotensin II. Acetylcholine increased both urine flow rate and sodium excretion (p < 0.01, p < 0.001, respectively), while captopril increased only sodium excretion (p < 0.025). Angiotensin II blocked the natriuresis due to captopril. None of the treatments altered urine osmolality (p > 0.4 in all cases). Acetylcholine increased the loads of water, sodium, chloride, and total solute delivered to the inner medullary collecting duct. Angiotensin II reduced delivery of water and solutes compared with captopril alone. None of the treatments affected load dependency of reabsorption of water, sodium, chloride, or total solute in the inner medullary collecting duct. We conclude that there is, at most, a weak interaction between medullary blood flow and reabsorption from the inner medullary collecting duct.

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ANGIOTENSIN II BLOCKADE IN EXISTING HYPOVOLEMIA: EFFECTS OF CANDESARTAN IN THE PORCINE SPLANCHNIC AND RENAL CIRCULATION

Shock ◽

10.1097/00024382-200014040-00009 ◽

2000 ◽

Vol 14 (4) ◽

pp. 471-477 ◽

Cited By ~ 8

Author(s):

Mats Laesser ◽

Lars Fändriks ◽

Anders Pettersson ◽

Sara Ewert ◽

Anders Åneman

Keyword(s):

Angiotensin Ii ◽

Renal Circulation

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Cholesterol feeding does not alter renal hemodynamic response to acetylcholine and angiotensin II in rabbits

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1997.272.3.r940 ◽

1997 ◽

Vol 272 (3) ◽

pp. R940-R947

Author(s):

J. F. Carroll ◽

H. L. Mizelle ◽

K. Cockrell ◽

J. F. Reckelhoff ◽

B. R. Clower ◽

...

Keyword(s):

Angiotensin Ii ◽

Control Diet ◽

Aortic Ring ◽

High Cholesterol Diet ◽

Ang Ii ◽

Cholesterol Diet ◽

Cholesterol Feeding ◽

Renal Circulation ◽

Renal Vascular ◽

Renal Responses

Aortic ring studies have demonstrated a decrease in endothelium-dependent relaxation or an enhanced response to vasoconstrictors in rabbits fed a high-cholesterol diet. Whether such abnormalities exist in the renal circulation is unclear. The purpose of this study was to determine functional renal responses to acetylcholine (ACh) or angiotensin II (ANG II) infusion in anesthetized rabbits after 8-10 wk of either a control diet (ACh, n = 6; ANG II, n = 6) or a 1% cholesterol diet (ACh, n = 7; ANG II, n = 7). Mean arterial pressure (MAP), renal blood flow (RBF), and glomerular filtration rate (GFR) were measured. Renal vascular resistance (RVR) was calculated as MAP/RBF. For ANG II experiments, captopril (15 microg x kg(-1) x min(-1)) was infused to suppress endogenous ANG II production. After two control clearance periods, either ACh (1 microg x kg(-1) x min(-1)) or ANG II (0.5 ng x kg(-1) x min(-1)) was infused into the renal artery; RBF was allowed to stabilize before experimental clearances. RBF increased with ACh (control: 25 +/- 2 to 39 +/- 2 ml/min; cholesterol: 26 +/- 2 to 40 +/- 3 ml/min) and decreased with ANG II infusions (control: 40 +/- 4 to 25 +/- 3 ml/min; cholesterol: 36 +/- 3 to 24 +/- 2 ml/min). Nitrate/nitrite excretion also increased with ACh infusion (control: 2.3 +/- 1.0 to 5.2 +/- 1.8 nmol x kg(-1) x min(-1); cholesterol: 2.3 +/- 0.3 to 6.0 +/- 1.3 nmol x kg(-1) x min(-1)). However, there were no significant differences between control and cholesterol groups in either response. GFR was unaltered during ACh and ANG II infusions. MAP, RVR, and urinary sodium and potassium excretion did not differ between groups in response to either drug. These results suggest that, despite significant hypercholesterolemia and large-vessel atherosclerosis, both nitric oxideinduced vasodilation and endothelium-dependent modulation of ANG II vasoconstriction in the renal circulation are unaffected by cholesterol feeding.

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Role of angiotensin II, alpha-adrenergic system, and arginine vasopressin on arterial pressure in rat

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1984.246.1.h25 ◽

1984 ◽

Vol 246 (1) ◽

pp. H25-H30 ◽

Cited By ~ 1

Author(s):

M. S. Paller ◽

S. L. Linas

Keyword(s):

Angiotensin Ii ◽

Arterial Pressure ◽

Arginine Vasopressin ◽

Adrenergic Receptor ◽

Enzyme Inhibitor ◽

Adrenergic System ◽

Ang Ii ◽

Conscious Rat ◽

Profound Hypotension

Three pressor systems regulate arterial pressure (MAP): angiotensin II (ANG II), the alpha-adrenergic system, and arginine vasopressin (AVP). In this study we determined the ability of each system to support MAP in the conscious rat when the other two systems were inactivated. After administration of the converting-enzyme inhibitor teprotide (CEI) and the alpha-adrenergic receptor antagonist phenoxybenzamine (POB), MAP decreased 40% as a result of a 45% decrease in peripheral vascular resistance (PVR). Despite hypotension, plasma AVP levels were not increased, and an AVP pressor antagonist (AVP-A) did not result in a further decrease in MAP. Thus the profound hypotension after POB plus CEI was the result of inhibition of all three systems. POB, rather than CEI, prevented AVP release since following hypotensive hemorrhage, plasma levels reached 51 +/- 13 pg/ml with CEI but only 4.7 +/- 0.8 pg/ml with POB. To study the pressor effect of AVP alone, AVP was infused in POB plus CEI-treated rats. AVP increased MAP (from 68 +/- 4 to 92 +/- 5 mmHg; P less than 0.005) and plasma AVP (to 13.8 +/- 1.9 pg/ml). Since POB inhibited both the AVP and the alpha-adrenergic system, the role of ANG II alone was determined in POB-treated rats. In the presence of ANG II MAP was 97 +/- 1 mmHg. To study the alpha-adrenergic system, MAP was determined in CEI plus AVP-A-treated rats. In the presence of an intact alpha-adrenergic system MAP was 101 +/- 1 mmHg. We conclude that PVR and MAP are profoundly decreased in the absence of all three pressor systems.(ABSTRACT TRUNCATED AT 250 WORDS)

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Renal synthesis and urinary excretion of eicosanoids during pregnancy in rats

AJP Renal Physiology ◽

10.1152/ajprenal.1987.253.6.f1197 ◽

1987 ◽

Vol 253 (6) ◽

pp. F1197-F1205 ◽

Cited By ~ 1

Author(s):

K. P. Conrad ◽

M. J. Dunn

Keyword(s):

Angiotensin Ii ◽

Urinary Excretion ◽

Previous Investigation ◽

Renal Hemodynamics ◽

Renal Circulation ◽

Pregnant Rats ◽

Cyclooxygenase Inhibition ◽

Cortical Slices

We tested whether vasodilatory prostaglandins (PGs) mediate the adaptation of the maternal renal circulation to pregnancy by assessing production of PGs by kidney tissues in vitro. We reasoned that if PGs are crucial, then local synthetic rates of these hormones would most likely be increased. Glomeruli harvested from gravid rats of gestational days 6, 12, and 20 did not demonstrate greater basal or stimulated syntheses of PGF2 alpha, PGE2, or 6-keto-PGF1 alpha than those from virgin controls. Production of PGE2 and 6-keto-PGF1 alpha by renal cortical slices obtained from pregnant rats was not greater than that of virgins either. Urine 24-h excretory rates of PGE2 and 6-keto-PGF1 alpha, but not PGF2 alpha, were significantly increased during pregnancy (all P less than 0.05 from prepregnant levels). During midgestation, when urinary excretion of PGE2 and 6-keto-PGF1 alpha was greatest, medullary syntheses of these PGs were found to be comparable between virgin and gravid animals. The present study, which fails to show augmented synthesis of PGs by renal tissues derived from gravid rats, is consistent with our previous investigation in which cyclooxygenase inhibition did not reduce the gestational increase of renal hemodynamics or restore the attenuated renal pressor responsiveness to exogenous angiotensin II. Taken together, we conclude that in rats, PGs most likely do not mediate the alterations in the renal circulation observed during pregnancy.

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