Angiotensin I conversion and vascular reactivity in pathophysiological states in dogs

1980 ◽  
Vol 48 (2) ◽  
pp. 308-312 ◽  
Author(s):  
P. J. Leuenberger ◽  
S. A. Stalcup ◽  
L. M. Greenbaum ◽  
R. B. Mellins ◽  
G. M. Turino
Keyword(s):  
Blood Pressure ◽  
Enzyme Activity ◽  
Angiotensin Ii ◽  
Vascular Reactivity ◽  
Blood Pressure Response ◽  
Acute Hypoxia ◽  
Pressure Response ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Arterial Blood

To determine if angiotension converting enzyme activity is altered by acute pathophysiological insults, we assessed angiotensin I conversion using a blood pressure response technique in anesthetized dogs studied during acute 100% O2 breathing and acute acid-base derangements. Also, we determined systemic vascular reactivity to angiotensin II by measuring the magnitude and duration of the arterial blood pressure response to intra-arterial injections of angiotensin II under these same conditions. Angiotensin I conversion found in normoxia [91 +/- 7 (SD)%] was unchanged by acute acidosis, alkalosis, and hyperoxia. During acute hyperoxia the mean half time of the hypertensive response increased from 68 +/- 25 (SD) s at a PaO2 of 112 +/- 18 (SD) Torr to 100 +/- 34 (SD) s at a PaO2 of 491 +/- 47 (SD) Torr (P less than 0.01). No other pathophysiological condition studied had any effect on reactivity of systemic vasculature to angiotensin II. We conclude that, except during acute hypoxia as previously shown, converting enzyme activity is resistant to other pathophysiological insults and that vascular responsiveness to angiotensin II is enhanced by hyperoxia.

The Effect of Captopril on Blood Pressure and Angiotensins I, II and III in Sodium-Depleted Dogs: Problems Associated with the Measurement of Angiotensin II after Inhibition of Converting Enzyme

1980 ◽  
Vol 58 (6) ◽  
pp. 445-450 ◽  
Author(s):  
J. J. Morton ◽  
M. Tree ◽  
J. Casals-Stenzel
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Fold Increase ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Active Inhibitor ◽  
Arterial Blood ◽  
Rapid Fall ◽  
Angiotensin Iii ◽  
Plasma Angiotensin

1. Changes in arterial blood pressure, blood angiotensin I, plasma angiotensin II and plasma angiotensin III were measured in conscious sodium—depleted dogs after infusion of captopril, an orally active inhibitor of converting enzyme. 2. Angiotensins II and III were measured after chromatography to remove angiotensin I, which increased in concentration after inhibition of converting enzyme and which interfered in the direct assay for angiotensin II. 3. Infusion of captopril at 20, 200, 2000 and 6000 μg h−1 kg−1, each for 3 h, produced a rapid fall in blood pressure and in concentration of angiotensin II. Angiotensin II was undetectable at 6000 μg h−1 kg−1 (mean pre-infusion value for all samples was 39 ± sd 15 pmol/I, n = 14) 4. The percentage fall in blood pressure correlated with the percentage fall in plasma angiotensin II (r = 0.65, P<0.001) 5. These results suggest that the initial fall in blood pressure may be mediated in part by the suppression of angiotensin II. 6. Blood angiotensin I concentration rose with each rate of infusion of drug to a maximum 16-fold increase at 6000 μg h−1 kg−1 (26−416 pmol/l). The rise in angiotensin I was inversely related to the fall in angiotensin II (r = −0.68, P<0.001)

Cardiovascular consequences of microinjection of vasopressin and angiotensin II in the area postrema

1993 ◽  
Vol 265 (3) ◽  
pp. R625-R631 ◽  
Author(s):  
V. L. Lowes ◽  
L. E. McLean ◽  
N. W. Kasting ◽  
A. V. Ferguson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Area Postrema ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Systemic Administration ◽  
Pressure Response ◽  
Arterial Blood ◽  
At1 Antagonist

Microinjection of angiotensin II (ANG II) into the area postrema (AP) of urethan-anesthetized male Sprague-Dawley rats elicited statistically significant increases in mean arterial blood pressure at doses ranging from 10 pg to 500 ng (10 pg, mean +/- SE, 10.8 +/- 1.1 mmHg, P < 0.001; 250 ng, 15.2 +/- 2.6 mmHg, P < 0.001). Heart rate was also significantly increased at doses > 10 pg, although these increases were not dose dependent. Systemic administration of losartan (Dup-753), an AT1 antagonist, was able to significantly reduce the pressor response to 250 ng ANG (post-losartan: 81.9 +/- 9.5% reduction in blood pressure response, P < 0.0001), whereas PD123319, an AT2 antagonist, was without significant effect (P > 0.1). Microinjection of vasopressin (VP) (10 pg-500 ng) into the AP also resulted in statistically significant increases in blood pressure at doses ranging from 10 to 100 pg (10 pg, 7.0 +/- 1.5 mmHg, P < 0.05) and 100-500 ng (250 ng, 12.2 +/- 1.8 mmHg, P < 0.0001). Small but significant changes in heart rate were observed only at 100 pg and 100 ng. Systemic administration of a V1 antagonist significantly attenuated the increases in blood pressure in response to 50, 100, and 250 ng VP (250 ng, post-V1 antagonist: 66.4 +/- 8.6% reduction in blood pressure response, P < 0.001), whereas [desamino,D-Arg8]vasopressin (DDAVP), a V2 agonist, had a depressor effect when microinjected directly into the AP (250 ng, -9.9 +/- 1.6 mmHg, P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals BLOOD PRESSURE RESPONSE TO [1-SARCOSINE, 8-ISOLEUCINE]ANGIOTENSIN II IN PATIENTS WITH LIVER CIRRHOSIS AND ASCITES

1979 ◽  
Vol 43 (1) ◽  
pp. 37-41 ◽  
Author(s):  
TAKESHI HATA ◽  
TOSHIO OGIHARA ◽  
HIROSHI MIKAMI ◽  
MITSUAKI NAKAMARU ◽  
TAKASHI MANDAI ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Liver Cirrhosis ◽  
Angiotensin Ii ◽  
Blood Pressure Response ◽  
Pressure Response

Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Jolanta Gutkowska ◽  
Gaétan Thibault ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Ace Inhibition ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

scholarly journals Blood pressure response to angiotensin II is enhanced in obese Zucker rats and is attributed to an aldosterone-dependent mechanism

2012 ◽  
Vol 166 (8) ◽  
pp. 2417-2429 ◽  
Author(s):  
Helge Müller-Fielitz ◽  
Margot Lau ◽  
Olaf Jöhren ◽  
Florian Stellmacher ◽  
Markus Schwaninger ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Pressure Response ◽  
Pressure Response ◽  
Zucker Rats ◽  
Obese Zucker Rats ◽  
Dependent Mechanism

Role of arteria baroreceptor input on thirst and urinary responses to intracerebroventricular angiotensin II

1993 ◽  
Vol 265 (3) ◽  
pp. R591-R595 ◽  
Author(s):  
R. L. Thunhorst ◽  
S. J. Lewis ◽  
A. K. Johnson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Arterial Blood ◽  
Endogenous Formation

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.

Brain angiotensin receptors and sympathoadrenal regulation during insulin-induced hypoglycemia

2001 ◽  
Vol 280 (4) ◽  
pp. R1162-R1168 ◽  
Author(s):  
René H. Worck ◽  
Dennis Staahltoft ◽  
Thomas E. N. Jonassen ◽  
Erik Frandsen ◽  
Hans Ibsen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibition ◽  
Blood Pressure Response ◽  
Pressure Response ◽  
Angiotensin Receptors ◽  
Converting Enzyme ◽  
Reflex Regulation ◽  
Conscious Rats ◽  
Converting Enzyme Inhibition

Simultaneous blockade of systemic AT1 and AT2 receptors or converting enzyme inhibition (CEI) attenuates the hypoglycemia-induced reflex increase of epinephrine (Epi). To examine the role of brain AT1 and AT2 receptors in the reflex regulation of Epi release, we measured catecholamines, hemodynamics, and renin during insulin-induced hypoglycemia in conscious rats pretreated intracerebroventricularly with losartan, PD-123319, losartan and PD-123319, or vehicle. Epi and norepinephrine (NE) increased 60-and 3-fold, respectively. However, the gain of the reflex increase in plasma Epi (Δplasma Epi/Δplasma glucose) and the overall Epi and NE responses were similar in all groups. The ensuing blood pressure response was similar between groups, but the corresponding bradycardia was augmented after PD-123319 ( P < 0.05 vs. vehicle) or combined losartan and PD-123319 ( P < 0.01 vs. vehicle). The findings indicate 1) brain angiotensin receptors are not essential for the reflex regulation of Epi release during hypoglycemia and 2) the gain of baroreceptor-mediated bradycardia is increased by blockade of brain AT2 receptors in this model.

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