Effect of [Sar1, Ala8]-angiotensin II and hypophysectomy on the intestinal resistance vessels and blood pressure following furosemide-induced volume depletion

1976 ◽  
Vol 54 (3) ◽  
pp. 373-380 ◽  
Author(s):  
J. Robert McNeill ◽  
William C. Wilcox ◽  
Raoul Regnault
Keyword(s):  
Blood Pressure ◽  
Control System ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Adrenal Glands ◽  
The Other ◽  
Volume Depletion ◽  
Competitive Antagonist ◽  
Vasoconstrictor Response ◽  
Resistance Vessels

Intravenous administration of furosemide (2 mg/kg) caused intestinal vasoconstriction in various groups of pentobarbital-anesthetized cats. [Sar1, Ala8]-angiotensin II, a specific competitive antagonist of angiotensin II, was infused 60 min after administration of furosemide, a time when the intestinal vasoconstrictor response to the diuretic was maximal or near maximal. In hypophysectomized animals, infusion of the antagonist abolished the intestinal vasoconstriction and caused a significant fall in arterial pressure even when the intestinal nerves and adrenal glands remained intact. In contrast, the antagonist had little effect when the pituitary gland remained intact. The results suggest that endogenous angiotensin and vasopressin are overlapping mechanisms which constrict the intestinal resistance vessels and support arterial pressure following furosemide-induced volume depletion. In the absence of one control system, the other compensates to maintain the responses.

Vasopressin and angiotensin: reciprocal mechanisms controlling mesenteric conductance

1977 ◽  
Vol 232 (3) ◽  
pp. H260-H266
Author(s):  
J. R. McNeill ◽  
W. C. Wilcox ◽  
C. C. Pang
Keyword(s):  
Control System ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
The Other ◽  
Small Decrease ◽  
Prolonged Infusion ◽  
Resistance Vessels ◽  
Angiotensin Ii Antagonist ◽  
Small Intestinal ◽  
Anesthetized Cat

Intravenous infusions of [Sar1-Ala8]angiotensin II, acute hypophysectomy, and acute intestinal denervation were carried out in 15 pentobarbital-anesthetized cats. Infusion of the angiotensin II antagonist caused only a small increase in superior mesenteric arterial conductance and a small decrease in arterial pressure in intact animals, but the changes were subypophysectomy alone caused only a small intestinal vasodilatation and little change in arterial pressure. However, the responses to hypophysectomy were much larger when the gland was removed during a prolonged infusion of the angiotensin II antagonist. Intestinal denervation caused only minor changes in mesenteric conductance and arterial pressure, and the responses to [Sar1-Ala8]angiotensin II and hypophysectomy were largely unaltered by the presence or absence of the intestinal innervation. The results suggest that the renin-angiotensin and vasopressin systems are reciprocal overlapping mechanisms that exert a significant vasoconstrictor influence on the intestinal resistance vessels in the anesthetized cat. In the absence of one control system, the other appears to compensate to maintain resistance.

Hypophysectomy and saralasin on mesenteric vasoconstrictor response to vasopressin

1979 ◽  
Vol 236 (2) ◽  
pp. H200-H205
Author(s):  
C. C. Pang ◽  
W. C. Wilcox ◽  
J. R. McNeill
Keyword(s):  
Angiotensin Ii ◽  
Plateau Phase ◽  
Dose Response Relationship ◽  
Competitive Antagonist ◽  
Stressed Animal ◽  
Vasoconstrictor Response ◽  
Resistance Vessels ◽  
Before And After ◽  
High Doses ◽  
Relationship Of

The dose-response relationship of the mesenteric resistance vessels to vasopressin was studied in anesthetized laparotomized cats before and after hypophysectomy and again during the plateau phase of the response to a prolonged infusion of [Sar1-Ala8] angiotensin II (saralasin), a competitive antagonist of angiotensin II. Hypophysectomy and saralasin each caused an increase in superior mesenteric arterial conductance. Before hypophysectomy infusion of 0.5 mU/(min.kg) of vasopressin caused mesenteric conductance to decrease from 0.168 to 0.156 ml/(min.kg.mmHg), a change of only 0.012 units. After hypophysectomy, the same dose reduced conductance from 0.227 to 0.179 mU/(min.kg.mmHg), a change of 0.048 units. During the plateau phase of the response to saralasin, 0.5 mU/(min.kg) of vasopressin reduced conductance from 0.281 to 0.201 ml/(min.kg.mmHg), a change of 0.079 units. Hypophysectomy and saralasin had little effect on the mesenteric vasoconstrictor response to high doses of vasopressin (2.0-10 mU/(min.kg). The ineffectiveness of low doses of vasopressin on the mesenteric resistance vessels of the intact anesthetized, surgically stressed animal may be due in part to the already constricted state of the bed caused by endogenous vasopressin and angiotensin and in part due to an opposing vasodilator influence, the reflex withdrawal of the vasoconstrictor effect of endogenous vasopressin.

Abnormal vascular function and morphology in preeclampsia: a study of isolated resistance vessels

1985 ◽  
Vol 69 (4) ◽  
pp. 477-482 ◽  
Author(s):  
C. Aalkjaer ◽  
H. Danielsen ◽  
P. Johannesen ◽  
E. B. Pedersen ◽  
A. Rasmussen ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Pregnant Women ◽  
Vascular Function ◽  
Direct Evidence ◽  
The Other ◽  
Vascular Changes ◽  
Direct Information ◽  
Vascular Abnormalities ◽  
Media Thickness ◽  
Resistance Vessels

1. In order to obtain direct information about vascular changes associated with pre-eclampsia, the morphological and functional characteristics of isolated omental resistance vessels from 11 women with pre-eclampsia, 10 normotensive pregnant women and eight normotensive nonpregnant women were determined. 2. In vessels from the women with preeclampsia, the ratio of media thickness to lumen diameter was increased, compared with that in vessels from the other two groups. 3. The vessels from the women with preeclampsia had an increased responsiveness to angiotensin II and a decreased rate of relaxation, but only when compared with the vessels from the normotensive pregnant women. However, no difference in responsiveness to noradrenaline was found between any of the groups. 4. The angiotensin II responsiveness of the vessels from the women with pre-eclampsia and from the non-pregnant women were similar, suggesting that pre-eclampsia is associated with an absence of the change in vascular function which normally occurs during pregnancy. 5. The study provides direct evidence for an involvement of vascular abnormalities in the pathogenesis of pre-eclampsia.

Effect of baroreceptor denervation on stimulation of drinking by angiotensin II in conscious dogs

1991 ◽  
Vol 260 (3) ◽  
pp. E333-E337 ◽  
Author(s):  
C. K. Klingbeil ◽  
V. L. Brooks ◽  
E. W. Quillen ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Plasma Osmolality ◽  
Plasma Angiotensin ◽  
High Doses ◽  
Stimulation Of

Angiotensin II causes marked stimulation of drinking when it is injected centrally but is a relatively weak dipsogen when administered intravenously. However, it has been proposed that the dipsogenic action of systemically administered angiotensin II may be counteracted by the pressor action of the peptide. To test this hypothesis, the dipsogenic action of angiotensin II was investigated in dogs, in which low and high baroreceptor influences had been eliminated by denervation of the carotid sinus, aortic arch, and heart. In five sham-operated dogs, infusion of angiotensin II at 10 and 20 ng.kg-1.min-1 increased plasma angiotensin II concentration to 109.2 +/- 6.9 and 219.2 +/- 38.5 pg/ml and mean arterial pressure by 20 and 29 mmHg, respectively, but did not induce drinking. In four baroreceptor-denervated dogs, the angiotensin II infusions produced similar increases in plasma angiotensin II concentration and mean arterial pressure but, in contrast to the results in the sham-operated dogs, produced a dose-related stimulation of drinking. Water intake with the low and high doses of angiotensin II was 111 +/- 44 and 255 +/- 36 ml, respectively. The drinking responses to an increase in plasma osmolality produced by infusion of hypertonic sodium chloride were not different in the sham-operated and baroreceptor-denervated dogs. These results demonstrate that baroreceptor denervation increases the dipsogenic potency of intravenous angiotensin II and provides further support for the hypothesis that the dipsogenic action of intravenous angiotensin II is counteracted by the rise in blood pressure.

P4559Assess of angiotensin receptor blockers therapy associated to mineralocorticoid receptor antagonists or to calcium channel blockers plus hydrochlorothiazide according central haemodynamic parameters

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C A Paterno Marchioli
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Mineralocorticoid Receptor ◽  
Channel Blockers ◽  
Mineralocorticoid Receptor Antagonists ◽  
Hypertensive Patients ◽  
Haemodynamic Parameters ◽  
Significant Difference ◽  
Receptor Blockers

Abstract Background Protective effect of Angiotensin-II Receptor Blockers (ARBs) on major cardiovascular events might be partly independent of the degree of blood pressure reduction. Calcium channel blockers (CCBs), lower arterial pressure by decreasing total peripheral resistance without reducing cardiac output. Hydrochlorothiazide (Hctz) is one of the most commonly prescribed antihypertensive drugs worldwide, but associated with more frequent adverse effects, such as hypokalaemia, hyponatraemia, hyperuricaemia and may increase the glycaemia, It sensitizes the endothelium to the action of angiotensin II, might act on the aldosterone release. The phenomenon of “aldosterone escape” occurs even in the presence of combination therapy with ARBs. The harmful effects of aldosterone are innumerable: induced cardiac and renal fibrosis, sodium and water retention, inflammation, oxidative stress, arrhythmias, glucose intolerance, insulin resistance, among others, that are involved in arterial and myocardium remodelling. Mineralocorticoid Receptor Antagonists (MRAs) therapy improve diastolic function, decrease plasma volume and vascular/myocardial fibrosis. Purpose This study aimed to assess the responses of two groups of therapy such as ARBs associated to MRAs or to CCBs+Hctz according to central haemodynamic parameters (CHPs) in hypertensive patients, both genders, with normal kidney function. Methods For this cross-sectional retrospective study, data were collected from 391 hypertensive patients who were assisted in the hypertension centre. Female/male 239/152, each gender divided into two groups of therapy: ARB+MRA/ARB+CCB+Hctz. Female 210/29 (average age 57/70) and male 125/27 (average age 55/61). The CHPs were measured with a SphygmoCor System PVX (AtCor-Medical Australia), a validated device employing the high-fidelity technique of applanation tonometry according to established protocols. Also, the difference of Augmentation Index (Diff-AIx) between the observed values and the expected levels was assessed according to normal range by age. No patients had cardiovascular, endocrine, renal and metabolic decompensated diseases. Results After measuring the body mass index, waist circumference and heart rate, the two therapy groups were confronted, both genders, had not found the statistically significant difference. The results of CHPs (Central Aortic Pressure, End-Systolic Pressure, Mean Arterial Pressure, Pulse Pressure, Augmentation Pressure), systolic and diastolic blood pressure during association of ARBs+MRAs therapy compared to ARBs+CCBs+Hctz, both genders, showed the lowest values with a highly statistically significant difference. In the female/male the Diff-AIx was found p=0.05/0.04. Conclusion These findings suggest that ARBs+MRAs treatment reaches the best haemodynamic conditions because improve the levels of CHPs and arterial stiffness (Diff-AIx) giving an adequate reduction of the stress to the arterial-ventricular coupling.

Control of blood pressure and hindlimb conductance during hemorrhage in conscious renal hypertensive rabbits

1995 ◽  
Vol 268 (6) ◽  
pp. H2302-H2310 ◽  
Author(s):  
G. Weichert ◽  
C. A. Courneya
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Similar Pattern ◽  
Ang Ii ◽  
Autonomic Nervous

We examined the response to hemorrhage in conscious normotensive and hypertensive rabbits under control conditions and during efferent blockade of 1) the hormones vasopressin (AVP) and angiotensin II (ANG II), 2) the autonomic nervous system, and 3) autonomic and hormonal inputs. We recorded mean arterial pressure, heart rate, and hindlimb conductance. The response to hemorrhage was unchanged with hormonal blockade alone. Blockade of the autonomic nervous system caused a faster rate of blood pressure decline, but the rate of decrease in hindlimb conductance was maintained at control levels. Blocking the autonomic nervous system and the hormones resulted in rapid blood pressure decline and an increase in hindlimb conductance. Although the three types of efferent blockade had a similar pattern of effects in normotensive and hypertensive rabbits, hypertensive rabbits exhibited less cardiovascular support during hemorrhage than normotensive rabbits. During hemorrhage, hypertensive rabbits had an attenuation of hindlimb vasoconstriction, a reduction in the heart rate-mean arterial pressure relationship, and reduced ability to maintain blood pressure compared with normotensive rabbits.

EFFECTS OF PROLONGED INFUSIONS OF POTASSIUM CHLORIDE, ADRENOCORTICOTROPHIN OR ANGIOTENSIN II UPON SERUM ALDOSTERONE CONCENTRATION AND THE CONVERSION OF CORTICOSTERONE TO ALDOSTERONE IN RATS

1979 ◽  
Vol 90 (4) ◽  
pp. 680-691 ◽  
Author(s):  
Jan Komor ◽  
Jürg Müller
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Potassium Chloride ◽  
Conversion Rate ◽  
Potassium Deficiency ◽  
The Other ◽  
Serum Aldosterone ◽  
Acth Treatment ◽  
Sodium And Potassium

ABSTRACT The temporal relation between alterations in serum aldosterone and in the conversion of labelled corticosterone to aldosterone by incubated adrenal tissue was studied in conscious rats receiving long-term infusions of KCl, ACTH or angiotensin II. When potassium-deficient rats were given KCl, a marked increase in serum aldosterone was observed only after 12 h, i.e. at a time when the conversion of corticosterone to aldosterone had become normal. After 24 h of ACTH infusion into sodiumand potassium-replete rats the serum aldosterone was markedly elevated, whereas the conversion of corticosterone to aldosterone was significantly decreased. After 48 h of continued ACTH infusion the serum aldosterone returned to normal and there was a further decrease in the conversion rate. A 24-h angiotensin II infusion into sodium- and potassium-replete rats induced significant increases in both the serum aldosterone and the conversion. After 48 h of continued angiotensin infusion the serum aldosterone returned to normal while the conversion and the blood pressure remained elevated. These results indicate that the activity of the enzymes involved in the final steps of aldosterone biosynthesis may become ratelimiting for the secretion of aldosterone during potassium deficiency and during prolonged ACTH treatment. On the other hand, the observed transiency of aldosterone stimulation by exogenous angiotensin II was not due to a suppression of the final steps of aldosterone biosynthesis and remains unexplained.

Control of sodium excretion by angiotensin II: intrarenal mechanisms and blood pressure regulation

1986 ◽  
Vol 250 (6) ◽  
pp. R960-R972 ◽  
Author(s):  
J. E. Hall
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Pressure Control ◽  
Ang Ii ◽  
Aldosterone Secretion ◽  
Body Fluid Volume ◽  
Proximal Tubular ◽  
Renal Medullary Blood Flow ◽  
Pressure Natriuresis

Angiotensin II (ANG II) is one of the body's most powerful regulators of Na excretion, operating through extrarenal mechanisms, such as stimulation of aldosterone secretion, as well as intrarenal mechanisms. Considerable evidence suggests that the intrarenal actions of ANG II are quantitatively more important than changes in aldosterone secretion in the normal day-to-day regulation of Na balance and arterial pressure. ANG II at physiological concentrations increases proximal tubular reabsorption, but further studies are needed to determine whether ANG II also has an important effect on more distal tubular segments. ANG II also markedly constricts efferent arterioles, tending to increase Na reabsorption by altering peritubular capillary physical forces and also helping to prevent excessive decreases in glomerular filtration rate. ANG II may also decrease Na excretion and increase urine concentrating ability by reducing renal medullary blood flow. Regulation of Na excretion by ANG II is closely linked with arterial pressure control and volume homeostasis through the renal pressure natriuresis mechanism. Under many physiological conditions, such as changes in Na intake, ANG II greatly multiplies the effectiveness of the pressure natriuresis mechanism to prevent fluctuations in body fluid volume and arterial pressure. In circumstances associated with circulatory depression, such as decreased cardiac function, reductions in blood pressure and increased ANG II formation cause Na retention until arterial pressure is restored to normal. However, in pathophysiological conditions in which ANG II is inappropriately elevated, increased arterial pressure (hypertension) is required for the kidney to "escape" the potent antinatriuretic actions of ANG II and to return Na excretion to normal via the pressure natriuresis mechanism.

Cardioaccelerator action of angiotensin

1962 ◽  
Vol 202 (2) ◽  
pp. 237-240 ◽  
Author(s):  
S. D. Nishith ◽  
L. D. Davis ◽  
W. B. Youmans
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Abdominal Aorta ◽  
Intravenous Infusion ◽  
Control Level ◽  
Arterial Blood ◽  
Initial Decrease ◽  
Slow Intravenous Infusion

Effects of synthetic angiotensin II on heart rate and blood pressure were determined in dogs under the influence of morphine (3 mg/kg) and chloralose (90 mg/kg). Angiotensin in total doses of 2.5–20 µg, rapidly injected intravenously in intact dogs, caused an initial decrease in heart rate followed by a rise above the control level, despite the continued elevation of arterial blood pressure. When the degree of rise in arterial pressure was buffered by a mechanical compensator connected with the abdominal aorta, rapid intravenous angiotensin injection produced no initial cardioinhibitory phase, and the magnitude of the accleration of heart rate was much greater than in the unbuffered animal. Slow intravenous infusion of angiotensin in some cases caused only a rise in heart rate. In sinoaortic denervated animals both blood pressure and heart rate were greatly increased when a total dose of 10 µg angiotensin was rapidly injected intravenously. Thus, it is demonstrated that the cardioinhibitory response to angiotensin depends largely or exclusively on reflex effects from sinoaortic pressoreceptors, and that angiotensin has a strong cardioaccelerator action which is exerted through the efferent nerves to the heart.

Assessment of Autonomic and Non-Autonomic Components of Resting Hindlimb Vascular Resistance and Reactivity to Pressor Substances in Renal Hypertensive Rabbits

1976 ◽  
Vol 51 (s3) ◽  
pp. 57s-59s
Author(s):  
J. A. Angus ◽  
M. J. West ◽  
P. I. Korner
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Structural Changes ◽  
Resistance Vessels ◽  
Structural Differences ◽  
Before And After ◽  
Autonomic Blockade ◽  
Autonomic Component

1. Hindlimb vascular resistance (HVR) was measured before and after pharmacological autonomic blockade in unanaesthetized renal cellophan-wrap hypertensive or normotensive rabbits with previously implanted Doppler ultrasonic flowmeters. 2. When the blood pressure was restored to resting values after autonomic block, the elevated resting HVR in the hypertensive rabbits was entirely accounted for by an increased non-autonomic component (i.e. HVR after block). If the pressure was not restored after block the autonomic component (i.e. resting HVR minus non-autonomic HVR) was overestimated and the non-autonomic component was underestimated. 3. During maximum vasodilatation the minimum HVR was significantly higher in the hypertensive rabbits than in the normotensive group, probably due to structural differences of resistance vessels. 4. Reactivity of the hindlimb bed to noradrenaline, angiotensin II and vasopressin injections was approximately twice as great in the hypertensive rabbits as in the sham-operated group, probably as a consequence of the structural changes.

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