Circulatory Effects of Angiotensin

Buñag, Ruben D.

doi:10.1007/978-3-642-65600-2_24

Cited by 22 publications

(11 citation statements)

References 79 publications

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“…It is known that All has a pronounced positive inotropic effect on the isolated myocardium. 33 This effect is not detectable during All infusion in vivo, probably due to baroreceptor response to increased vascular resistance and BP. ' 6 In the recumbent position in the present study, an elimination of the inotropic effect of All could not be uncovered; in fact, an increase in CO and SV was found.…”

Section: Figure 4 Changes In Systolic (Sbp) Diastolic (Dbp) and Mementioning

confidence: 97%

Reflex-hemodynamic adjustments and baroreflex sensitivity during converting enzyme inhibition with MK-421 in normal humans.

et al. 1983

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SUMMARY Invasive hemodynamic measurements and determination of baroreflex sensitivity were carried out in 12 mildly sodium-depleted normotensive volunteers in a randomized double-blind crossover study with a single dose of converting enzyme inhibitor, MK-421, and placebo. In supine humans at rest, MK-421 caused a reduction in blood pressure through a fall in total peripheral resistance and an increase in arterial compliance. Thus, MK-421 appears to dilate both resistance vessels and larger arteries. Cardiac output increased, but contrary to the effects of other vasodilators, the increase was due to a higher stroke volume with an unchanged heart rate. The lack of heart rate response may well reflect enhanced central parasympathetic cardiac inhibition. Head-up tilt on MK-421 caused an additional decrease in blood pressure in 65% of the subjects. The major determinant for the blood pressure fall during tilt and converting enzyme inhibition was a decrease in cardiac performance, while the reflex increase of arteriolar and venous tone was largely unimpaired. The decreased stroke volume may be secondary to elimination of a positive inotropic effect of angiotensin II (All). It is also conceivable that in the absence of AH the inotropic response to sympathetic activation is inadequate during tilt in these sodium-depleted normotensive individuals. Baroreflex sensitivity to blood pressure increase (i.v. phenylephrine) was enhanced after MK 421. Arterial compliance was increased, and this may explain the altered baroreceptor sensitivity. However, a possible central nervous enhancement of baroreceptor sensitivity after MK-421 could not be ruled out in this study.

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Section: Figure 4 Changes In Systolic (Sbp) Diastolic (Dbp) and Mementioning

confidence: 97%

Reflex-hemodynamic adjustments and baroreflex sensitivity during converting enzyme inhibition with MK-421 in normal humans.

et al. 1983

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“…In intact adult animals, angiotensin II in fusion is known to produce potent vasocon striction in the systemic circulation [17], For the pulmonary circulation, there are conflict ing results from studies on the role of endog enous angiotensin II when angiotensin II an tagonists or converting-enzyme inhibitors have been administered [11]. However, ad ministration of exogenous angiotensin II, it self, in the isolated perfused lung consis tently results in increased pulmonary vascu lar resistance [18], More recently, Goll et al [11], using conscious dogs, showed that an giotensin II infusion at 0.06 pg/kg/min pro duced systemic hypertension and resulted in active, nonflow-dependent constriction of the pulmonary circulation.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic Responses to Angiotensin II in the Newborn Lamb

Goetzman¹,

Bennett²

1991

Dev Pharmacol Ther

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Angiotensin II is known to increase both pulmonary and systemic arteriolar tone in adult animals. Its influence on these vascular beds shortly after birth is less well understood. Therefore, we studied the effects of infusions of angiotensin II (0.1 μg/kg/min) on pulmonary and systemic hemodynamics in 13 anesthesized newborn lambs. Systemic vascular resistance increased significantly from a mean of 0.079 ± 0.03 to 0.094 ± 0.04 mm Hg/ml/min during angiotensin II infusion while the mean pulmonary vascular resistance was unchanged at 0.024 ± 0.01 mm Hg/ml/min. Interestingly, cardiac output increased significantly by 18.9% during angiotensin II infusion. During hypoxemia produced by ventilating with 10-12% oxygen, the responses to angiotensin II infusion were similar to those obtained during normoxia. The absence of an effect on pulmonary vascular resistance and the increase in cardiac output were not predicted based on results reported for older animals. The mechanisms responsible for these age-related differences are unknown. Our findings have implications regarding the potential clinical use of angiotensin II as a modulator of blood pressure in the hypotensive newborn.

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“…Because i.v. AH causes direct vasoconstriction and a baroreceptormediated reflex withdrawal of sympathetic nerve activity 17 while, conversely, vertebral artery All produces a neurogenically mediated increase in vascular resistance, 3 ' 18 it is possible to suggest thaj the action of the AVP antagonist was linked to the mechanism that results in the activation of sympathetic nerve activity by All. 16 Since the modulatory effect of the AVP inhibitor upon the magnitude of the intravertebrally elicited pressor response to All could not be duplicated by giving this compound either via the vertebral artery route or into a vein, it does not appear likely that this action is exercised by the blockade of a vasopressinergic site that is either located in the periphery or is reached through a gap in the blood brain barrier of the vertebral artery territory.…”

Section: V-99mentioning

confidence: 99%

Arginine vasopressin modulates the central action of angiotensin II in the dog.

Michelini¹,

Barnes²,

Ferrario³

1983

Hypertension

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SUMMARY Endogenous vasopressin may interact with central autonomic nervous system factors in the regulation of cardiovascular function. In 25 morphine/chloralose-anesthetized dogs, we studied the magnitude of the pressor response produced by an infusion of angiotensin II (All) into the vertebral arteries (VA), before and after intracisternal (n = 10), intravertebral (n = 9), or intravenous (n = 6) administration of a competitive antagonist of arginine vasopressin (AVP) [d(CH 2 )5iyr(Me) AVP]. The dose response curve to vertebral artery infusion of AH (range 2-20 ng/ kg/mih) was significantly (p < 0.05) shifted to the right of control after injection of the AVP antagonist (10 Mg/kg) into the cisterna magna; the ED at 20 mm Hg being almost double after central AVP blockade. This effect of AVP blockade was confined only to the cardiovascular response mediated by All via the vertebral arteries. When pressor doses of All were injected into either a vein (i.v.) or the cisterna magna of these same dogs, the increases in mean blood pressure were the same before and after AVP antagonist treatment. In another group of anesthetized dogs, we investigated whether the reduced reactivity to intravertebral All could be duplicated by giving the AVP antagonist either via the vertebral artery or i.v. Only the cisterna magna route was effective in causing a blunting of the pressor response to vertebral artery AH. These data demonstrate a previously unknown interaction between vasopressin and the centrally mediated pressor response to intravertebral AH. T is well established that in the dog the area postrema of the fourth ventricle has a role in the neural control of cardiovascular function by acting, in part, to enhance central vasomotor sympathetic activity in response to increased blood levels of angiotensin II (All).1 " 5 In addition, recent data suggest that the effects of AH at the dog's area postrema may depend upon the activity of endogenous brain peptides such as the opioid system. 6 Other studies have indicated that there are reciprocal direct connections between the supraoptic (SON) and paraventricular nuclei (PVN) of the hypothalamus and the nucleus tractus solitarii (NTS) in the brain stem. These observations, in conjunction with the recent reports that hypertension is associated with alterations in vasopressin levels in the brain stem of spontaneously hypertensive rats (SHRs), 10 make this peptide another possible candidate to interact with AH in determining the degree of sympathetic activation at the brain stem. To investigate one facet of the function of brain vasopressin upon the reflex regulation of arterial pressure, we determined whether blockade of the activity of this neuropeptide system alters the ability of AH to exert an increase in sympathetic activity via the area postrema pressor pathway. MethodsExperiments were performed in 25 male mongrel dogs (body weight = 21.6 ± 0.4 kg) anesthetized with alpha-chloralose (65 mg/kg, i.v.) after premedication with morphine (2 mg/kg, i.m.) and respirated mechanically. S...

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Circulatory Effects of Angiotensin

Cited by 22 publications

References 79 publications

Reflex-hemodynamic adjustments and baroreflex sensitivity during converting enzyme inhibition with MK-421 in normal humans.

Reflex-hemodynamic adjustments and baroreflex sensitivity during converting enzyme inhibition with MK-421 in normal humans.

Hemodynamic Responses to Angiotensin II in the Newborn Lamb

Arginine vasopressin modulates the central action of angiotensin II in the dog.

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