Anesthesia alters pulmonary vasoregulation by angiotensin II and captopril

Nyhan, Daniel; Chen, B. B.; Fehr, D. M.; Rock, Peter; Murray, Paul A.

doi:10.1152/jappl.1992.72.2.636

Cited by 18 publications

(8 citation statements)

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“…When Q is kept constant, PVR is directly proportional to the Ppa–Ppao gradient [19-21]. In contrast, in the large series of published studies on angiotensin II in HPV, this methodology was used only by Murray and coworkers [6,7]. Whether angiotensin II is a mediator of HPV is controversial.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the results of the pilot experiments examining the dose–effect relationship of both medications support maximal inhibition of the renin–angiotensin cascade. Nyhan and coworkers [7], using pressure–flow plots in normoxic conditions, showed that angiotensin II produced pulmonary vasoconstriction in conscious as well as in dogs anaesthetized with pentobarbital. However, the pulmonary vasodilator response to captopril observed in conscious dogs was reversed to a paradoxical vasoconstriction in pentobarbital anaesthetized dogs.…”

Section: Discussionmentioning

confidence: 99%

“…There exists a variety of conflicting data concerning the possible role of angiotensin II in HPV. Some studies showed that inhibition of the renin–angiotensin cascade, by means of angiotensin-converting enzyme (ACE) inhibition [6-10] or angiotensin II receptor blockade [9,11-14], reduces pulmonary vascular tone in normoxia [6,7] and hypoxia [8-14]. However, other studies did not confirm the pulmonary vasodilating effect of an ACE inhibitor [15,16] and of an angiotensin II receptor antagonist [17,18].…”

Section: Introductionmentioning

confidence: 99%

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Endogenous angiotensin II in the regulation of hypoxic pulmonary vasoconstriction in anaesthetized dogs

Hubloue

Rondelet²,

Kerbaul³

et al. 2004

Crit Care

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Introduction The role played by several vasoactive mediators that are synthesized and released by the pulmonary vascular endothelium in the regulation of hypoxic pulmonary vasoconstriction (HPV) remains unclear. As a potent vasoconstrictor, angiotensin II could be involved. We tested the hypothesis that angiotensin-converting enzyme inhibition by enalaprilat and type 1 angiotensin II receptor blockade by candesartan would inhibit HPV. Methods HPV was evaluated in anaesthetized dogs, with an intact pulmonary circulation, by examining the increase in the Ppa-Ppao gradient (mean pulmonary artery pressure minus occluded pulmonary artery pressure) that occurred in response to hypoxia (inspiratory oxygen fraction of 0.1) at constant pulmonary blood flow. Plasma renin activity and angiotensin II immunoreactivity were measured to determine whether activation or inhibition of the renin-angiotensin system was present. Results Administration of enalaprilat and candesartan did not affect the Ppa-Ppao gradient at baseline or during hypoxia. Plasma renin activity and angiotensin II immunoreactivity increased during hypoxia, and subsequent measurements were consistent with effective angiotensin-converting enzyme inhibition after administration of enalaprilat, and with angiotensin receptor blockade after administration of candesartan. Conclusion These results suggest that, although the renin-angiotensin system was activated in hypoxia, angiotensin II is not normally involved in mediating acute HPV.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Endogenous angiotensin II in the regulation of hypoxic pulmonary vasoconstriction in anaesthetized dogs

Hubloue

Rondelet²,

Kerbaul³

et al. 2004

Crit Care

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“…Exogenous ANG II caused vasoconstriction in lungs of cats (1552), dogs (625,1405), humans (258), mice (494), pigs (1221), rabbits (2063), and rats (121, 566, 1240, 2039) as well as in isolated pulmonary arteries of dogs (1887) and rats (200,1652). Under normoxic conditions, some studies showed that ACE inhibition or angiotensin II receptor blockade reduced pulmonary vasomotor tone (259, 625, 1405), suggesting basal activation of the renin-angiotensin system; however, others failed to confirm these effects (720,823,959,997,1552).…”

Section: Angiotensin IImentioning

confidence: 99%

Hypoxic Pulmonary Vasoconstriction

Sylvester

Shimoda

Aaronson

et al. 2012

Physiological Reviews

607

621

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It has been known for more than 60 years, and suspected for over 100, that alveolar hypoxia causes pulmonary vasoconstriction by means of mechanisms local to the lung. For the last 20 years, it has been clear that the essential sensor, transduction, and effector mechanisms responsible for hypoxic pulmonary vasoconstriction (HPV) reside in the pulmonary arterial smooth muscle cell. The main focus of this review is the cellular and molecular work performed to clarify these intrinsic mechanisms and to determine how they are facilitated and inhibited by the extrinsic influences of other cells. Because the interaction of intrinsic and extrinsic mechanisms is likely to shape expression of HPV in vivo, we relate results obtained in cells to HPV in more intact preparations, such as intact and isolated lungs and isolated pulmonary vessels. Finally, we evaluate evidence regarding the contribution of HPV to the physiological and pathophysiological processes involved in the transition from fetal to neonatal life, pulmonary gas exchange, high-altitude pulmonary edema, and pulmonary hypertension. Although understanding of HPV has advanced significantly, major areas of ignorance and uncertainty await resolution.

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“…In point of fact, the lung endothelium is the primary site of metabolism of angiotensin I, with approximately 60% to 80% of plasma angiotensin I converted to ANG II in a single pass through the pulmonary circulation. Exogenous ANG II causes pulmonary vasoconstriction in most species, both in isolated vessel and intact lung preparations (37,70,87,160,185,222,404,408,462,506,534,614,682). Some studies suggest that basal activation of the renin-angiotensin system and production of ANG II exerts a slight vasoconstrictor effect on the pulmonary circulation (222,462), although other studies failed to show an effect of ANG II blockade at baseline (246,276,323,335,506).…”

Section: Angiotensin IImentioning

confidence: 99%

Lung Circulation

Suresh

Shimoda

2016

Comprehensive Physiology

111

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The circulation of the lung is unique both in volume and function. For example, it is the only organ with two circulations: the pulmonary circulation, the main function of which is gas exchange, and the bronchial circulation, a systemic vascular supply that provides oxygenated blood to the walls of the conducting airways, pulmonary arteries and veins. The pulmonary circulation accommodates the entire cardiac output, maintaining high blood flow at low intravascular arterial pressure. As compared with the systemic circulation, pulmonary arteries have thinner walls with much less vascular smooth muscle and a relative lack of basal tone. Factors controlling pulmonary blood flow include vascular structure, gravity, mechanical effects of breathing, and the influence of neural and humoral factors. Pulmonary vascular tone is also altered by hypoxia, which causes pulmonary vasoconstriction. If the hypoxic stimulus persists for a prolonged period, contraction is accompanied by remodeling of the vasculature, resulting in pulmonary hypertension. In addition, genetic and environmental factors can also confer susceptibility to development of pulmonary hypertension. Under normal conditions, the endothelium forms a tight barrier, actively regulating interstitial fluid homeostasis. Infection and inflammation compromise normal barrier homeostasis, resulting in increased permeability and edema formation. This article focuses on reviewing the basics of the lung circulation (pulmonary and bronchial), normal development and transition at birth and vasoregulation. Mechanisms contributing to pathological conditions in the pulmonary circulation, in particular when barrier function is disrupted and during development of pulmonary hypertension, will also be discussed.

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Anesthesia alters pulmonary vasoregulation by angiotensin II and captopril

Cited by 18 publications

References 0 publications

Endogenous angiotensin II in the regulation of hypoxic pulmonary vasoconstriction in anaesthetized dogs

Endogenous angiotensin II in the regulation of hypoxic pulmonary vasoconstriction in anaesthetized dogs

Hypoxic Pulmonary Vasoconstriction

Lung Circulation

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