Mechanisms of hypoxic vasodilation in ferret pulmonary arteries

Wiener, Charles; Banta, Meggan R.; Dowless, Michele; Flavahan, Nicholas A.; Sylvester, J. T.

doi:10.1152/ajplung.1995.269.3.l351

Cited by 12 publications

(19 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar results were obtained from prestimulated proximal pulmonary arteries in rabbit (413) and first-and third-order pulmonary arteries in pig (578, 991,1045). On the other hand, phase 2 HPV did not occur in proximal pulmonary arteries of orders 3-5 in ferret (2089) or orders 4 -5 in pig (991). The reasons for these differences are unknown.…”

Section: Pulmonary Arteriessupporting

confidence: 69%

“…K Ca channel inhibition had no effect on resting E m in PASMC from adult animals (53, 1334,1438,1599,1623,1776,1949,2170,2179). Moreover, K Ca channel inhibitors did not alter tone in isolated pulmonary vessels (53, 1360,2089) or P PA in isolated lungs (751). Collectively, these results provide strong evidence that K Ca channels do not contribute significantly to basal E m in adult PASMC.…”

Section: Membrane Potentialmentioning

confidence: 79%

“…Relationships between the level of hypoxia and magnitude of phase 1 vasoconstriction in prestimulated rat proximal pulmonary arteries suggested that the response began to occur at ϳ8% O 2 , and was half-maximum at ϳ3% O 2 and maximum at 0% O 2 (1651,1652,1691). These O 2 concentrations were shifted to higher values when the intensity of prestimulation was increased (1652) or when measurements were made in a rat strain more responsive to hypoxia (1691 656,799,814,900,903,935,991,1043,1045,1131,1151,1413,1430,1651,1652,1691,1896,1961,1976,2018,2089,2185). Moreover, substantial data suggested that the endothelium dependence of phase 1 was caused by an hypoxia-induced decrease in endothelial NO production, leading to smooth muscle contraction (506, 656,814,903,934,935,991,1151,1413,1430,1691,1896,1976,2018).…”

Section: Pulmonary Arteriesmentioning

confidence: 98%

“…At durations Յ20 min in rats (1413,1651,1652,1691,1715,1767,2185) and Յ30 min in other species, including cow (1430), dog (375, 429), ferret (2089), guinea pig (1818), human (394, 815), pig (1282,1976), rabbit (399, 903,1417), and sheep (392, 393, 1959 -1961), severe hypoxia caused either vasoconstriction or vasoconstriction followed by vasodilation, perhaps representing partial or complete phase 1 responses, respectively. As with phase 1 during prolonged hypoxia, these responses were occasionally preceded by a brief vasodilation (506, 656,876,1151,1207,1208).…”

Section: Pulmonary Arteriesmentioning

confidence: 99%

See 3 more Smart Citations

Hypoxic Pulmonary Vasoconstriction

Sylvester

Shimoda

Aaronson

et al. 2012

Physiological Reviews

Self Cite

607

621

View full text Add to dashboard Cite

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.

show abstract

Section: Pulmonary Arteriessupporting

confidence: 69%

Section: Membrane Potentialmentioning

confidence: 79%

Section: Pulmonary Arteriesmentioning

confidence: 98%

Section: Pulmonary Arteriesmentioning

confidence: 99%

See 2 more Smart Citations

Hypoxic Pulmonary Vasoconstriction

Sylvester

Shimoda

Aaronson

et al. 2012

Physiological Reviews

Self Cite

607

621

View full text Add to dashboard Cite

show abstract

“…41 ATP-sensitive K ϩ channels contribute to the mechanism of metabolic coronary vasodilation and are the final pathway of action of various mediators of endothelium-independent vasodilation. Estradiol at high concentration, 42 hypoxia, 43 acidosis, 44 and hyperinsulinemia 45 act on arterial wall by such a mechanism. Lactate induces skeletal muscle arteriolar dilation that is dependent on H 2 O 2 -mediated activation of vascular smooth muscle guanylate cyclase and is independent of endothelium-mediated dilators.…”

Section: Discussionmentioning

confidence: 99%

Noninvasive detection of vascular dysfunction in alcoholic patients

Maiorano

Bartolomucci

Contursi

et al. 1999

American Journal of Hypertension

View full text Add to dashboard Cite

Vasodilation is impaired in various conditions, such as hypercholesterolemia and tobacco use. We evaluated brachial artery flow-mediated vasodilation (FMD) after blood pressure (BP) cuff occlusion using high-resolution B-mode ultrasound in 20 alcoholics, without any coexisting conditions such as smoking, hypertension, or cholesterolemia, after a 3-month period of abstinence. They were compared with a control group of 20 alcohol-free healthy subjects. We measured the diameter of the brachial artery under baseline conditions, during reactive hyperemia (with increased flow causing endothelium-dependent dilatation), and after administration of sublingual glyceryl trinitrate (GTN), an endothelium-independent dilator. We performed an echocardiographic study (Esaote Au3) according to guidelines of the American Society of Echocardiography to assess left ventricular mass (LVM), wall thickness, systolic stress, and diastolic function changes. FMD (% diameter change) was significantly less in the alcoholic patients than in the controls (6.03 ؎ 3.67 v 13.7 ؎ 4.65; P < .05), whereas no difference was noted after GTN administration (13.7 ؎ 7.97 v 16.0 ؎ 5.12, P ‫؍‬ NS). Echocardiographic study showed no differences between the study group for LVM, wall thickness, and systolic stress; diastolic function expressed as E/A ratio inversion was significantly impaired. These data demonstrate an impairment of endothelial-dependent vasodilatation in chronic alcohol abusers, which may contribute to the excess prevalence of cardiovascular diseases in these individuals. Am J Hypertens 1999;12:137-144

show abstract

Molecular and Functional Significance of Ca²⁺‐Activated Cl⁻ Channels in Pulmonary Arterial Smooth Muscle

et al. 2015

View full text Add to dashboard Cite

Increased peripheral resistance of small distal pulmonary arteries is a hallmark signature of pulmonary hypertension (PH) and is believed to be the consequence of enhanced vasoconstriction to agonists, thickening of the arterial wall due to remodeling, and increased thrombosis. The elevation in arterial tone in PH is attributable, at least in part, to smooth muscle cells of PH patients being more depolarized and displaying higher intracellular Ca 2+ levels than cells from normal subjects. It is now clear that downregulation of voltage-dependent K + channels (e.g., Kv1.5) and increased expression and activity of voltage-dependent (Cav1.2) and voltage-independent (e.g., canonical and vanilloid transient receptor potential [TRPC and TRPV]) Ca 2+ channels play an important role in the functional remodeling of pulmonary arteries in PH. This review focuses on an anion-permeable channel that is now considered a novel excitatory mechanism in the systemic and pulmonary circulations. It is permeable to Cl − and is activated by a rise in intracellular Ca 2+ concentration (Ca 2+-activated Cl − channel, or CaCC). The first section outlines the biophysical and pharmacological properties of the channel and ends with a description of the molecular candidate genes postulated to encode for CaCCs, with particular emphasis on the bestrophin and the newly discovered TMEM16 and anoctamin families of genes. The second section provides a review of the various sources of Ca 2+ activating CaCCs, which include stimulation by mobilization from intracellular Ca 2+ stores and Ca 2+ entry through voltage-dependent and voltage-independent Ca 2+ channels. The third and final section summarizes recent findings that suggest a potentially important role for CaCCs and the gene TMEM16A in PH.Keywords: calcium-activated chloride channels, pulmonary hypertension, TMEM16A, anoctamin, bestrophin. . They are widely distributed small-conductance channels located in the plasma membrane of many cell types and are hypothesized to serve important functions in sperm maturation, fluid transport across epithelial tissues, cardiac repolarization, olfactory transduction, photoreceptor stimulation, neuronal and skeletal muscle excitation, cardiac repolarization, and vascular smooth muscle excitability and contraction. For more information on the general properties and role of CaCCs in various cell types and tissues, the reader is invited to consult excellent reviews on this topic. [1][2][3][4][5][6][7][8][9][10][11] Byrne and Large 12 were the first to report the existence of a Ca 2+ -activated Cl − conductance in smooth muscle by describing its general properties in rat anococcygeus smooth muscle. Since this initial discovery, that group and others have described this conductance in a variety of smooth muscle cells, including vascular smooth muscle cells (VSMCs). 1,4,7 The identification in 2008 by three independent groups of the TMEM16, or anoctamin, family of genes as novel candidates for CaCCs 13-15 sparked a renewed interest in refining our understan...

show abstract

Mechanisms of hypoxic vasodilation in ferret pulmonary arteries

Cited by 12 publications

References 0 publications

Hypoxic Pulmonary Vasoconstriction

Hypoxic Pulmonary Vasoconstriction

Noninvasive detection of vascular dysfunction in alcoholic patients

Molecular and Functional Significance of Ca²⁺‐Activated Cl⁻ Channels in Pulmonary Arterial Smooth Muscle

Contact Info

Product

Resources

About

Mechanisms of hypoxic vasodilation in ferret pulmonary arteries

Cited by 12 publications

References 0 publications

Hypoxic Pulmonary Vasoconstriction

Hypoxic Pulmonary Vasoconstriction

Noninvasive detection of vascular dysfunction in alcoholic patients

Molecular and Functional Significance of Ca2+‐Activated Cl− Channels in Pulmonary Arterial Smooth Muscle

Contact Info

Product

Resources

About

Molecular and Functional Significance of Ca²⁺‐Activated Cl⁻ Channels in Pulmonary Arterial Smooth Muscle