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PubMed2006

Thiol oxidation causes pulmonary vasodilation by activating K+ channels and inhibiting store-operated Ca2+ channels.

Cellular redox change regulates pulmonary vascular tone by affecting function of membrane and cytoplasmic proteins, enzymes, and second messengers. This study was designed to test the hypothesis that functional modulation of ion channels by thiol oxidation contributes to regulation of excitation-contraction coupling in isolated pulmonary artery (PA) rings. Acute treatment with the thiol oxidant diamide produced a dose-dependent relaxation in PA rings; the IC50 was 335 and 58 microM for 40 mM K+ - and 2 microM phenylephrine-induced PA contraction, respectively. The diamide-mediated pulmonary vasodilation was affected by neither functional removal of endothelium nor 8-bromoguanosine-3'-5'-cyclic monophosphate (50 microM) and HA-1004 (30 microM). A rise in extracellular K+ concentration (from 20 to 80 mM) attenuated the thiol oxidant-induced PA relaxation. Passive store depletion by cyclopiazonic acid (50 microM) and active store depletion by phenylephrine (in the absence of external Ca2+ both induced PA contraction due to capacitative Ca2+ entry. Thiol oxidation by diamide significantly attenuated capacitative Ca2+ entry-induced PA contraction due to active and passive store depletion. The PA rings isolated from left and right PA branches appeared to respond differently to store depletion. Although the active tension induced by passive store depletion was comparable, the active tension induced by active store depletion was 3.5-fold greater in right branches than in left branches. These data indicate that thiol oxidation causes pulmonary vasodilation by activating K+ channels and inhibiting store-operated Ca2+ channels, which subsequently attenuate Ca2+ influx and decrease cytosolic free Ca2+ concentration in pulmonary artery smooth muscle cells. The mechanisms involved in thiol oxidation-mediated pulmonary vasodilation or activation of K+ channels and inhibition of store-operated Ca2+ channels appear to be independent of functional endothelium and of the cGMP-dependent protein kinase pathway.

Animals↗
PubMed2001

Arterial compliance abnormalities in isolated systolic hypertension.

Arterial compliance measurements using intraarterial pulse contour analysis and a modified Windkessel model were carried out in 19 patients with isolated systolic hypertension (> or = 160/< or = 90 mm Hg) and compared to measurements in 29 patients with essential hypertension (diastolic blood pressure [BP] > or = 95 mm Hg) and 47 normotensive control subjects. Arterial capacitive compliance was significantly lower in isolated systolic hypertension than in essential hypertension (P < .0002) and significantly lower in essential hypertension than in normotensive control subjects (P < .0001). Although the isolated systolic hypertension group was older than the essential hypertension group, the reduction of capacitive compliance in isolated systolic hypertension persisted even when comparison was made with a more nearly age-matched group of essential hypertension. In contrast, oscillatory compliance was reduced similarly in isolated systolic hypertension and essential hypertension compared to normotensive control subjects (P < .0001). Although pulse pressure was greater in isolated systolic hypertension than in essential hypertension, only a weak correlation (r = -0.34) existed between pulse pressure and capacitive compliance. These data indicate that both essential hypertension and isolated systolic hypertension patients exhibit comparably abnormal structure or tone of the small vessels that are the site of oscillations or reflections in the arterial vasculature. In isolated systolic hypertension there is a profound reduction in large artery or capacitive compliance that accounts for the increase in systolic BP and decrease in diastolic BP. This abnormality cannot be accurately assessed by pulse pressure alone.

Aged↗
PubMed1995

The role of capacitative Ca2+ influx in the alpha 1B-adrenoceptor-mediated contraction to phenylephrine of the rat spleen.

1. The mechanism of contraction to phenylephrine in the rat spleen (mediated via alpha 1B-adrenoceptors) has been studied in functional experiments. 2. The concentration-dependent contraction of the rat spleen to cumulative additions of phenylephrine (pD2 4.8 +/- 0.1) was not significantly reduced by the selective protein kinase C (PKC) inhibitor, calphostin C (10(-6)M) or potentiated by the DAG kinase inhibitor, R59022 (10(-6) M). 3. Contraction of the rat spleen in normal Krebs solution containing Ca2+ (2.5 mM) to a single concentration of phenylephrine (3 x 10(-4) M) produced a maximal response consisting of an initial phasic component and a more slowly developing tonic component. However in Ca(2+)-free Krebs solution (containing EGTA), phenylephrine (3 x 10(-4)M) produced only a phasic contraction which was reduced to 46 +/- 3% maximum response to phenylephrine in normal Krebs solution. 4. In some tissues after the contraction to phenylephrine (3 x 10(-4) M) in Ca(2+)-free Krebs solution (containing EGTA), the phenylephrine was washed out and the tissue was allowed to recover. After 2 h, upon addition of Ca2+ (2.5 mM) to the Krebs solution (EGTA now removed) a tonic contraction developed in the tissue (97 +/- 4% maximum response to phenylephrine). 5. Cyclopiazonic acid produced a tonic contraction of the rat spleen with a maximum effect at 10(-5) M (202 +/- 8% maximum response compared with that to phenylephrine). The contraction to CPA (10(-5) M) was reduced in Ca(2+)-free Krebs solution containing EGTA (30 +/- 4% of the maximum response to phenylephrine). One hour after the end of the contraction in Ca(2+)-free Krebs solution (EGTA now removed), upon addition of Ca2+ (2.5 mM) to the Krebs solution a tonic contraction developed in the tissue (263 +/- 12% maximum response to phenylephrine). 6 In Ca2+-free Krebs solution, after the spleen had been incubated with cyclopiazonic acid for 30 min,the subsequent contraction to phenylephrine (3 x 10-4 M) was reduced from 46+/-3% to 9+/-2%maximum response to phenylephrine.7 Cumulative contractions to phenylephrine and the contraction to cyclopiazonic acid (10-5 M) in the spleen were not significantly affected by nifedipine (10-6 M). The non-selective Ca2+channel blocker,SK&F 96365 (3 x 10-5 M) reduced the maximum response for the cumulative additions of phenylephrine to 35+/-1% and the contraction to CPA (10-5 M) from 202+/-8% to 108+/-8% maximum response to phenylephrine.8 The tyrosine kinase inhibitors genistein (3 x 10-5 M and tyrphostin 23 (10-4 M), reduced the maximum response to phenylephrine in the spleen to 51+/-4% and 44+/-5% respectively and the maximum contraction to cyclopiazonic acid (3 x 10-6 M) in the spleen from 132 +/- 6% to 82 +/-5% and 80 +/- 7% maximum response to phenylephrine respectively without affecting contractions to K+.9 In conclusion, these results are consistent with the contraction of the rat spleen to phenylephrine consisting of an initial phasic contraction due to release of intracellular Ca2+ and a larger tonic contraction due to capacitative Ca2+ influx through non-voltage-gated Ca2+ channels and which may involve a tyrosine kinase. This suggests that inositol triphosphate but not diacylglycerol is involved in the contraction.

Adrenergic alpha-1 Receptor Agonists↗
PubMed1998

Characterization of two different Ca2+ entry pathways dependent on depletion of internal Ca2+ pools in rat aorta.

Ryanodine (10 microM), thapsigargin (1 microM) and cyclopiazonic acid (10 microM) produced a slow, sustained contractile response in rat aorta that only can be observed in Ca2+-containing solution. In Ca2+-free medium, no response to the drugs was obtained, which suggests that the contraction elicited in presence of Ca2+ is mainly due to the contribution of extracellular influx. This Ca2+ entry does not depend on the opening of dihydropyridine-dependent Ca2+-channels for nimodipine does not affect this. Noradrenaline (1 microM) induced a biphasic response in Ca2+-free medium that was mediated by two different Ca2+ compartments, one of which is common to caffeine (10 mM), and is also depleted by ryanodine (10 microM), thapsigargin (1 microM) and cyclopiazonic acid (10 microM). This compartment loses its Ca2+ content after long exposure (65 min) to Ca2+-free EDTA-containing solution and its refilling was also affected by the three agents tested. The other compartment depleted by noradrenaline, but not by caffeine, was also insensitive to ryanodine, thapsigargin and cyclopiazonic acid, and did not lose its Ca2+ after 65 min in Ca2+-free medium. Contractions induced by noradrenaline (1 microM) or caffeine (10 mM) in Ca2+-free medium were not affected by ryanodine, thapsigargin and cyclopiazonic acid when these agents were added 1 min before or during the response to each agonist. After depletion of internal Ca2+ stores sensitive to noradrenaline, an increase in the resting tone (IRT) of rat aorta was observed when Ca2+ was added again in absence of the agonist. This IRT was not affected by treatment with ryanodine, thapsigargin and cyclopiazonic acid, and represents a Ca2+ entry pathway dependent on the depletion of the noradrenaline-sensitive Ca2+ compartment. In conclusion, we can differentiate two Ca2+ entry pathways in rat aorta that depend on the previous depletion of two internal Ca2+ compartments: One corresponds to the classic capacitative Ca2+ entry model and is promoted by depletion of the internal pool sensitive to noradreanline, caffeine, ryanodine, thapsigargin and cyclopiazonic acid, the other is dependent only on depletion of an alpha1-adrenoceptor-sensitive Ca2+ pool.

Animals↗
PubMed1994

[Cardiovascular physiology. Elasticity and viscoelasticity of the circulatory system. I. Physical basis. II. Arteries].

The vascular walls and the myocardium have the mechanical behaviour of viscoelastic materials. This paper consists in the first two parts of a review on elasticity and viscoelasticity in the circulatory system. The main elastic and viscoelastic properties of the arterial walls and some of its consequences are studied and some of its quantification theories are exposed, proceeded by the Physical and Biophysical basis necessary to the understanding of phenomena concerned in the totality of the work. Arterial stress and strain are analysed and the notions of arterial static elastic modulus, stiffness or elastance and compliance or capacitance such as the concepts of dynamic or viscoelastic modulus and stiffness are developed. Creep, stress relaxation, histeresis and pulse waves dispersion and atenuation effects are described.

Arteries↗
PubMed2001

Pharmacological evidence for capacitative Ca(2+) entry in cannulated and pressurized skeletal muscle arterioles.

Arteriolar myogenic tone shows a marked dependency on extracellular Ca(2+). The contribution played by mechanisms such as intracellular Ca(2+) release and capacitative entry, however, are less certain. The present studies aimed to demonstrate functional evidence for involvement of such mechanisms in myogenic tone and reactivity. Single cremaster arterioles were denuded of endothelium, pressurized under no-flow conditions and loaded with fura 2-AM for measurement of changes in intracellular Ca(2+) [Ca(2+)](i). The cell permeable, putative, IP(3) receptor antagonist 2APB (2 aminoethoxydiphenyl borate) was used to determine the possible role of IP(3) receptor-mediated mechanisms in arteriolar myogenic tone and reactivity. Arterioles dilated in response to increasing concentrations of 2APB (1 - 300 microM) without a concomitant change in global [Ca(2+)](i). Also 2APB (50 microM) completely inhibited the myogenic constriction in response to a step change in luminal pressure (50 - 120 mmHg) with no apparent effect on pressure-mediated increases in [Ca(2+)](i). 2APB markedly attenuated the constrictor response and [Ca(2+)](i) increase stimulated by phenylephrine but not KCl. Capacitative Ca(2+) influx in arterioles was demonstrated either by re-addition of extracellular [Ca(2+)] following pre-treatment with 1 or 10 microM nifedipine in Ca(2+) free buffer or exposure of vessels to thapsigargin (1 microM) to induce store depletion. In both cases 2APB inhibited the increase in [Ca(2+)](i). Capacitative Ca(2+) entry showed an inverse relationship with intraluminal pressure over the range 10 - 120 mmHg. Consistent with an effect on a Ca(2+) entry pathway, 2APB had no effect on intracellular (caffeine releasable) Ca(2+) stores while decreasing the rate of Mn(2+) quench of fura 2 fluorescence. The results provide functional evidence for capacitative Ca(2+) entry in intact arteriolar smooth muscle. The effectiveness of 2APB in inhibiting both non-voltage gated Ca(2+) entry and responsiveness to an acute pressure step is consistent with the involvement of an axis involving IP(3)-mediated and or capacitative Ca(2+) entry mechanisms in myogenic reactivity. Given the lack of effect of 2APB on pressure-induced changes in global [Ca(2+)](i) it is suggested that such mechanisms participate on a localized level to couple the myogenic stimulus to contraction.

Actins↗
PubMed1982

[Adrenoreactivity of the vessels of the small intestine during adaptation to high altitude in the cat].

Responses of the resistance and capacitance vessels of small intestine to adrenergic stimulation and blockade were studied in acute experiments on cats after 3-30 days of high altitude adaptation (the Pamirs, 3370 m). In comparison to control (Dushanbe, 830 m) constrictor responses of the resistance vessels to noradrenaline and adrenaline were significantly increases at high altitude, whereas the dilator responses to beta-stimulator propranolol were obviously reduced. Changes of venous blood outflow from small intestine in response to catecholamines at high altitude exceeded the control values. Pharmacological analysis suggests that the reactivity of alpha-adrenoreceptors of the small intestine resistance and capacitance vessels at high altitude was increased, whereas the beta-reactivity of the resistance vessels was reduced. Crucial shifts of the adrenoreactivity occurred after 3-5 and 14-16 days of the adaptation.

Adaptation, Physiological↗
PubMedDate not supplied

Comparative vasodilator effects of magnesium salts on rat mesenteric arterioles and venules.

In vivo studies were undertaken to investigate the comparative effects of different magnesium (Mg) salts (i.e., MgCl2, MgSO4, Mg acetate, Mg aspartate HCl) on arterioles (10-20 microns i.d.) and venules (15-30 microns i.d.) of the mesenteric circulation of the pentobarbitone-anesthetized rat. Perivascular administration of these Mg salts (topical doses = 0.1-100 mumoles) produced dose-dependent vasodilatation (5-50% increases in lumen size) of arterioles and venules almost instantaneously. Arterioles were more sensitive than venules to topical MgCl2 and MgSO4 but not to either Mg aspartate HCl or Mg acetate. Intra-arterial infusion of the Mg salts (1-40 mumoles/min, i.e., 5-400 mumol/kg/min for 20 min) at each dose produced vasodilatation, i.e. 10-80% increases in lumen size of mesenteric arterioles; doses above 10 mumoles/min sometimes produced bleeding from venules. Systemic i.v. infusion (1-40 mumoles/min) of all 4 Mg salts lowered systolic and diastolic arterial blood pressure dose-dependently; however, the degree or presence of vasodilatation noted in the microvessels was not always correlated with the falls in arterial blood pressure. Intravenous administration of the Mg salts resulted in dose-dependent elevation in plasma Mg (0.3-4.7 mg/dl, over control levels); increments in plasma Mg were noted as soon as 1 min after the start of the infusion. Plasma Mg levels wre higher with inorganic salts and peaked more rapidly. Large i.v. doses of Mg salts (i.e., greater than 20 mumoles/min) induced some bleeding from the venules which varied with the anion. Administration of a variety of pharmacological receptor antagonists and a cyclo-oxygenase inhibitor did not interfere with vasodilatation of arterioles or venules induced by Mg salts. These results indicate that magnesium ions: 1) are vasodilators of intact microscopic mesenteric resistance and capacitance microvessels; and 2) bring about vasodilatation by direct actions on microvascular smooth muscle cells. In addition, our data indicate that the anion associated with Mg appears to exert significant influences on microvascular tone.

Animals↗
PubMed2001

Ion channels and their functional role in vascular endothelium.

Endothelial cells (EC) form a unique signal-transducing surface in the vascular system. The abundance of ion channels in the plasma membrane of these nonexcitable cells has raised questions about their functional role. This review presents evidence for the involvement of ion channels in endothelial cell functions controlled by intracellular Ca(2+) signals, such as the production and release of many vasoactive factors, e.g., nitric oxide and PGI(2). In addition, ion channels may be involved in the regulation of the traffic of macromolecules by endocytosis, transcytosis, the biosynthetic-secretory pathway, and exocytosis, e.g., tissue factor pathway inhibitor, von Willebrand factor, and tissue plasminogen activator. Ion channels are also involved in controlling intercellular permeability, EC proliferation, and angiogenesis. These functions are supported or triggered via ion channels, which either provide Ca(2+)-entry pathways or stabilize the driving force for Ca(2+) influx through these pathways. These Ca(2+)-entry pathways comprise agonist-activated nonselective Ca(2+)-permeable cation channels, cyclic nucleotide-activated nonselective cation channels, and store-operated Ca(2+) channels or capacitative Ca(2+) entry. At least some of these channels appear to be expressed by genes of the trp family. The driving force for Ca(2+) entry is mainly controlled by large-conductance Ca(2+)-dependent BK(Ca) channels (slo), inwardly rectifying K(+) channels (Kir2.1), and at least two types of Cl( -) channels, i.e., the Ca(2+)-activated Cl(-) channel and the housekeeping, volume-regulated anion channel (VRAC). In addition to their essential function in Ca(2+) signaling, VRAC channels are multifunctional, operate as a transport pathway for amino acids and organic osmolytes, and are possibly involved in endothelial cell proliferation and angiogenesis. Finally, we have also highlighted the role of ion channels as mechanosensors in EC. Plasmalemmal ion channels may signal rapid changes in hemodynamic forces, such as shear stress and biaxial tensile stress, but also changes in cell shape and cell volume to the cytoskeleton and the intracellular machinery for metabolite traffic and gene expression.

Animals↗
PubMed2002

Modulation of endothelial inward-rectifier K+ current by optical isomers of cholesterol.

Membrane potential of aortic endothelial cells under resting conditions is dominated by inward-rectifier K(+) channels belonging to the Kir 2 family. Regulation of endothelial Kir by membrane cholesterol was studied in bovine aortic endothelial cells by altering the sterol composition of the cell membrane. Our results show that enriching the cells with cholesterol decreases the Kir current density, whereas depleting the cells of cholesterol increases the density of the current. The dependence of the Kir current density on the level of cellular cholesterol fits a sigmoid curve with the highest sensitivity of the Kir current at normal physiological levels of cholesterol. To investigate the mechanism of Kir regulation by cholesterol, endogenous cholesterol was substituted by its optical isomer, epicholesterol. Substitution of approximately 50% of cholesterol by epicholesterol results in an early and significant increase in the Kir current density. Furthermore, substitution of cholesterol by epicholesterol has a stronger facilitative effect on the current than cholesterol depletion. Neither single channel properties nor membrane capacitance were significantly affected by the changes in the membrane sterol composition. These results suggest that 1) cholesterol modulates cellular K(+) conductance by changing the number of the active channels and 2) that specific cholesterol-protein interactions are critical for the regulation of endothelial Kir.

Animals↗
PubMed2005

Effects of induction of capacitative calcium entry on equine laminar microvessels.

OBJECTIVE: To determine the effects of induction of capacitative Ca2+ entry on tone in equine laminar arteries and veins. SAMPLE POPULATION: Laminar arteries and veins from 6 adult mixed-breed horses. PROCEDURE: Arteries and veins were isolated and mounted on small vessel myographs for the measurement of isometric tension. Capacitative Ca2+ entry was induced by incubating the vessels with the specific Ca2+-ATPase inhibitor thapsigargin (100nM) in a Ca2+-free physiologic salt solution. Capacitative Ca2+ entry-associated contractile responses were determined by the subsequent addition of 2mM Ca2+ to the solution bathing the vessels; in some experiments, either the voltage-gated Ca2+ blocker diltiazem (10microM) or the putative capacitative Ca2+ entry inhibitor trifluoromethylphenylimidazole (300microM) was added to the bathing solution 15 minutes prior to a second 2mM Ca2+ exposure. The Sr2+ permeability of the capacitative Ca2+ entry pathway in laminar vessels was assessed by exposing the vessels to 4mM Sr2+ after induction of capacitative Ca2+ entry with thapsigargin. RESULTS: Induction of capacitative Ca2+ entry elicited robust contractile responses in laminar veins but did not increase tone in laminar arteries. In laminar veins, capacitative Ca2+ entry-induced contractile responses were unaffected by preincubation with diltiazem, attenuated by trifluoromethylphenylimidazole, and were impermeable to Sr+. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that induction of capacitative Ca2+ entry elicits vasoconstriction in equine laminar veins but not in laminar arteries and should therefore be considered a potential mechanism by which selective venoconstriction occurs in horses during the development of acute laminitis.

Animals↗
PubMedDate not supplied

Comparative hemodynamic effects of MK-422, a converting enzyme inhibitor, and a renin inhibitor in dogs with acute left ventricular failure.

The angiotensin-converting enzyme (ACE) inhibitor MK-422 (enalaprilat) was compared with the potent renin inhibitor SCRIP for its ability to improve left ventricular function in closed-chest dogs. Acute left ventricular failure (ALVF) was induced by repeated embolization (EMB) of the left coronary arterial vasculature with 50-micron plastic microspheres. Baseline stability data were obtained in 30 dogs in which the evolution of ALVF was monitored over time. Guided by a progressive rise in left ventricular end-diastolic pressure (LVEDP), a stepwise perturbation of the coronary circulation with microspheres over 30 min caused reductions in left ventricular dP/dt and cardiac output, averaging 47 and 40%, respectively. EMB reduced heart rate (20 beats/min) and mean arterial pressure by approximately 20 mm Hg which, along with other hemodynamic variables remained stable after induction of heart failure. MK-422 (100 micrograms/kg i.v.) given 45 min after ALVF was induced, decreased mean arterial pressure by 20 mm Hg (p less than 0.05) and reduced total peripheral resistance (TPR) from 5,453 to 4,150 dyne X s X cm-5 (p less than 0.05). The decline in LVEDP (from 14 +/- 1 to 11 +/- 1 mm Hg) and TPR suggests that MK-422 dilates resistance and, conceivably, capacitance vessels. In dogs with sham EMB (vehicle injections into coronary circulation), MK-422 reduced arterial pressure but had no important effects on the other hemodynamic indices.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1976

DPAVP: a vasopressin analog with selective microvascular and RES actions for the treatment of circulatory shock in rats.

The present study indicates that: (a) local administration of low concentrations of an analog of vasopressin, 1-deamino-[2-phenylalanine, 8-arginine]-vasopressin (DPAVP), constricts venules in the rat splanchnic terminal vascular bed of normal animals, unlike that seen for catecholamines; (b) maximal concentrations of DPAVP narrow but do not occlude both arterioles and venules: (c) microscopic muscular venules (31-39 mu i.d.) do not narrow more than 20% in response to the vasopressin analog DPAVP; and (d) terminal arterioles (17-23 mu i.d.) do not narrow more than 50% in response to DPAVP. Systemic administration of DPAVP to rats subjected to hemorrhage or bowel ischemia shock more than doubles survival rates over control rats receiving Ringer solution. Infusion of DPAVP produces a dose-dependent effect on arterial blood pressure, microscopic capacitance vessels, large arterioles and small arteries. In addition, i.v. administration of DPAVP: (a) returns arterial hematocrit towards normal after shock; and (b) regenerates and sustains vasomotion and venular tone, decreases microvascular hyperreactivity characteristic of shock syndromes, restores constricted arteriolar lumen sizes towards normal, predisposes to a splanchnic microbed virtually free of stasis, petechiae and leukocytic sticking, and restores capillary perfusion and outflow to near-normal. Further, DPAVP effectively restores the early reticuloendothelial system (RES) phagocytic depression, characteristic of shock syndromes, to normal; the latter eventuating in RES hyper-phagocytic activity. These findings indicate it is possible to synthesize vasoactive molecules which: (a) exert selective microvascular and RES phagocytic effects; and (b) are highly beneficial in the therapy of low-flow states, at least in rats.

Animals↗
PubMed1992

Vasodilator properties of nitroglycerin and isosorbide dinitrate during cardiopulmonary bypass.

In a placebo-controlled trial, we have studied the vasodilator properties of bolus doses of nitroglycerin (TNG) and isosorbide dinitrate (ISDN) in 32 patients during cardiopulmonary bypass with a constant pump flow. Blood volume of the venous reservoir and mean arterial pressure were recorded for 10 min after drug administration to detect changes in venous capacitance and arteriolar resistance, respectively. The venous capacitance-increasing effects of TNG 200 micrograms and ISDN 1,600 micrograms were initially identical and significant at 2 and 3 min after the bolus. Thereafter, the effect of TNG began to decline, while that of ISDN remained significant until the end of the study. TNG 200 micrograms decreased arterial pressure slightly more than ISDN 1,600 micrograms, but the effect of both drugs lasted for only 1-2 min. TNG and ISDN were equipotent in increasing venous capacitance when administered in a bolus dose ratio of 1:8 during CPB, but the venodilator effect of ISDN lasted longer than that of TNG. The duration of the arteriolar dilator effect was very short with both drugs.

Adult↗
PubMed1984

Effects of dihydroergotamine on hemodynamic molsidomine actions in anesthetized dogs.

In pentobarbital-anesthetized mongrel dogs the intravenous actions of 0.50 mg/kg molsidomine on pulmonary artery and left ventricular (LV) end-diastolic pressures and internal heart dimensions (preload), left ventricular systolic and peripheral blood pressures, and total peripheral resistance (afterload), as well as on heart rate, dP/dt, stroke volume, and cardiac output (heart performance) were studied for 2 h. Hemodynamic molsidomine effects were influenced by increasing amounts of intravenously infused dihydroergotamine solution (DHE, 1-64 micrograms X kg-1 X min-1). Molsidomine decreased preload, stroke volume, and cardiac output for over 2 h but decreased ventricular and peripheral pressures for 45 min. Systemic vascular resistance showed a tendency to decrease while heart rate and LV dP/dtmax were not altered. DHE infusion reversed molsidomine effects on the preload and afterload of the heart. The diminished stroke volume was elevated so that cardiac output also increased. Total peripheral resistance increased while heart rate fell in a dose-dependent fashion. The LV dP/dtmax remained unchanged until the highest dose of 64 micrograms X kg-1 X min-1 DHE elevated the isovolumic myocardial contractility. These experiments indicate that DHE can reverse the intravenous molsidomine effects on hemodynamics. Most likely, this is mediated through peripheral vasoconstriction of venous capacitance vessels, thereby affecting molsidomine's action on postcapillary beds of the circulation.

Anesthesia↗
PubMed1980

[The effects of dihydroergotamine on volume content and compliance of the extrathoracic capacitance vessels of man under anesthesia during extracorporeal circulation in hypothermia (author's transl)].

The influence of dihydroergotamine on volume content and compliance of the extrathoracic capacitance vessels during extracorporeal circulation was investigated. Compared with an untreated control group the compliance decreased (0.44 ml/mm Hg/kg b. wt.) and 490 ml of blood was mobilized and shifted from the circulation into the blood reservoir of the machine. Therefore DHE counteracts the effects of venous pooling.

Anesthesia, General↗
PubMed1987

Dynamic peripheral nerve metabolic and vascular responses to exsanguination.

We studied the dynamic effects of exsanguination of approximately one-third of rat blood volume over 3-12 min on energy metabolism and blood flow in rat sciatic nerves. Nerve high-energy phosphate compounds were relatively well maintained. There was a modest stimulation of anaerobic metabolism at slow rates of exsanguination, and glucose stores were slightly increased. These findings indicate that when stressed because of significant blood loss, compensatory mechanisms, presumably adrenosympathetic mediated, are effective in vivo. We recorded nerve blood flow (NBF), endoneurial oxygen tension, and mean arterial pressure simultaneously; NBF was linearly related to blood pressure (BP) over a wide range of BPs, confirming that NBF does not significantly autoregulate. Endoneurium underwent oxygen-exchange, indicating that peripheral nerve microvasculature is physiologically nutritive. NBF fell before and at a faster rate than BP, indicating that it is a capacitive system. Nerves also adapted to declining oxygen supplies, presumably by reducing their oxygen consumption. The physiological implications of such a system are discussed.

Anaerobiosis↗
PubMed2006

Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta.

The ability of estradiol to affect phenylephrine-induced contraction and the subsequent increase in resting tone, associated with capacitative Ca(2+) entry across the plasma membrane, was evaluated in rat aortic rings incubated in Ca(2+)-free solution. The incubation with estradiol (1-100 nM, 5 min) inhibited both the phenylephrine-induced contraction and the IRT. Neither cycloheximide (1 microM; inhibitor of protein synthesis) nor tamoxifen (1 microM; blocker of estrogenic receptors) modified the effects of estradiol. Estradiol (100 microM) also blocked the contractile response to serotonin (10 microM) but not to caffeine (10 mM). In addition, estradiol (100 microM) inhibited the contractile responses to cyclopiazonic acid (1 microM; selective Ca(2+)-ATPase inhibitor) associated with capacitative Ca(2+) influx through non-L-type Ca(2+) channels. Finally, estradiol inhibited the Ca(2+)-induced increases in intracellular free Ca(2+) (after pretreatment with phenylephrine) in cultured rat aorta smooth muscle cells incubated in Ca(2+)-free solution. In conclusion, estradiol interfered in a concentration-dependent manner with Ca(2+)-dependent contractile effects mediated by the stimuli of alpha(1)-adrenergic and serotonergic receptors and inhibited the capacitative Ca(2+) influx through both L-type and non-L-type Ca(2+) channels. Such effects are in essence nongenomic and not mediated by the intracellular estrogenic receptor.

Animals↗