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PubMed2001

Capacitative Ca(2+) entry in agonist-induced pulmonary vasoconstriction.

Agonist-induced increases in cytosolic Ca(2+) concentration ([Ca(2+)](cyt)) in pulmonary artery (PA) smooth muscle cells (SMCs) consist of a transient Ca(2+) release from intracellular stores followed by a sustained Ca(2+) influx. Depletion of intracellular Ca(2+) stores triggers capacitative Ca(2+) entry (CCE), which contributes to the sustained increase in [Ca(2+)](cyt) and the refilling of Ca(2+) into the stores. In isolated PAs superfused with Ca(2+)-free solution, phenylephrine induced a transient contraction, apparently by a rise in [Ca(2+)](cyt) due to Ca(2+) release from the intracellular stores. The transient contraction lasted for 3-4 min until the Ca(2+) store was depleted. Restoration of extracellular Ca(2+) in the presence of phentolamine produced a contraction potentially due to a rise in [Ca(2+)](cyt) via CCE. The store-operated Ca(2+) channel blocker Ni(2+) reduced the store depletion-activated Ca(2+) currents, decreased CCE, and inhibited the CCE-mediated contraction. In single PASMCs, we identified, using RT-PCR, five transient receptor potential gene transcripts. These results suggest that CCE, potentially through transient receptor potential-encoded Ca(2+) channels, plays an important role in agonist-mediated PA contraction.

Animals↗
PubMed1999

Anandamide-induced mobilization of cytosolic Ca2+ in endothelial cells.

1. Experiments were designed to determine whether anandamide affects cytosolic Ca2+ concentrations in endothelial cells and, if so, whether CB1 cannabinoid receptors are involved. To this effect, human umbilical vein-derived EA.hy926 endothelial cells were loaded with fura-2 to monitor changes in cytosolic Ca2+ using conventional fluorescence spectrometry methods. 2. Anandamide induced an increase in Ca2+ in endothelial cells which, in contrast to histamine, developed slowly and was transient. Anandamide caused a concentration-dependent release of Ca2+ from intracellular stores without triggering capacitative Ca2+ entry, contrary to histamine or the endoplasmic reticulum Ca2+ -ATPase inhibitor thapsigargin. 3. Anandamide pretreatment slightly reduced the mobilization of Ca2+ from intracellular stores that was evoked by histamine. The mobilization of Ca2+ from intracellular stores evoked by anandamide was impaired by 10 mM caffeine. 4. Anandamide and histamine each significantly increased NO synthase activity in EA.hy926 cells, as determined by the enhanced conversion of L-[3H]-arginine to L-[3H]-citruline. 5. The CB1 cannabinoid receptor antagonist SR141716A (1 microM) only produced a marginal reduction of the mobilization of Ca2+ produced by 5 microM anandamide. However, at 5 microM SR141716A elicited the release of Ca2+ from intracellular stores. This concentration strongly impaired the mobilization of cytosolic Ca2+ evoked by either anandamide, histamine or thapsigargin. 6. Pretreatment of the cells with either 200 microM phenylmethylsulphonyl fluoride (to inhibit the conversion of anandamide into arachidonic acid) or 400 ng ml(-1) pertussis toxin (to uncouple CB1 cannabinoid receptors from Gi/o proteins) had no significant effect on the mobilization of cytosolic Ca2+ evoked by either anandamide, or histamine. 7. Taken together the results demonstrate that anandamide mobilizes Ca2+ from a caffeine-sensitive intracellular Ca2+ store that functionally overlaps in part with the internal stores mobilized by histamine. However, a classical CB1 cannabinoid receptor-mediated and pertussis toxin-sensitive mechanism does not mediate this novel effect of anandamide in endothelial cells. 8. The mobilization of cytosolic Ca2+ in endothelial cells may account for the endothelium-dependent and NO-mediated vasodilator actions of anandamide. Due to its non-specific inhibition of Ca2+ signalling in endothelial cells, SR141716A may not be used to assess the physiological involvement of endogenous cannabinoids to endothelium-dependent control of vascular smooth muscle tone.

Arachidonic Acids↗
PubMed1999

Histamine alters cadherin-mediated sites of endothelial adhesion.

We tested the hypothesis that histamine alters the focal apposition of endothelial cells by acting on sites of cadherin-mediated cell-cell adhesion. Focal apposition was measured as the impedance of a cell-covered electrode, which was partitioned into a cell-matrix resistance, a cell-cell resistance, and membrane capacitance. Histamine causes an immediate, short-lived decrease in the impedance of an electrode covered with human umbilical vein endothelial (HUVE) cells. ECV304 cells are a line of spontaneously transformed HUVE cells that do not express the endothelial cadherin, cadherin-5. Histamine increased ECV304 cell calcium to 600 nM. Histamine did not increase myosin light chain phosphorylation of control or transfected ECV304 cells. ECV304 cells transfected with either E-cadherin or cadherin-5 on a dexamethasone-responsive plasmid (pLKneo) increased their cell-cell resistance when stimulated with dexamethasone, whereas ECV304 cells transfected with pLKneo-lacZ did not. Histamine did not affect the impedance of ECV304 cells transfected with pLKneo-lacZ. In contrast, histamine decreased the cell-cell resistance of ECV304 cells transfected with either pLKneo-E-cadherin or pLKneo-cadherin-5. From these data, we conclude that histamine acts on sites of cadherin-mediated cell-cell apposition.

Animals↗
PubMed1988

Influences of pressure surrounding the heart and intracardiac pressure on the diastolic coronary pressure-flow relation in excised canine heart.

We investigated the change in the instantaneous diastolic left coronary pressure-flow relation (DPFR) when the pressure surrounding the heart (SHP), right heart pressure (RHP), and left heart pressure (LHP) were systematically varied. Eight excised and maximally vasodilated canine hearts placed in an air-tight chamber were used. To obtain a capacitance-free DPFR, coronary perfusion pressure was slowly decreased (about 2 mm Hg/sec) during a prolonged diastole. The zero-flow pressure (Pf = 0) and the slope of the DPFR were analyzed. The mean values of the slope did not change significantly throughout the interventions. The mean value of Pf = 0 in the control state (SHP = RHP = LHP = 0 mm Hg) was 6.0 +/- 2.0 mm Hg (mean +/- SD, n = 8), significantly higher than the venous outflow pressure, RHP (p less than 0.001), and the other two pressures (p less than 0.001). When SHP was raised to 15 and 30 mm Hg, while the other pressures remained at 0 mm Hg, the mean values of Pf = 0 increased to 20.9 +/- 2.4 and 35.6 +/- 3.1 mm Hg (p less than 0.001 and p less than 0.0005, respectively, vs. control). The mean values of Pf = 0 when only RHP was elevated to 15 and 30 mm Hg were 16.0 +/- 1.5 and 29.3 +/- 1.5 mm Hg (p less than 0.001 and p less than 0.0005 vs. control). On elevation of LHP to 15 and 30 mm Hg, the mean values of Pf = 0 were 12.0 +/- 2.8 and 17.3 +/- 3.6 mm Hg (p less than 0.01 and p less than 0.01 vs. control). When both SHP and LHP were almost evenly elevated to about 15 and 30 mm Hg, the mean values of Pf = 0 were raised to 22.0 +/- 2.9 and 35.3 +/- 3.2 mm Hg, respectively. These mean values were not significantly different from those when only SHP was elevated to the comparable levels. The observation that Pf = 0 exceeded RHP in the control state and that RHP, which was elevated above the preceding Pf = 0, was identical with the present Pf = 0 supports the vascular waterfall mechanism when RHP is low. Furthermore, the evidence that the degree of DPFR shift was almost linearly dependent on the SHP level rather than on the LHP level indicates that the pressure on the epicardial side is one of the factors that determines the pressure at the top of the vascular waterfall.

Animals↗
PubMed2004

Venous excess: a new approach to cardiovascular control and its teaching.

The circulatory control system is driven partly by factors relating to the arterial side and partly by factors relating to the venous side. Students are generally provided with a conceptually clear account of the arterial side, based on sound homeostatic mechanisms of negative feedback from a well-defined error signal, arterial pressure. However, on the venous side, teaching is often based on the notion of venous return, a concept that, as normally presented, is imprecise and intangible, a frequent cause of confusion that may lead to errors of clinical practice. Although one can trace these misconceptions back to some of Guyton's publications, Guyton himself was well aware of the complexities of venous resistance and capacitance but has not always been well served by subsequent misinterpretation. The fundamental problem with venous return that makes it inappropriate for controlling the circulation is that it lacks the essential requirement of being an error signal. We propose instead a new variable, venous excess, which represents the accumulation of any mismatch between the rate of blood entering the great veins and the rate of leaving, the cardiac output. As well as being directly observable without intervention (in a patient's jugular vein), it meets all of the requirements of an error signal: via the Starling mechanism it stimulates cardiac output, regulates venous compliance, and in the longer term is an important determinant of fluid intake and excretion, and these effects act to reduce the original perturbation. Based on this concept, we suggest a simple and secure basis for teaching the control of the circulation that avoids undue reliance on entities that are difficult to specify or measure and emphasizes the role of feedback and the similarities between the arterial and venous mechanisms.

Animals↗
PubMed1980

Idiopathic orthostatic hypotension: circulating noradrenaline and ultrastructure of saphenous vein.

The present study indicates that patients who can be clinically classified as idiopathic orthostatic hypotensives of the peripheral type are heterogeneous. There is the typical hypoadrenergic type characterized by low levels of circulating noradrenaline, much reduced or absent noradrenaline stores, and correspondingly little or no adrenergic innervation in the saphenous vein, a major capacitance vessel, as confirmed by ultrastructural examination. In one patient of this type, an abnormally high occurrence of mast cells in the blood vessel wall was noted. There also exists a category of individuals of the hyperadrenergic type, analogous to certain diabetics with noradrenergic abnormalities. These patients also are characterized by low levels of circulating noradrenaline, but noradrenaline stores are high; an exaggerated release of neurotransmitter occurs in response to stimuli; the saphenous vein with noradrenergic innervation remains ultrastructurally normal; however, the effector cell response are greatly blunted. In one patient of this type, the smooth muscle cells of the saphenous vein contained excessively high glycogen deposits. Further, it should be anticipated that a variety of intermediate types can be found as exemplified by one patient with variable, low to normal levels of circulating noradrenaline, a sluggish response to release neurotransmitter upon postural challenge, and considerable innervation of saphenous vein but with the majority of axons and terminals undergoing active degeneration.

Adrenergic Fibers↗
PubMed1997

Effects of age on Ca2+ currents in small mesenteric artery myocytes from Wistar-Kyoto and spontaneously hypertensive rats.

The purpose of this study was to test the hypothesis that differences in voltage-gated Ca2+ channels increase with age during the development of sustained hypertension in the spontaneously hypertensive rat (SHR). Using patch-clamp methods, we measured whole-cell Ca2+ currents in freshly isolated myocytes from small mesenteric arteries of juvenile (5 to 7 weeks), young (10 to 12 weeks), and mature (19 to 23 weeks) Wistar-Kyoto rats (WKY) and SHR. Indirect tail artery systolic pressure increased progressively with age in SHR (from 125 +/- 5 to 159 +/- 5 to 192 +/- 5 mm Hg) but only in the younger WKY (from 107 +/- 6 to 130 +/- 4 to 136 +/- 4 mm Hg). Peak Ca2+ current density (current per cell capacitance) was larger in SHR than WKY myocytes at all ages (at 6 weeks, 3.5 +/- 0.4 versus 2.3 +/- 0.2 pA/pF; at 12 weeks, 3.8 +/- 0.2 versus 3.1 +/- 0.2; at 20 weeks. 4.9 +/- 0.4 versus 3.3 +/- 0.4). Cell capacitance (surface area) was significantly smaller in 12-week-old SHR than WKY (25.2 +/- 1.1 versus 31.8 +/- 1.6 pF), but no differences were found in the 6- or 20-week-old groups. There were significant differences in Ca2+ current with strain, age, and voltage but no significant age-strain interactions. The ratio of peak Ca2+ current for SHR to that of WKY declined linearly with voltage at all ages suggesting differences in the voltage dependence of Ca2+ current activation. The voltage dependence of Ca2+ current was shifted to the left in SHR compared with WKY at all ages. Activation curves were shifted significantly in the negative-voltage direction only in 20-week-old SHR myocytes. We have found differences with age in Ca2+ current density and its voltage dependence in SHR compared with WKY during the phase of development in which blood pressure becomes established in the SHR. The net effect of these differences predicts a larger Ca2+ current in SHR at voltages in the physiological range of membrane potential.

Aging↗
PubMed2001

Propofol attenuates capacitative calcium entry in pulmonary artery smooth muscle cells.

BACKGROUND: Depletion of intracellular Ca2+ stores results in capacitative Ca2+ entry (CCE) in pulmonary artery smooth muscle cells (PASMCs). The authors aimed to investigate the effects of propofol on CCE and to assess the extent to which protein kinase C (PKC) and tyrosine kinases mediate propofol-induced changes in CCE. METHODS: Pulmonary artery smooth muscle cells were cultured from explants of canine intrapulmonary artery. Fura 2-loaded PASMCs were placed in a dish (37 degrees C) on an inverted fluorescence microscope. Intracellular Ca2+ concentration was measured using fura 2 in PASMCs using a dual-wavelength spectrofluorometer. Thapsigargin (1 microM), a sarcoplasmic reticulum Ca2+-adenosine triphosphatase inhibitor, was used to deplete intracellular Ca2+ stores after removing extracellular Ca2+. CCE was activated when extracellular Ca2+ (2.2 mM) was restored. RESULTS: Thapsigargin caused a transient increase in intracellular Ca2+ concentration (182+/-11%). Restoring extracellular calcium (to induce CCE) resulted in a peak (246+/-12% of baseline) and a sustained (187+/-7% of baseline) increase in intracellular Ca2+ concentration. Propofol (1, 10, 100 microM) attenuated CCE in a dose-dependent manner (peak: 85+/-3, 70+/-4, 62+/-4%; sustained: 94+/-5, 80+/-5, 72+/-5% of control respectively). Tyrosine kinase inhibition (tyrphostin 23) attenuated CCE (peak: 67+/-4%; sustained: 74+/-5% of control), but the propofol-induced decrease in CCE was still apparent after tyrosine kinases inhibition. PKC activation (phorbol 12-myristate 13-acetate) attenuated CCE (peak: 48+/-1%; sustained: 53+/-3% of control), whereas PKC inhibition (bisindolylmaleimide) potentiated CCE (peak: 132+/-11%; sustained: 120+/-4% of control). Moreover, PKC inhibition abolished the propofol-induced attenuation of CCE. CONCLUSION: Tyrosine kinases activate and PKC inhibits CCE in PASMCs. Propofol attenuates CCE primarily via a PKC-dependent pathway. CCE should be considered a possible cellular target for anesthetic agents that alter vascular smooth muscle tone.

Anesthetics, Intravenous↗
PubMedDate not supplied

Left ventricular function in early primary hypertension. Functional consequences of cardiovascular structural changes.

An increase in left ventricular (LV) wall thickness will lead to decreased LV distensibility during both LV passive filling and left atrial contraction. Reduced LV distensibility will change the filling pattern of the left ventricle, and a proportionally smaller part of the stroke volume will be delivered during the passive filling of the preceding diastole and a larger part during late diastole by a more powerful left atrial contraction. With a more pronounced increase in LV wall thickness a reduced distensibility of venous capacitance vessels (functional or structural) will probably help to preserve LV pump function by influencing LV filling and use of the Frank-Starling mechanism. LV wall stress (peak and end-systolic) is high and LV intrinsic contractility is normal or supernormal in early primary hypertension, as judged from the relationship between end-systolic wall stress and different indices of LV function (fractional shortening, mean velocity of circumferential fiber shortening, ejection fraction). Great differences in peak systolic wall stress may be recorded among groups with comparable values for LV end-systolic wall stress, which may be explained by very different degrees of cardiovascular structural changes, with higher values for peak systolic wall stress seen in hypertension caused by high output than those values seen in hypertension caused by high total peripheral resistance. Signs of supernormal LV systolic function are common in high output hypertension, which is also at least partly due to an increase in LV end-diastolic volume and use of the Frank-Starling mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed2006

Descending vasa recta endothelium is an electrical syncytium.

We examined gap junction coupling of descending vasa recta (DVR). DVR endothelial cells or pericytes were depolarized to record the associated capacitance transients. Virtually all endothelia and some pericytes exhibited prolonged transients lasting 10-30 ms. Carbenoxolone (100 microM) and 18beta-glycyrrhetinic acid (18betaGRA; 100 microM) markedly shortened the endothelial transients. Carbenoxolone and heptanol (2 mM) reduced the pericyte capacitance transients when they were prolonged. Lucifer yellow (LY; 2 mM) was dialyzed into the cytoplasm of endothelial cells and pericytes. LY spread diffusely along the endothelial monolayer, whereas in most pericytes, it was confined to a single cell. In some pericytes, complex patterns of LY spreading were observed. DVR cells were depolarized by voltage clamp as fluorescence of bis(1,3-dibarbituric acid)-trimethine oxanol [DiBAC(4)(3)] was monitored approximately 200 microm away. A 40-mV endothelial depolarization was accompanied by a 26.1 +/- 5.5-mV change in DiBAC(4)(3) fluorescence. DiBAC(4)(3) fluorescence did not change after 18betaGRA or when pericytes were depolarized. Similarly, propagated cytoplasmic Ca(2+) responses arising from mechanical perturbation of the DVR wall were attenuated by 18betaGRA or heptanol. Connexin (Cx) immunostaining showed predominant linear Cx40 and Cx43 in endothelia, whereas Cx37 stained smooth muscle actin-positive pericytes. We conclude that the DVR endothelium is an electrical syncytium and that gap junction coupling in DVR pericytes exists but is less pronounced.

Animals↗
PubMed1995

Mathematical model that characterizes transmitral and pulmonary venous flow velocity patterns.

The transmitral and pulmonary venous flow velocity (TMFV and PVFV, respectively) patterns are related to the physiological state of the left heart by use of an electrical analog model. Filling of left ventricle (LV) through the mitral valve is characterized by a quadratic Bernoulli's resistance in series with an inertance. Filling of the left atrium (LA) through the pulmonary veins is represented by a lumped network of linear resistance, capacitance, and inertance. LV and LA are each represented by a time-varying elastance. A volume dependency is incorporated into the LV model to produce physiological pressure-volume loops and Starling curves. The state-space representation of the analog model consists of 10 simultaneous differential equations, which are solved by numerical integration. Model validity is supported by the following. First, the expected effects of aging and decreasing LV compliance on TMFV and PVFV are accurately represented by the model. Second, the model-generated TMFV and PVFV waveforms fit well to pulsed-Doppler recordings in normal and postinfarct patients. It is shown that the TMFV deceleration time is prolonged by the increase in LV compliance and, to a lesser extent, by the increase in LA compliance. A shift from diastolic dominance to systolic dominance in PVFV occurs when LA compliance or pulmonary perfusion pressure increases or when LV compliance or mitral valve area decreases. The present model should serve as a useful theoretical basis for echocardiographic evaluation of LV and LA functions.

Animals↗
PubMed1991

Differential effects of pentobarbital on intracerebral arterioles and venules of rats in vitro.

The vasoactive properties of pentobarbital (PB) were studied in intracerebral arterioles and venules (diameter, 30-90 microns). These vessels mediate changes in cerebrovascular resistance and capacitance, respectively. Mean control vessel diameters of arterioles and venules at pH 7.3 were 53.9 +/- 2.8 microns and 78.4 +/- 4.3 microns, respectively. Both arterioles and venules dilated when the pH of the extraluminal solution was lowered to 6.8 and constricted when the pH was raised to 7.6. PB, 10(-6) to 10(-2) mol/L, dilated intracerebral arterioles in a dose-dependent manner at pH 7.3, reaching a maximal dilation of 129.7 +/- 3.1% of control diameter at a dose of 10(-3) mol/L. In contrast, PB at 10(-6) to 10(-2) mol/L failed to produce significant changes in the diameter of intracerebral venules. In addition, PB at 10(-3) mol/L significantly inhibited arteriolar constriction induced by KCl (120 mmol/L), but not venular constriction. The present study suggests that intracerebral venules are relatively less responsive to PB than cerebral arterioles and peripheral veins. In addition to its effect on cerebral metabolism. PB may act to redistribute venous blood volume from cerebral veins to more responsive peripheral veins, thereby decreasing intracranial blood volume and intracranial pressure.

Animals↗
PubMed1990

Effect of acidosis on contraction of microvascular smooth muscle by alpha 1- and alpha 2-adrenoceptors. Implications for neural and metabolic regulation.

Our previous studies have identified that adrenergic regulation of large arterioles and venules in skeletal muscle uses both postjunctional alpha 1- and alpha 2-adrenoceptors, whereas terminal arterioles appear to be subserved primarily by alpha 2-receptors. Adrenergic constriction of terminal arterioles is known to be particularly susceptible to inhibition by increased tissue metabolic rate. The purpose of this study was to examine the influence of tissue acidosis on alpha 1- and alpha 2-adrenoceptor constriction of skeletal muscle microvessels to determine if this differential receptor distribution might have significance in neural-metabolic interactions. Intravital microscopy of rat cremaster skeletal muscle was used to obtain concentration-response curves (diameter changes) of large distributing arterioles (mean diameter, 100 microns), small precapillary arterioles (20 microns), and capacitance venules (150 microns) for addition to the tissue bath of alpha-adrenergic agonists during normal pH (7.4) and during tissue bath acidosis (pH 7.1) produced by increasing bath PCO2. The following alpha-agonists were used: phenylephrine (alpha 1), B-HT 933 (alpha 2), and norepinephrine (mixed alpha 1/alpha 2). Acidosis had no effect on baseline diameter of the three vessel types, indicating a lack of effect on "intrinsic tone." Acidosis also had no effect on large microvessel sensitivity to phenylephrine but markedly reduced responses to B-HT 933. Acidosis had no effect on large arteriolar and venular sensitivity to norepinephrine but markedly decreased (x300) small precapillary arteriolar sensitivity. These data suggest that 1) alpha 2- but not alpha 1-adrenoceptor-mediated constriction of microvessels may be selectively sensitive to modest reductions in tissue pH, and 2) the prevalence of alpha 2-receptors on terminal arterioles and the marked sensitivity of alpha 2 constriction to tissue acidosis may contribute to the particular susceptibility of neural constriction at this level of the microcirculation to metabolic inhibition.

Acidosis↗
PubMed2000

ATP-sensitive potassium channels in capillaries isolated from guinea-pig heart.

The full-length cDNAs of two different alpha-subunits (Kir6.1 and Kir6.2) and partial cDNAs of three different beta-subunits (SUR1, SUR2A and SUR2B) of ATP-sensitive potassium (KATP) channels of the guinea-pig (gp) were obtained by screening a cDNA library from the ventricle of guinea-pig heart. Cell-specific reverse-transcriptase PCR with gene-specific intron-spanning primers showed that gpKir6.1, gpKir6.2 and gpSUR2B were expressed in a purified fraction of capillary endothelial cells. In cardiomyocytes, gpKir6.1, gpKir6.2, gpSUR1 and gpSUR2A were detected. Patch-clamp measurements were carried out in isolated capillary fragments consisting of 3-15 endothelial cells. The membrane capacitance measured in the whole-cell mode was 19.9 +/- 1.0 pF and was independent of the length of the capillary fragment, which suggests that the endothelial cells were not electrically coupled under our experimental conditions. The perforated-patch technique was used to measure the steady-state current-voltage relation of capillary endothelial cells. Application of K+ channel openers (rilmakalim or diazoxide) or metabolic inhibition (250 microM 2,4-dinitrophenol plus 10 mM deoxyglucose) induced a current that reversed near the calculated K+ equilibrium potential. Rilmakalim (1 microM), diazoxide (300 microM) and metabolic inhibition increased the slope conductance measured at -55 mV by a factor of 9.0 (+/-1.8), 2.5 (+/-0.2) and 3.9 (+/-1.7), respectively. The effects were reversed by glibenclamide (1 microM). Our results suggest that capillary endothelial cells from guinea-pig heart express KATP channels composed of SUR2B and Kir6.1 and/or Kir6.2 subunits. The hyperpolarization elicited by the opening of KATP channels may lead to an increase in free cytosolic Ca2+, and thus modulate the synthesis of NO and the permeability of the capillary wall.

Adenosine Triphosphate↗
PubMed1986

Haemodynamic responses to stimulation of the splanchnic and cardiac sympathetic nerves in the anaesthetized cat.

The changes in cardiac output and mean right atrial pressure (R.A.P.) evoked at different circulating blood volumes by stimulation of the splanchnic sympathetic nerves were investigated in adrenalectomized cats under chloralose anaesthesia, with unopened chests and spontaneous respiration and with active vascular reflexes. The cardiac autonomic nerves were cut or blocked pharmacologically. Stimulation of the distal ends of the splanchnic nerves at 4 Hz caused aortic pressure and R.A.P. to rise to maximum values at 2 min before declining slowly. Cardiac output rose more slowly to a steady state at 3 min; at higher circulating volumes it fell initially. Although the output increments were slower in development they were better sustained than those in total peripheral resistance. The proportionate output increments were largest and the R.A.P. increments least at low circulating volumes whereas at high volumes the R.A.P. increments were large but the output changes were small or negative; the pattern of changes resembled that resulting from infusion of blood. Stimulation of the cardiac sympathetic nerves evoked a rise in output and a fall in R.A.P. related in magnitude to the initial value of R.A.P. On simultaneous stimulation of the splanchnic and cardiac sympathetic nerves the changes in output combined whereas the R.A.P. changes cancelled, to give output increments of 25-50% with little change in R.A.P. at all circulating volumes. At high circulating volumes infusion of blood did not usually alter output or aortic pressure, but splanchnic nerve stimulation increased peripheral resistance and aortic pressure and commonly evoked a rise in left ventricular stroke work which could not be accounted for by known adrenergic mechanisms or by elevation of left ventricular end-diastolic pressure. Portal venous pressure was consistently elevated by splanchnic nerve stimulation; it rose more slowly than did aortic pressure or R.A.P. and was independent of a changing central venous pressure provided this did not exceed +5 mmHg. The cardiac output increments were not related to changes in the ratio between the input and output resistances of the portal vein and it is concluded that displacement blood from the peripheral to the central vasculature was induced by contraction capacitance vessels.

Adrenalectomy↗
PubMed1991

Nicardipine inhibits the endothelin-1-induced constriction of systemic capacitance and resistance vessels.

We estimated the effects of intravenous injection of endothelin-1 (ET-1; 400 pmol/kg) on the systemic capacitance and resistance vessels in anesthetized mongrel dogs by measuring changes in the mean circulatory pressure (MCP) and total peripheral resistance (TPR), respectively. In addition, the present study investigated the inhibiting action of nicardipine (NIC; 10 micrograms/kg bolus injection followed by 1.0-2.0 micrograms/kg/min continuous infusion) against the vasoconstrictor action of ET-1. We examined the effects of ET-1 (30 to 1,000 pmol/0.1 ml) on the femoral arterial system by measuring the percent changes in the perfusion pressure (% delta PP) of the femoral artery perfused with a constant flow, and investigated the effect of NIC on the vasoconstrictor action of ET-1 in this preparation. We obtained the following results: (a) Intravenous injection of ET-1 raised both TPR and MCP. However, in the presence of NIC, ET-1 raised TPR without influencing MCP. (b) Intra-arterial injection of ET-1 caused a dose-dependent increase in % delta PP. NIC shifted the dose-response curve of ET-1 for % delta PP to the right in a parallel fashion.

Animals↗
PubMed1984

Effect of arterial impedance changes on the end-systolic pressure-volume relation.

To study the end-systolic pressure-volume relationship of left ventricle ejection against physiological afterload, we imposed seven simulated arterial impedances on excised canine left ventricles connected to a newly developed servo-pump system. We set each of the impedance parameters (resistance, capacitance, and characteristic impedance) to 50, 100, and 200% of normal value (resistance: 3 mm Hg sec/ml; capacitance: 0.4 ml/mm Hg; characteristic impedance: 0.2 mm Hg sec/ml), while leaving the other parameters normal. Under a given impedance, the end-systolic pressure-volume relationship was determined by preloading the ventricle at four different end-diastolic volumes. There was no significant change in the slope of the end-systolic pressure-volume relationship with changes in any of the afterloading impedance parameters. However, the volume intercept of the end-systolic pressure-volume relationship decreased significantly with resistance from 5.5 +/- 1.0 (SE) ml at resistance equal to 1.5 mm Hg sec/ml to 0.6 +/- 1.8 ml at resistance equal to 6 mm Hg sec/ml (P less than 0.01). The volume axis intercept also decreased with characteristic impedance, from 5.9 +/- 2.0 ml at a characteristic impedance of 0.1 mm Hg sec/ml to 5.4 +/- 2.1 ml at a characteristic impedance of 0.4 mm Hg sec/ml, (P less than 0.05). We conclude that the slope of the end-systolic pressure-volume relationship is insensitive to a wide range of changes in afterload impedance, but its volume intercept is dependent on resistance and characteristic impedance.

Animals↗
PubMed1986

The action potential and underlying ionic currents in proximal rat middle cerebral arterioles.

The active and passive electrical properties of isolated segments (length 120-220 microns, diameter 60-150 micron) of proximal rat middle cerebral arterioles (less than 1 mm from parent artery) were analysed using a single-electrode current or voltage clamp. The voltage response to a current step exhibited an exponential time course. The mean resistance and time constant was 102 M omega and 265 ms corresponding to approximate specific resistance and capacitance of 60 k omega/cm and 4 micro F/cm2. Membrane resistance was constant in the range -55 to -80 mV. At potentials more negative than -80 mV there was a decrease in membrane resistance resulting in activation of an inward rectifier. At membrane potentials less negative than -50 mV the membrane resistance decreased; larger depolarizations (greater than -40 mV) initiated small regenerative responses. External application of tetraethylammonium chloride caused membrane depolarization (10-15 mV), spontaneous discharge of action potentials and rhythmic arteriolar constriction. Action potentials studied with the membrane held at -60 mV had a large rapid depolarizing component, an after-depolarization and a small slower after-hyperpolarization. Tetrodotoxin (TTX) had no effect on the action potential. However, both the fast and slow components of the action potential were suppressed by extracellular removal of calcium ions and/or addition of cobalt ions, nifedipine or verapamil. Voltage-clamp studies demonstrated an inward rectifying current at membrane potentials more negative than -80 mV. At depolarized potentials at least four separate currents were activated; two separate calcium currents and two outward currents.

Action Potentials↗