Autonomic neural regulation of intact Purkinje system of dogs

To characterize autonomic influences on the Purkinje system in vivo, we measured Purkinje relative refractory period (PRRP) in response to sympathetic (SNS) and vagal nerve stimulation (VNS). Effects of SNS on PRRP were primarily mediated via beta-adrenergic mechanisms because shortening of PRRP during SNS [from 215 +/- 7 (SE) to 202 +/- 8 ms, P less than 0.01] was entirely blocked by metoprolol (1 mg/kg). Vagal influences in the ambient state did not prolong PRRP, even when effective refractory period of adjacent muscle did prolong. When VNS was augmented with physostigmine, PRRP prolonged from 205 +/- 12 to 212 +/- 13 ms, P less than 0.05. Similar provocation of parasympathetic effects on PRRP occurred when VNS was performed during SNS; PRRP prolonged from 188 +/- 9 to 193 +/- 9 ms, P less than 0.05. Also, when alpha-adrenergic stimulation was produced by phenylephrine infusion (25 micrograms.kg-1.min-1) in the presence of metoprolol (1 mg/kg), which prolonged PRRP from 242 +/- 8 to 246 +/- 9 ms, P less than 0.05, the addition of VNS further prolonged PRRP from 246 +/- 9 to 253 +/- 9 ms, P less than 0.05. Thus some refractory period responses in the Purkinje system were similar to adjacent muscle, because beta-adrenergic activation shortened refractory period and vagal stimulation antagonized the shortening. Findings unique to Purkinje tissue were refractory period prolongation by vagal stimulation when facilitated by concurrent prolongation of refractory period during alpha-adrenergic stimulation.

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Autonomic control of ventricular refractoriness

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1981.241.6.h878 ◽

1981 ◽

Vol 241 (6) ◽

pp. H878-H882 ◽

Cited By ~ 2

Author(s):

S. Nattel ◽

D. E. Euler ◽

J. F. Spear ◽

E. N. Moore

Keyword(s):

Regression Model ◽

Right Ventricular ◽

Nerve Stimulation ◽

Refractory Period ◽

Regional Variation ◽

Vagal Stimulation ◽

Left Ventricular ◽

Sympathetic Stimulation ◽

Multilinear Regression

The effects of vagal and sympathetic stimulation on canine ventricular refractoriness were studied in vivo. Sympathetic stimulation reduced the left ventricular refractory period to an extent linearly related to the logarithm of nerve stimulation frequency. Vagal stimulation had no effect in the absence of sympathetic stimulation but produced a frequency-dependent attenuation of sympathetic effects when the two systems were stimulated simultaneously. The effects of combined vagal and sympathetic stimulation were best described by a multilinear regression model using the logarithm of vagal and sympathetic frequency as covariates. The magnitude of vagal attenuation of sympathetic effects did not show any regional variation at the five widely spaced sites (2 right ventricular, 3 left ventricular) studied.

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Inotropic sensitivity to beta-adrenergic stimulation in early sepsis

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.255.4.h699 ◽

1988 ◽

Vol 255 (4) ◽

pp. H699-H703 ◽

Cited By ~ 4

Author(s):

L. W. Smith ◽

K. H. McDonough

Keyword(s):

Contractile Function ◽

Plasma Catecholamines ◽

Left Ventricular ◽

Adrenergic Stimulation ◽

Maximal Increase ◽

Beta Adrenergic ◽

Arterial Blood ◽

Myocardial Contractile ◽

Early Sepsis

In early sepsis, maintenance of in vivo cardiovascular performance is at least partly dependent on sympathetic support to hearts with intrinsic contractile defects. Yet prolonged sympathetic stimulation, as occurs in sepsis, would be expected to alter the heart's ability to respond to this stimulation. We have investigated myocardial inotropic sensitivity to beta-adrenergic stimulation in a model of sepsis in which animals, at the time studied, exhibited bacteremia, normal arterial blood pressure and cardiac output, elevated heart rate, and elevated plasma catecholamines. Intrinsic myocardial contractile function, as assessed by the maximal rate of left ventricular pressure development (LV dP/dtmax) in an isovolumically contracting heart preparation, was significantly depressed in septic animals. To determine whether hearts from septic animals could respond normally to beta-adrenergic stimulation, we studied inotropic response to a bolus of isoproterenol in these isolated hearts. With maximal isoproterenol stimulation, hearts from septic animals were able to attain the same dP/dtmax as were hearts from control animals. With lower levels of isoproterenol, there was also no difference in inotropic indexes between the two groups when response was expressed as a percent of the maximal increase in dP/dtmax achieved with isoproterenol. These results suggest that in early sepsis, despite intrinsic myocardial contractile dysfunction, the ability of the heart to modulate its inotropic state in response in beta-adrenergic stimulation is intact.

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Escape from vasoconstriction in the gastric microcirculation

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1975.228.6.1893 ◽

1975 ◽

Vol 228 (6) ◽

pp. 1893-1895 ◽

Cited By ~ 18

Author(s):

Paul H. Guth ◽

Esther Smith

Keyword(s):

Nerve Stimulation ◽

Splanchnic Nerve ◽

System Response ◽

In Vivo Microscopy ◽

Adrenergic Stimulation ◽

Resistance Vessels ◽

Autoregulatory Escape ◽

Splanchnic Nerve Stimulation ◽

Gastric Microcirculation

Escape of splanchnic resistance vessels from vasoconstriction due to adrenergic stimulation has been attributed to increasing submucosal blood flow due to dilation of submucosal arteriovenous anastomoses (shunts). This postulate, as applied to the rat gastric microcirculation, was studied by in vivo microscopy. Using an image-splitting TV microscope recording system, response of gastric submucosal arterioles (13–33 µm) to 3 min of left splanchnic nerve stimulation, norepinephrine superfusion, and vasopressin superfusion was measured. All stimuli produced initial vasoconstriction. Escape occurred in all rats with nerve stimulation and norepinephrine, but in only one of five with vasopressin. No shunts were seen. The study demonstrates that the gastric submucosal arterioles exhibit an escape phenomenon, suggesting that "autoregulatory escape" in other splanchnic beds also may be due to relaxation of constricted vessels and not to opening of shunts.

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In vivo and in vitro cardiac responses to beta-adrenergic stimulation in volume-overload heart failure

Journal of Molecular and Cellular Cardiology ◽

10.1016/j.yjmcc.2012.11.013 ◽

2013 ◽

Vol 57 ◽

pp. 47-58 ◽

Cited By ~ 17

Author(s):

Anuradha Guggilam ◽

Kirk R. Hutchinson ◽

T. Aaron West ◽

Amy P. Kelly ◽

Maarten L. Galantowicz ◽

...

Keyword(s):

Heart Failure ◽

Volume Overload ◽

Adrenergic Stimulation ◽

Beta Adrenergic ◽

Cardiac Responses

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Energy metabolism in trout red cells: consequences of adrenergic stimulation in vivo and in vitro

Journal of Experimental Biology ◽

10.1242/jeb.143.1.133 ◽

1989 ◽

Vol 143 (1) ◽

pp. 133-147 ◽

Cited By ~ 3

Author(s):

R. A. Ferguson ◽

B. L. Tufts ◽

R. G. Boutilier

Keyword(s):

Ph Regulation ◽

Red Cells ◽

Red Cell ◽

Adrenergic Stimulation ◽

Beta Adrenergic ◽

Extracellular Acidosis ◽

Metabolic Functions ◽

The Face

beta-Adrenergic stimulation of salmonid red cells results in a rapid decrease (within 5 min) in the nucleotide triphosphate:haemoglobin ratio (NTP:Hb), which is thereafter maintained at a constant level, presumably through increased ATP turnover via matched aerobic metabolism and energy-consuming processes. Addition of the beta-adrenergic agonist isoproterenol to rainbow trout red cells in vitro leads to a rise in intracellular pH (pHi), a corresponding decrease in extracellular pH (pHe) and an increase in red cell oxygen consumption (MO2). Moreover, the extent to which red cell pHi is maintained constant in the face of an acute extracellular acidosis in vitro or in vivo is proportional to the adrenergically stimulated increase in red cell MO2. In the absence of oxygen, these red cells remain capable of pH regulation, but cannot maintain NTP:Hb constant. As a result, membrane and metabolic functions become uncoupled in the stimulated deoxygenated cells.

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Inhibition of nitric oxide synthase augments myocardial contractile responses to beta-adrenergic stimulation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.271.6.h2646 ◽

1996 ◽

Vol 271 (6) ◽

pp. H2646-H2652 ◽

Cited By ~ 12

Author(s):

J. F. Keaney ◽

J. M. Hare ◽

J. L. Balligand ◽

J. Loscalzo ◽

T. W. Smith ◽

...

Keyword(s):

Nitric Oxide ◽

Myocardial Contractility ◽

Adrenergic Stimulation ◽

Maximum Increase ◽

Beta Adrenergic ◽

Before And After ◽

Nos Inhibitor ◽

Oxide Synthase

Recent in vitro evidence suggests a role for nitric oxide (NO) in the modulation of myocardial contractility. The specific role of NO in the control of cardiac function in vivo, however, remains unclear. We investigated the effect of NO synthase (NOS) inhibition on myocardial contractility in response to beta-adrenergic stimulation in autonomically blocked dogs. Intracoronary infusions of dobutamine (1-50 micrograms/min) and isoproterenol (0.1 and 0.5 microgram/min) were performed before and after the intracoronary administration of the specific NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME). Intracoronary dobutamine resulted in a dose-dependent increase in peak first derivative of pressure (dP/dtmax) to a maximum of 195 +/- 10% (P < 0.001). After inhibition of NOS with intracoronary L-NAME at rates of 0.1 and 1 mg/min, the response to dobutamine was significantly enhanced with dP/dtmax, increasing 276 +/- 17 and 317 +/- 26%, respectively (P < 0.001). Intracoronary isoproterenol resulted in a maximum increase in dP/dtmax of 116 +/- 15% (P < 0.001) that further increased to 154 +/- 17 and 157 +/- 18% after NOS inhibition with 0.1 and 1 mg/min L-NAME, respectively (both P < 0.002). L-NAME had no effect on baseline dP/dtmax but did produce a reduction in myocardial guanosine 3',5'-cyclic monophosphate content. These results suggest a role for NO in the control of myocardial contractility in response to beta-adrenergic stimulation in vivo.

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Escape from vasoconstriction in the gastric microcirculation

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1975.228.6.1880 ◽

1975 ◽

Vol 228 (6) ◽

pp. 1880-1886 ◽

Cited By ~ 12

Author(s):

PH Guth ◽

E Smith

Keyword(s):

Nerve Stimulation ◽

Splanchnic Nerve ◽

System Response ◽

In Vivo Microscopy ◽

Adrenergic Stimulation ◽

Resistance Vessels ◽

Autoregulatory Escape ◽

Splanchnic Nerve Stimulation ◽

Gastric Microcirculation

Escape of splanchic resistance vessels from vasconstriction due to adrenergic stimulation has been attributed to increasing submucosal blood flow due to dilation of submucosal arteriovenous anastomes (shunts). This postulate, as applied to the rat gastric microcirculation, was studied by in vivo microscopy. Using an image-splittingTV microscope recording system, response of gastric submucosal arterioles (13-33 mum)to 3 min of left splanchnic nerve stimulation, norepinephrine superfision, and vasopressin superfission was measured. All stimuli produced initial vasoconstriction.Escape occurred in all rats with nerve stimulation and norepinephrine, but in onlyone of five with vasopressin. No shunts were seen. The study demonstrates that thegastric submucosal arterioles exhibit an escape phenomenon, suggesting that "autoregulatory escape" in other splanchic beds also may be due to relaxation of constricted vessels and not to opening of shunts.

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Refractory period response of cardiac Purkinje tissue to alpha 1- and alpha 2-adrenergic influences

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.1.h376 ◽

1994 ◽

Vol 267 (1) ◽

pp. H376-H382 ◽

Cited By ~ 4

Author(s):

D. G. Cable ◽

T. E. Rath ◽

E. R. Dreyer ◽

J. B. Martins

Keyword(s):

Mean Arterial Pressure ◽

Cell Membrane ◽

Arterial Pressure ◽

Refractory Period ◽

Adrenergic Stimulation ◽

Relative Refractory Period ◽

Wb 4101 ◽

Adrenergic Antagonists

Our purpose was to characterize Purkinje responses in vivo to alpha 1- and alpha 2-adrenergic stimulation in sinoaortically denervated and vagotomized dogs pretreated with metoprolol (1 mg/kg). We measured Purkinje relative refractory period (PRRP) responses to norepinephrine (NE) and phenylephrine (PE) with prazosin and/or yohimbine, WB-4101, and chloralethylclonidine (CEC) in varying doses. Results were as follows: PE infusion (25 micrograms.kg-1.min-1) prolonged PRRP (9.6 +/- 1.4 ms; a 4.1 +/- 0.4% change). Prazosin blocked PRRP prolongation with PE at 7 x 10(-8) M/kg (P < 0.05). Yohimbine did not attenuate PRRP prolongation with PE either alone or in combination with prazosin. NE infusion (0.8 micrograms.kg-1.min-1) also prolonged PRRP (9.2 +/- 2.3 ms; a 4.8 +/- 1.0% change). In contrast neither prazosin nor yohimbine at any dose (up to 10(-6) M/kg) totally blocked the prolongation with NE infusion. However, with prazosin (2 x 10(-7) M/kg) pretreatment, yohimbine blocked PRRP prolongation, significant at 7 x 10(-8) M/kg (P < 0.05). In separate experiments with yohimbine pretreatment at 7 x 10(-8) M/kg, PRRP prolongation with either PE or NE infusion was blocked equipotently with WB-4101 and CEC at 7 x 10(-8) M/kg. However, CEC did not block mean arterial pressure (MAP) responses to PE or NE infusion unlike WB-4101. We concluded that both subclasses of alpha 1-adrenergic antagonists equipotently block PRRP prolongation by alpha-agonists despite different effects on MAP. Purkinje refractoriness is also prolonged by alpha 2-adrenergic stimulation acting at the cell membrane.

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