scholarly journals Phasic negative intrathoracic pressures enhance the vascular responses to stimulation of pulmonary arterial baroreceptors in closed-chest anaesthetized dogs

2004 ◽  
Vol 555 (3) ◽  
pp. 815-824 ◽  
Author(s):  
Jonathan P. Moore ◽  
Roger Hainsworth ◽  
Mark J. Drinkhill
Keyword(s):  
Vascular Responses ◽  
Closed Chest ◽  
Arterial Baroreceptors ◽  
Pulmonary Arterial ◽  
Stimulation Of

Cardiovascular afferent inputs to ventral tegmental area

1997 ◽  
Vol 272 (6) ◽  
pp. R1998-R2003 ◽  
Author(s):  
G. J. Kirouac ◽  
J. Ciriello
Keyword(s):  
Ventral Tegmental Area ◽  
Discharge Rate ◽  
Onset Latency ◽  
Selective Activation ◽  
Unit Recording ◽  
Arterial Baroreceptors ◽  
Reflex Activation ◽  
Afferent Inputs ◽  
Ventral Tegmental ◽  
Stimulation Of

Extracellular single-unit recording experiments were done in alpha-chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of selective activation of arterial baroreceptors and stimulation of cardiovascular depressor sites in the nucleus of the solitary tract (NTS) on the discharge rate of neurons in the ventral tegmental area (VTA). Electrical stimulation of the aortic depressor nerve (ADN), which is known to carry aortic baroreceptor afferent fibers only, excited 12 of 21 (mean onset latency 42.4 +/- 8.8 ms) and inhibited 2 of 21 (mean onset latency 42.5 +/- 6.5 ms) single units in the VTA. The discharge rate of VTA units was also altered during the reflex activation of arterial baroreceptors by the acute rise in arterial pressure (AP) to systemic injections of phenylephrine (10 micrograms/kg i.v.): 12 of 44 units were excited and 15 of 44 were inhibited. Units that responded to either ADN stimulation or the reflex activation of the baroreflex also responded to stimulation of depressor sites in the NTS. An additional 12 units that were found in barodenervated controls to be responsive to NTS stimulation were nonresponsive to selective activation of arterial baroreceptors. These data indicate that cardiovascular afferent inputs modulate the activity of neurons in the VTA and suggest that changes in systemic AP may exert an effect on the activity of neurons involved in mesolimbic and mesocortical function.

Left heart and arterial baroreceptors interact in control of plasma vasopressin, renin, and cortisol in awake dogs

1994 ◽  
Vol 266 (3) ◽  
pp. R879-R888 ◽  
Author(s):  
J. L. Andersen ◽  
L. J. Andersen ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Vena Cava ◽  
Plasma Renin ◽  
Significant Rise ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Arterial Hypotension ◽  
Left Heart ◽  
Arterial Baroreceptors ◽  
Plasma Arginine ◽  
Stimulation Of

Arterial hypotension induced by constriction of the ascending aorta (AA) causes increases in left atrial pressure (LAP) and plasma atrial natriuretic peptide (ANP), but no change in plasma arginine vasopressin (AVP), plasma renin activity (PRA), or cortisol. In the present study, we tested the hypothesis that the rise in left heart pressure during constriction of the AA suppressed the stimulation of AVP, renin, and cortisol secretion in response to arterial hypotension. Dogs were prepared with inflatable cuffs around the AA, the pulmonary artery (PA), and the thoracic inferior vena cava (IVC) and with catheters in the left and right atria and abdominal aorta. In one series of experiments, the AA was constricted to lower mean arterial pressure (MAP) 10 or 20% below control for 15 min. Then, either the PA or the IVC was constricted to bring LAP back to control levels but without altering the degree of arterial hypotension. Constriction of the AA alone led to significant increases in LAP and plasma ANP but no change in plasma AVP, cortisol, or PRA. Reducing LAP to control levels by constriction of either the PA or IVC led to significant and similar increases in plasma AVP, cortisol, and PRA. Plasma ANP fell significantly 10 min after LAP was normalized by constriction of the IVC but not when LAP was normalized by constriction of the PA, because PA constriction caused a significant rise in right atrial pressure that stimulated ANP secretion. The increases in plasma AVP and PRA after normalizing LAP by constriction of the PA were compared with the increases obtained during identical falls in MAP induced by constriction of the IVC alone, a maneuver that lowers LAP below control. The increases in plasma AVP in the two conditions were identical, indicating that the stimulation of left heart baroreceptors alone can account for the suppression of AVP secretion in response to unloading arterial baroreceptors. In contrast, there was a greater rise in PRA during hypotension caused by constriction of the IVC alone compared with the condition in which LAP was normalized but plasma ANP remained elevated. This suggests that increased left heart pressure inhibits renin secretion in response to arterial hypotension by reflex mechanisms and by increased plasma ANP concentration.

Evidence for a central role for vasopressin in cardiovascular regulation

1983 ◽  
Vol 244 (6) ◽  
pp. H852-H859 ◽  
Author(s):  
K. H. Berecek ◽  
R. L. Webb ◽  
M. J. Brody
Keyword(s):  
Vascular Resistance ◽  
Third Ventricle ◽  
Cardiovascular Responses ◽  
Cardiovascular Regulation ◽  
Brattleboro Rats ◽  
Vascular Responses ◽  
The Third ◽  
Neuronal Systems ◽  
Mesenteric Vascular Resistance ◽  
Stimulation Of

Central vasopressin (VP) may modulate the functional activity of specific neuronal systems involved in cardiovascular regulation. To test this hypothesis we compared cardiovascular (CV) responses to electrical stimulation of the anteroventral region of the third ventricle (AV3V) in Brattleboro rats homozygous for diabetes insipidus (DI), in heterozygous DI rats (DI-HZ) and in normal Long-Evans rats (LE). We also studied the effects of peripheral and intracerebroventricular (ivt) treatment of DI rats with VP and treatment of LE rats with an antipressor blocker of VP on cardiovascular responses to AV3V stimulation. Stimulation of the AV3V region in anesthetized LE rats produced a frequency-dependent increase in renal (RVR) and mesenteric vascular resistance (MVR), a decrease in hindquarter vascular resistance (HQVR), and a decrease in arterial pressure (AP) and heart rate (HR). DI and DI-HZ rats showed significantly greater decreases in AP and HR and lesser changes in RVR, MVR, and HQVR. The deficiency in vasoconstriction in DI rats appeared to be centrally mediated inasmuch as vascular responses to peripherally administered phenylephrine and nerve stimulation were comparable in LE and DI rats. Treatment of DI rats with VP peripherally improved CV responses to AV3V stimulation. An even greater improvement in CV responses to AV3V stimulation was obtained when DI were given ivt infusion of VP. Finally, following intravenous administration of an antipressor VP blocker LE rats showed a greater decrease in AP and HR and lesser resistance changes in response to AV3V stimulation. Our data suggest that cardiovascular responses elicited from stimulation of the AV3V region may depend, in part, on a central vasopressin mechanism.

Sulfhydryl-depleting agents, but not deferoxamine, modulate EDRF action in cultured pulmonary arterial cells

1993 ◽  
Vol 265 (3) ◽  
pp. L220-L227
Author(s):  
N. Marczin ◽  
U. S. Ryan ◽  
J. D. Catravas
Keyword(s):  
Diethyl Ester ◽  
Dependent Manner ◽  
Deferoxamine Mesylate ◽  
Pulmonary Arterial ◽  
Pulmonary Arterial Smooth Muscle ◽  
Low Molecular Weight Iron ◽  
Dose Dependent ◽  
Cgmp Formation ◽  
Stimulation Of

The potential role of intracellular sulfhydryls and iron on the biological activity of endothelium-derived relaxing factor (EDRF) released basally from bovine pulmonary arterial endothelial (BPAE) cells was investigated in a cultured cell bioassay system, by measuring N omega-nitro-L-arginine-sensitive guanosine 3',5'-cyclic monophosphate (cGMP) accumulation in rabbit pulmonary arterial smooth muscle (SM) cells. The role of sulfhydryls in the biosynthesis of EDRF was studied by selectively exposing the endothelial cells to thiol-depleting agents. Both N-ethylmaleimide (NEM) and maleic acid diethyl ester (DEM) inhibited EDRF-induced cGMP accumulation in a dose-dependent manner. To study the requirement of SM thiols in the metabolism of EDRF to a stimulator of cGMP formation, SM were selectively exposed to NEM and DEM before bioassay with control, untreated BPAE. DEM and NEM inhibited cGMP formation in response to EDRF by 30 and 68%, respectively. The requirement of SM sulfhydryls was further investigated in the stimulation of SM cGMP accumulation elicited by nitrosothiols [S-nitroso-L-cysteine, S-nitroso-mercaptoproprionic acid, and sodium nitroprusside (SNP)]. NEM pretreatment of SM cells abolished cGMP responses to all vasodilators; DEM did not affect the nitrosothiol responses but reduced by 30% the cGMP accumulation to SNP. The role of iron in the endothelial synthesis of EDRF was assessed by chelating endothelial low-molecular-weight iron compounds. Exposure of BPAE to deferoxamine mesylate had no effect on cGMP accumulation in SM, suggesting that deferoxamine-available iron is not necessary for the endothelial stimulation of SM cGMP formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Physiological effects of thermode and microwave stimulation of peripheral nerves

1962 ◽  
Vol 203 (2) ◽  
pp. 374-378 ◽  
Author(s):  
Robert D. McAfee
Keyword(s):  
Blood Pressure ◽  
Microwave Irradiation ◽  
Peripheral Nerve ◽  
Peripheral Nerves ◽  
Physiological Effect ◽  
Nerve Fibers ◽  
Physiological Effects ◽  
Vascular Responses ◽  
Total Body ◽  
Stimulation Of

Physiological effects produced in cats, dogs, rabbits, and rats by microwave irradiation (3-cm radar and 12.2-cm Microtherm) are duplicated in these animals by heating peripheral nerves with a warm-water or resistance-wire thermode. Identical effects occur when a temperature ranging between 45–47 C is attained by either of these means at a treated peripheral nerve or within tissue rich in peripheral nerve fibers. The response elicited by thermode or microwave stimulation includes arousal reactions, blood pressure and vascular responses, and signs of neurohumoral activity. We have demonstrated that the physiological effect of microwave radiation is a result of thermal stimulation of peripheral nerves which occurs independently of a significant increase in skin temperature or of total body heating.

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