Pressor Response to Adrenalin Shown by Spinal Dogs

1956 ◽  
Vol 186 (1) ◽  
pp. 85-88
Author(s):  
Paul K. Mooring ◽  
John Rathe ◽  
Walter S. Root
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Intravenous Injection ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Percentage Increase ◽  
Average Percentage ◽  
Anesthetized Dogs ◽  
Unanesthetized Animals ◽  
Acute Changes

Intravenous injection of Adrenalin (1 ml of 1:300,000–1:25,000) into 10 normal, anesthetized (Nembutal) dogs produced an average increase in mean arterial pressure which amounted to about 25 at the lower and 100 mm Hg at the higher doses. Essentially the same responses were shown by seven anesthetized, vagotomized dogs and five anesthetized, vagotomized animals in which the carotid regions were denervated. Eight anesthetized dogs with spinal cords cut between C8 and T1 showed after Adrenalin injection an average percentage increase in mean arterial pressure which was some threefold greater than that found in normal, anesthetized animals. This difference was increased still further by bilateral section of the vagi in eight spinal dogs. Section of the spinal cord one or two segments below C8 to T1 (4 dogs) decreased the response to Adrenalin. The increase in mean arterial pressure induced by the intravenous injection of Adrenalin was greater in six spinal dogs (C8 to T1) anesthetized with Nembutal than in two similar unanesthetized animals. Acute changes in plasma volume did not influence the magnitude of the blood pressure response to Adrenalin shown by four high spinal animals.

scholarly journals Developmental Changes in Hemodynamic Responses and Cardiovagal Modulation during Isometric Handgrip Exercise

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Styliani Goulopoulou ◽  
Bo Fernhall ◽  
Jill A. Kanaley
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Isometric Contraction ◽  
Pressor Response ◽  
Reflex Response ◽  
Group Differences ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Isometric Handgrip Exercise ◽  
Pressor Reflex

The purpose of this study was to examine differences in pressor response and cardiovagal modulation during isometric handgrip exercise (IHG) between children and adults. Beat-to-beat heart rate (HR) and blood pressure were measured in 23 prepubertal children and 23 adults at baseline and during IHG. Cardiovagal modulation was quantified by analysis of HR variability. Mean arterial pressure responses to IHG were greater in adults compared to children (P<.05) whereas there were no group differences in HR responses (P>.05). Children had a greater reduction in cardiovagal modulation in response to IHG compared to adults (P<.05). Changes in mean arterial pressure during IHG were correlated with baseline cardiovagal modulation and force produced during isometric contraction (P<.05). In conclusion, differences in pressor reflex response between children and adults cannot be solely explained by differences in autonomic modulation and appear to be associated with factors contributing to the force produced during isometric contraction.

Baroreflex attenuation after hypotension induced by vena caval occlusion in anesthetized dogs

1995 ◽  
Vol 268 (4) ◽  
pp. R859-R864
Author(s):  
F. Sawano ◽  
T. Shibamoto ◽  
T. Hayashi ◽  
Y. Saeki
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Systemic Hypotension ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Cardiopulmonary Receptors ◽  
Pressure Fall

We determined effects of vena caval occlusion-induced systemic hypotension of 50 mmHg lasting 10 min (VCO) on efferent sympathetic nerve activity (SNA) and sympathetic baroreflex responsiveness. We recorded simultaneously SNA to the kidney (RNA), heart (CNA), spleen (SpNA), and liver (HNA) in anesthetized dogs. Baroreflex sensitivity was assessed using the ratio of a reflex SNA increase to a mean arterial pressure fall, which was also induced by caval occlusion. During VCO, SNA initially and equivocally increased, followed by recovery toward baseline. Cervical vagotomy attenuated the VCO-induced initial sympathoexcitation and subsequently maintained SNA at higher levels than those of intact animals, a finding basically similar to hemorrhagic hypotension [S. Koyama, F. Sawano, Y. Matsuda, Y. Saeki, T. Shibamoto, T. Hayashi, Jr., Y. Matsubayashi, and M. Kawamoto. Am. J. Physiol. 262 (Regulatory Integrative Comp. Physiol. 31): R579-R585, 1992]. At 5 min after releasing VCO, the baroreflex responsiveness was significantly attenuated: RNA, 79 +/- 11%; CNA, 78 +/- 8%; HNA, 60 +/- 16%; SpNA, 81 +/- 13% of the corresponding baseline. Fifteen minutes after VCO, this attenuation disappeared. Either vagotomy or pretreatment with intravenous vasopressin V1 receptor antagonist abolished this baroreflex attenuation. In conclusion, systemic hypotension to 50 mmHg for 10 min causes transient attenuation of sympathetic baroreflex sensitivity due to circulating vasopressin released by unloading of cardiopulmonary receptors during hypotension.

Activation of neurons in the rostral ventrolateral medulla increases bronchomotor tone in dogs

1991 ◽  
Vol 71 (1) ◽  
pp. 210-216 ◽  
Author(s):  
J. R. Haselton ◽  
P. A. Padrid ◽  
M. P. Kaufman
Keyword(s):  
Smooth Muscle ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Ventrolateral Medulla ◽  
Adrenergic Blockade ◽  
Homocysteic Acid ◽  
Lung Resistance ◽  
Anesthetized Dogs ◽  
Total Lung Resistance ◽  
Bronchomotor Tone

Previous work from this laboratory has demonstrated that the chemical activation of cell bodies in the caudal ventrolateral medulla of chloralose-anesthetized dogs decreased bronchomotor tone by withdrawing cholinergic input to airway smooth muscle. In the present study we determined the bronchomotor responses to microinjection of DL-homocysteic acid (100 mM; 25–50 nl) into the rostral ventrolateral (RVL) medulla of chloralose-anesthetized dogs. Total lung resistance was used as a functional index of bronchomotor tone. Microinjection of DL-homocysteic acid into the 20 sites located in the lateral aspect of the RVL medulla increased both total lung resistance [from 6.5 +/- 0.4 to 9.1 +/- 0.8 (SE) cmH2O.l-1.s; P less than 0.05] and mean arterial pressure (from 125 +/- 5 to 148 +/- 8 mmHg; P less than 0.05). Microinjection of this amino acid into nine sites located in the medial aspect of the RVL medulla increased mean arterial pressure (from 130 +/- 6 to 153 +/- 6 mmHg; P less than 0.05) but had no effect on total lung resistance. We confirmed in three sites that the increase in total lung resistance evoked by microinjection of DL-homocysteic acid was accompanied by an increase in tracheal smooth muscle tension. The increase in total lung resistance evoked by DL-homocysteic acid was not affected by beta-adrenergic blockade but was abolished by muscarinic blockade.

Acute central effects of L-glutamate in pentobarbital-anesthetized dogs

1987 ◽  
Vol 252 (3) ◽  
pp. R594-R598
Author(s):  
J. E. Chelly ◽  
M. F. Doursout ◽  
J. P. Buckley
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Dose Effect ◽  
Central Effects ◽  
Intravenous Injections ◽  
Induced Hypertension ◽  
Anesthetized Dogs ◽  
The Right ◽  
Dose Dependent Increase ◽  
Dose Dependent

Microinjections of L-glutamate (10(-10) to 2 X 10(-8) mol/kg) into the nucleus of tractus solitarii produced a dose-dependent increase in mean arterial pressure and a decrease in heart rate. L-Glutamate-induced hypertension was prevented by spinal transection and pretreatment with atropine (1 mg/kg iv) reversed the bradycardia. L-Glutamate also produced a dose-dependent increase in mean arterial pressure when injected intravenously and into the cisterna magna, but the dose-effect curves were shifted to the right. Finally, pretreatment with hexamethonium (30 mg/kg iv) abolished the hypertension resulting from intravenous injections of L-glutamate. These data demonstrate that the nucleus of tractus solitarii may play a determinant role in the central pressor effects of L-glutamate. In addition, we demonstrated that this hypertension was due to a central sympathetic stimulation and that the autonomic nervous system also mediated the pressor effects of intravenous L-glutamate.

Effect of indomethacin on the pressor responses to sustained isometric contraction in humans

1993 ◽  
Vol 75 (1) ◽  
pp. 273-278 ◽  
Author(s):  
K. P. Davy ◽  
W. G. Herbert ◽  
J. H. Williams
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Voluntary Contraction ◽  
Plasma Norepinephrine ◽  
Isometric Handgrip ◽  
Double Blind ◽  
Muscle Ischemia ◽  
Stimulation Of

The purpose of this study was to test the hypothesis that prostaglandins participate in metaboreceptor stimulation of the pressor response to sustained isometric handgrip contraction in humans. To accomplish this, mean arterial pressure, heart rate (n = 10), and plasma norepinephrine levels (n = 8) were measured in healthy male subjects during sustained isometric handgrip at 40% of maximal voluntary contraction force to exhaustion and during a period of postcontraction muscle ischemia. The subjects were given a double-blind and counterbalanced administration of placebo or a single 100-mg dose of indomethacin. A period of 1 wk was allowed for systemic clearance of the drug. Mean arterial pressure increased 25 +/- 5 vs. 22 +/- 4 mmHg during the final minute of isometric handgrip contraction and 26 +/- 2 vs. 21 +/- 5 during the last minute of postcontraction muscle ischemia in the placebo vs. the indomethacin trial (P > 0.05), respectively. Heart rate was increased 21 +/- 4 vs. 17 +/- 3 beats/min during the final minute of isometric handgrip contraction in the placebo vs. the indomethacin trial (P > 0.05), respectively, and returned to control values during postcontraction muscle ischemia. Plasma norepinephrine levels increased 343 +/- 89 vs. 289 +/- 89 pg/ml after isometric handgrip contraction and 675 +/- 132 vs. 632 +/- 132 pg/ml after postcontraction muscle ischemia (P > 0.05) in the placebo vs. the indomethacin trial, respectively. These results suggest that prostaglandin inhibition does not significantly modulate muscle contraction-induced stimulation of mean arterial pressure, heart rate, or plasma norepinephrine levels.

Differential cardiovascular effects of central clonidine and B-HT 920 in conscious rats

1988 ◽  
Vol 66 (11) ◽  
pp. 1455-1460 ◽  
Author(s):  
Kathryn A. King ◽  
Catherine C. Y. Pang
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Cardiovascular Effects ◽  
Plasma Noradrenaline ◽  
Adrenoceptor Agonists ◽  
Noradrenaline And Adrenaline ◽  
Prior Administration

The effect of intracerebroventricular (i.c.v.) injection of the α2-adrenoceptor agonists clonidine and B-HT 920 on mean arterial pressure (MAP), heart rate (HR), and plasma concentrations of noradrenaline and adrenaline was examined in conscious unrestrained rats. The injection of 1.0 μg clonidine significantly decreased MAP and slightly decreased HR. Plasma noradrenaline and adrenaline levels were slightly but not significantly decreased after the injection of 1 μg clonidine. In contrast, the injection of 0.1–10.0 μg B-HT 920 increased MAP and decreased HR. Plasma noradrenaline and adrenaline levels were slightly increased after the injection of the 1- and 10-μg doses. The i.c. v. injection of the α2-antagonist rauwolscine slightly but not significantly increased MAP and plasma noradrenaline and adrenaline levels. The responses to i.c. v. injection of clonidine and B-HT 920 were not changed by prior administration of rauwolscine. Neither the pressor response to B-HT 920 nor the depressor response to clonidine was abolished by rauwolscine, suggesting that neither response was mediated by α2-adrenoceptors.

scholarly journals Spontaneous Flow Oscillations in the Cerebral Cortex during Acute Changes in Mean Arterial Pressure

1992 ◽  
Vol 12 (3) ◽  
pp. 491-499 ◽  
Author(s):  
Antal G. Hudetz ◽  
Richard J. Roman ◽  
David R. Harder
Keyword(s):  
Blood Flow ◽  
Cerebral Cortex ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Mean Flow ◽  
Flow Oscillations ◽  
The Mean ◽  
Acute Changes ◽  
Infusion Of Norepinephrine ◽  
Doppler Flowmeter

The purpose of this study was to characterize spontaneous oscillations of blood flow in the cerebral cortex of anesthetized rats under control conditions and after mean arterial pressure was altered by various means. Blood flow was monitored using a laser–Doppler flowmeter through the closed cranium. Spontaneous flow oscillations with amplitudes of 14–30% of the mean flow and frequencies of 4–11 cycles/min were recorded when arterial pressures were less than 90 mm Hg. Stepwise hemorrhagic hypotension and unilateral carotid occlusion increased the amplitude of oscillations. The amplitude of oscillations was negatively correlated with the level of mean arterial pressure after manipulation with norepinephrine or sodium nitroprusside. The oscillations were reversibly abolished during dilation of the cerebral circulation by elevating the inspired carbon dioxide content to 5%. The frequency of flow oscillations was very stable during all of the above maneuvers except during the infusion of norepinephrine, which increased the oscillation frequency slightly. The results suggest that flow oscillations are determined primarily by cerebral arterial pressure.

Cardiovascular responses to intrathecal vasopressin in conscious and anesthesized rats

1989 ◽  
Vol 256 (1) ◽  
pp. R193-R200 ◽  
Author(s):  
A. Martinez-Arizala ◽  
J. W. Holaday ◽  
J. B. Long
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Intrathecal Administration ◽  
Motor Dysfunction ◽  
Sprague Dawley ◽  
Cardiovascular Changes ◽  
Conscious Rats

Increases in mean arterial pressure and heart rate have been documented after the intrathecal administration of [Arg8]vasopressin (AVP) in rats. Prior studies in our laboratories with conscious rats indicated that these cardiovascular changes were associated with a marked hindlimb sensorimotor dysfunction. In this study, which represents the first systematic comparison of the effects of intrathecal AVP in conscious and anesthesized rats, we demonstrate that in conscious male Sprague-Dawley rats 1) the motor dysfunction induced by intrathecal AVP is accompanied by a rise in mean arterial pressure that is significantly greater than that produced by an equal intravenous dose of AVP, and 2) both paralytic and pressor effects of intrathecal but not intravenous AVP are blocked by the intrathecal administration of the V1-receptor antagonist d(CH2)5[Tyr(Me)2]AVP (V1-ANT) but are not blocked by intravenous phenoxybenzamine, hexamethonium, or [Sar1, Thr8]angiotensin II, an angiotensin II antagonist. In contrast, in anesthesized rats the arterial pressor response to intrathecal AVP was blocked by intrathecal V1-ANT, intravenous hexamethonium, and intravenous phenoxybenzamine. Furthermore, conscious but not anesthesized rats exhibited a tachyphylaxis to intrathecal AVP. These results indicate that intrathecal AVP produces both the cardiovascular changes and the sensorimotor deficits through interactions with centrally located V1-receptors. In addition, sympathetic catecholaminergic mechanisms mediate the rise in mean arterial pressure produced by intrathecal AVP in anesthesized rats, but they do not in conscious rats.

Mechanism of pressor effects by angiotensin in the nucleus tractus solitarius of rats

1984 ◽  
Vol 247 (3) ◽  
pp. R575-R581 ◽  
Author(s):  
R. Casto ◽  
M. I. Phillips
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Nucleus Tractus Solitarius ◽  
Pressor Response ◽  
Dose Range ◽  
Ang Ii ◽  
Sympathetic Activation ◽  
Vasopressin Antagonist ◽  
Hypophysectomized Rats ◽  
Intact Rats

We recently reported that microinjection of angiotensin II (ANG II) into the nucleus tractus solitarius (NTS) results in an increase in mean arterial pressure (MAP) in urethan-anesthetized rats in a dose range of 50-500 ng. To investigate the mechanism of this response, hexamethonium (20 mg/kg iv) was used to inhibit sympathetic activation. There was a highly significant (P less than 0.001) reduction in the magnitude of the pressor response (4.7 +/- 1.1 mmHg) compared with preblockade ANG II (500 ng) responses (15.5 +/- 1.6 mmHg). A vasopressin antagonist and hypophysectomized rats were used to study the contribution of pituitary vasopressin. Injection of 500 ng ANG II in hypophysectomized rats produced a pressor response (14.8 +/- 3.2 mmHg) indistinguishable from that in intact controls (15.5 +/- 1.6 mmHg). Pretreatment with the vasopressin antagonist d(CH2)5Tyr(Me)AVP (1 microgram iv) in intact rats also had no effect on the magnitude of the pressor response (15.7 +/- 1.7 mmHg). Microinjection of ANG I and II produces an increase in arterial pressure. It is concluded that the angiotensin pressor response in the NTS is mediated by activation of descending sympathetic fibers and is not dependent on release of blood-borne pressor agents from the pituitary.

Systemic inhibition of nitric oxide and prostaglandins in volume-induced natriuresis and hypertension

1998 ◽  
Vol 274 (1) ◽  
pp. R175-R180 ◽  
Author(s):  
James D. Krier ◽  
Juan Carlos Romero
Keyword(s):  
Nitric Oxide ◽  
Mean Arterial Pressure ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Significant Elevation ◽  
Synthesis Inhibition ◽  
Anesthetized Dogs ◽  
Change Map

Nitric oxide (NO) synthesis inhibition with N G-nitro-l-arginine methyl ester (l-NAME) (10 μg ⋅ kg−1 ⋅ min−1iv), cyclooxygenase inhibition with meclofenamate (Meclo; 5 mg/kg iv bolus), and combination of drugs (l-NAME+Meclo) were used to investigate the roles of NO and prostaglandins (PG) in the hemodynamic and natriuretic responses to isotonic saline volume expansion (VE; 5% body wt over 60 min) in anesthetized dogs. Before VE,l-NAME ( n = 6), Meclo ( n = 6), andl-NAME+Meclo ( n = 6) produced significant increments in mean arterial pressure (MAP) of 12 ± 2, 15 ± 3, and 17 ± 3 mmHg, respectively. VE did not change MAP in Meclo-treated dogs, but produced a significant elevation in the control dogs (14 ± 6 mmHg), inl-NAME-treated dogs (17 ± 6 mmHg), and in dogs pretreated withl-NAME+Meclo (12 ± 5 mmHg). VE alone induced marked natriuretic responses in the control (38 ± 9 to 562 ± 86 μmol/min),l-NAME (31 ± 9 to 664 ± 65 μmol/min), and Meclo groups (41 ± 10 to 699 ± 51 μmol/min). However, this natriuretic response was attenuated in dogs pretreated with l-NAME+Meclo (12 ± 4 to 185 ± 52 μmol/min). These results indicate that 1) blockade of both NO and PGs has significant diminishing effects on volume-induced natriuresis, 2) NO blockade alone impairs volume-induced natriuresis in a manner that requires further increases in MAP to restore the natriuresis, and 3) PG blockade alone does not curtail volume-induced natriuresis.

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