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.

Vascular and renal effects of leukotriene C4 in conscious rats

1985 ◽  
Vol 249 (5) ◽  
pp. F739-F744 ◽  
Author(s):  
J. Filep ◽  
B. Rigter ◽  
J. C. Frolich
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Statistical Significance ◽  
Renal Hemodynamics ◽  
Leukotriene C4 ◽  
Electrolyte Excretion ◽  
Renal Effects ◽  
Intravenous Injections ◽  
Induced Changes ◽  
Dose Dependent Increase

To investigate the possible renal effects of leukotriene C4 (LTC4) renal function was monitored in conscious unrestrained rats. Intravenous injections of 2, 4, and 8 micrograms/kg LTC4 markedly and dose-dependently elevated urine flow (by 64, 91, and 133%, respectively) with a concomitant increase in urinary sodium (61, 81, and 118%) and potassium (39, 50, and 76%) excretion. All changes were statistically significant. There was a tendency for glomerular filtration rate to increase, but this change reached statistical significance only after the highest dose of LTC4. Moreover, 8 micrograms/kg LTC4 reduced p-aminohippurate clearance by 33%. A dose-dependent increase in mean arterial pressure (15 mmHg at 2 micrograms/kg, 20 mmHg at 4 micrograms/kg, and 30 mmHg at 8 micrograms/kg) was observed following LTC4 administration. While the administration of FPL 55712, a putative antagonist of leukotrienes, had no effect on mean arterial pressure and kidney function, it significantly attenuated the vasopressor effect of LTC4 and practically completely abolished LTC4-induced changes in both renal hemodynamics and water and electrolyte excretion. These results raise the possibility that leukotrienes might be involved in the regulation of renal hemodynamics and could modify urinary electrolyte excretion under conditions in which leukotriene formation is enhanced.

Structural prerequisites for the hypotensive action of parathyroid hormone

1984 ◽  
Vol 246 (5) ◽  
pp. F551-F556 ◽  
Author(s):  
D. H. Ellison ◽  
D. A. McCarron
Keyword(s):  
Parathyroid Hormone ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Amino Acid Residues ◽  
Hypotensive Action ◽  
Intravenous Injections ◽  
Wistar Kyoto ◽  
Acute Changes ◽  
Urinary Phosphorus Excretion ◽  
Dose Dependent

We assessed the vascular, phosphaturic, and calcemic responses to several synthetic parathyroid hormone (PTH) analogues. Bovine (b) PTH (1-34), human (h) PTH (1-34), hPTH (53-84), [ Nle8 , Nle18 , Tyr34 ]bPTH (1-34), and [ Nle8 , Nle18 , Tyr34 ]bPTH (3-34) were administered in doses between 1 and 500 micrograms/kg as bolus intravenous injections to male Wistar-Kyoto rats aged 18-26 wk. Antagonism of the action of PTH was assessed in rats pretreated with 10 or 100 micrograms/kg [ Nle8 , Nle18 , Tyr34 ]bPTH (3-34) followed by 10 micrograms/kg of bPTH (1-34), or with 10 micrograms/kg hPTH (53-84) followed by 10 micrograms/kg hPTH (1-34). Bovine PTH (1-34), hPTH (1-34), and [ Nle8 , Nle18 , Tyr34 ]bPTH (1-34) produced virtually identical log dose-dependent hypotension, with 100 micrograms/kg of each analogue producing a 56% reduction in mean arterial pressure. Neither hPTH (53-84) nor [ Nle8 , Nle18 , Tyr34 ]bPTH (3-34) demonstrated any effect on mean arterial pressure at doses up to 500 micrograms/kg. Pretreatment with the inactive analogues failed to antagonize the vasodilating response to either bPTH (1-34) or hPTH (1-34). The vasoactive analogues significantly increased urinary phosphorus excretion while the inactive analogues did not modify it. hPTH (1-34) produced a modest decrease in serum Ca2+ at 1 min after injection. The results document that the vasodilating effect of PTH is a specific action of the peptide. Deletion of the first two amino acid residues abolishes both the phosphaturic and hypotensive effects of the peptide. Acute changes in serum Ca2+ do not appear to be a prerequisite for the vasodilatory response. Inactive analogues of PTH do not antagonize the vascular actions of the peptide.

Simultaneous evaluation of medullary secretory functions of normal and acutely denervated adrenals

1991 ◽  
Vol 260 (2) ◽  
pp. R306-R313 ◽  
Author(s):  
N. Yamaguchi ◽  
L. Lamarche ◽  
R. Briand
Keyword(s):  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Intravenous Injections ◽  
Simultaneous Evaluation ◽  
Bilateral Carotid ◽  
Anesthetized Dogs ◽  
Adrenal Response ◽  
The Right ◽  
Dose Dependent Increase

Adrenal medullary secretory function of the right innervated gland was simultaneously compared with that of contralateral acutely denervated gland in anesthetized dogs. During bilateral carotid artery occlusion (BCO), output (in ng/min) from right innervated gland of epinephrine and norepinephrine increased from 86.6 +/- 33.0 and 34.4 +/- 15.1 to 280.8 +/- 86.7 (P less than 0.01, n = 7) and 104.4 +/- 40.6 (P less than 0.01, n = 7), respectively. By contrast, epinephrine output from left denervated gland increased only slightly (P less than 0.05), and norepinephrine did not increase significantly. Net catecholamine output from left denervated gland was markedly attenuated by approximately 90% (P less than 0.01, n = 7) compared with that from right innervated gland. During BCO in the second group of dogs, catecholamine output from sham-denervated left gland increased significantly (P less than 0.01, n = 7) to an extent slightly lower than that observed in right innervated gland. In the third group, intravenous injections of dimethylphenylpiperazinium (5 and 15 micrograms/kg) resulted in a dose-dependent increase (P less than 0.05, n = 7) in catecholamine output from both right innervated and left denervated gland. The results indicate that the present procedure of acute surgical adrenal denervation can eliminate the centrally mediated adrenal response, whereas the medullary secretory response to blood-borne substances remains intact. This model may be a useful tool for studying neuronal and humoral medullary secretory functions in vivo under various experimentally induced stress conditions.

Baroreceptor-mediated compensation for hemodynamic effects of positive end-expiratory pressure

1999 ◽  
Vol 86 (1) ◽  
pp. 285-293 ◽  
Author(s):  
Stephen S. Blevins ◽  
Martha J. Connolly ◽  
Drew E. Carlson
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Baroreceptor Reflex ◽  
Right Atrial ◽  
Positive End Expiratory Pressure ◽  
Carotid Baroreceptor ◽  
The Right

The roles of the carotid arterial baroreceptor reflex and of vagally mediated mechanisms during positive end-expiratory pressure (PEEP) were determined in pentobarbital-anesthetized dogs with isolated carotid sinuses. Spontaneously breathing dogs were placed on PEEP (5–10 cmH2O) with the carotid sinus pressure set to the systemic arterial pressure (with feedback) or to a constant pressure (no feedback). Right atrial volume was measured with a conductance catheter. With carotid baroreceptor feedback before bilateral cervical vagotomy, total peripheral resistance increased ( P < 0.01) and mean arterial pressure decreased (−9.8 ± 4.3 mmHg) in response to PEEP. With no feedback after vagotomy, mean arterial pressure decreased to a greater extent (−45 ± 6 mmHg, P < 0.01), and total peripheral resistance decreased ( P < 0.05) in response to PEEP. In contrast, cardiac index decreased similarly during PEEP ( P < 0.01) for all baroreceptor and vagal inputs. This response comprised a decrease in the passive phase of right ventricular filling ( P< 0.01) that was not matched by the estimated increase in active right atrial output. Although the carotid baroreceptor reflex and vagally mediated mechanisms elicit vasoconstriction to compensate for the effects of PEEP on the arterial pressure, these processes fail to defend cardiac output because of the profound effect of PEEP on the passive filling of the right ventricle.

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.

Median preoptic nucleus ablation does not affect angiotensin II-induced hypertension

1986 ◽  
Vol 251 (1) ◽  
pp. H148-H152
Author(s):  
G. D. Fink ◽  
C. A. Bruner ◽  
M. L. Mangiapane
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Base Line ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Water Excretion ◽  
Median Preoptic Nucleus ◽  
Induced Hypertension

Previous studies implicated the ventral median preoptic nucleus (MNPOv) in cardiovascular responses to circulating and intracerebroventricular angiotensin II (ANG II) and in normal cardiovascular and fluid homoeostasis. In the present experiments, chronically catheterized rats received continuous (24 h/day) intravenous infusions of ANG II (10 ng/min) for 5 days, and changes in mean arterial pressure, heart rate, water intake and urinary electrolyte and water excretion were determined daily. Three groups of rats were compared as follows: 1) sham-operated control rats (n = 12), 2) rats with 20-70% of the MNPOv ablated electrolytically (n = 6), and 3) rats with over 90% of the MNPOv ablated (n = 5). The organum vasculosum of the lamina terminalis was intact in all three groups. Base-line values of all measured variables were identical in the three groups on two control days preceding ANG II infusion and on two recovery days after infusion. During the administration of ANG II for 5 days, mean arterial pressure rose significantly (and similarly) in all three groups of rats; no other variable was significantly affected by ANG II infusion. These results suggest that neural pathways originating in, or passing through, the MNPOv region are not critical in the pathogenesis of ANG II-induced hypertension in the rat.

Rho kinase and Ca2+ entry mediate increased pulmonary and systemic vascular resistance in l-NAME-treated rats

2007 ◽  
Vol 293 (5) ◽  
pp. L1306-L1313 ◽  
Author(s):  
Jasdeep S. Dhaliwal ◽  
David B. Casey ◽  
Anthony J. Greco ◽  
Adeleke M. Badejo ◽  
Thomas B. Gallen ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Rho Kinase ◽  
Systemic Arterial Pressure ◽  
Intravenous Injections ◽  
Pulmonary Arterial ◽  
Dose Dependent

The small GTP-binding protein and its downstream effector Rho kinase play an important role in the regulation of vasoconstrictor tone. Rho kinase activation maintains increased pulmonary vascular tone and mediates the vasoconstrictor response to nitric oxide (NO) synthesis inhibition in chronically hypoxic rats and in the ovine fetal lung. However, the role of Rho kinase in mediating pulmonary vasoconstriction after NO synthesis inhibition has not been examined in the intact rat. To address this question, cardiovascular responses to the Rho kinase inhibitor fasudil were studied at baseline and after administration of an NO synthesis inhibitor. In the intact rat, intravenous injections of fasudil cause dose-dependent decreases in systemic arterial pressure, small decreases in pulmonary arterial pressure, and increases in cardiac output. l-NAME caused a significant increase in pulmonary and systemic arterial pressures and a decrease in cardiac output. The intravenous injections of fasudil after l-NAME caused dose-dependent decreases in pulmonary and systemic arterial pressure and increases in cardiac output, and the percent decreases in pulmonary arterial pressure in response to the lower doses of fasudil were greater than decreases in systemic arterial pressure. The Ca++ entry blocker isradipine also decreased pulmonary and systemic arterial pressure in l-NAME-treated rats. Infusion of sodium nitroprusside restored pulmonary arterial pressure to baseline values after administration of l-NAME. These data provide evidence in support of the hypothesis that increases in pulmonary and systemic vascular resistance following l-NAME treatment are mediated by Rho kinase and Ca++ entry through L-type channels, and that responses to l-NAME can be reversed by an NO donor.

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.

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