Cardiovascular effects of cadmium on intravenous and intracerebroventricular administration in rats

1983 ◽  
Vol 61 (11) ◽  
pp. 1430-1432 ◽  
Author(s):  
V. N. Puri ◽  
R. N. Sur
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Cadmium Acetate ◽  
Cardiovascular Responses ◽  
Cadmium Exposure ◽  
Intracerebroventricular Administration

Cardiovascular responses to the intravenous (i.v.) and the intracerebroventricular (i.c.v.) administration of cadmium acetate were evaluated in rats anaesthetized with urethane. Cadmium acetate (1 mg/kg i.v.) caused an initial fall followed by a persistent rise in blood pressure. Cadmium acetate (1 μg i.c.v.) produced a more marked hypertensive effect. In the spinal-transected rat, the effect of intravenous cadmium was reduced but the effect of intraventricularly administered cadmium was completely abolished. It is, therefore, suggested that both central and peripheral mechanisms are involved in the pressor response to cadmium exposure.

Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

scholarly journals Tai-chi-chuan and yoga onpostexercise hypotension: comparison to aerobic and resistance exercise

2016 ◽  
Vol 29 (3) ◽  
pp. 543-552
Author(s):  
João Douglas Alves ◽  
Jorge Luiz de Brito Gomes ◽  
Caio Victor Coutinho de Oliveira ◽  
José Victor de Miranda Henriques Alves ◽  
Fabiana Ranielle de Siqueira Nogueira ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Young Women ◽  
Tai Chi ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Tai Chi Chuan ◽  
Post Exercise ◽  
Significant Difference ◽  
Apparently Healthy

Abstract Introduction: Tai-Chi-Chuan and Yoga have becoming popular practices. However is unclear the cardiovascular effects, and if they present similar behavior to aerobic and resistance sessions. Objective: To evaluate the cardiovascular responses during the session and post-exercise hypotension (PEH) of Tai Chi Chuan (TS) and Yoga (YS) in comparison to aerobic (AS) and resistance (SR) exercises. Methods: Fourteen young women (22.3 ± 2 years) apparently healthy performed four sessions (AS, RS, TS and YS). The heart rate (HR), systolic (SBP) and diastolic blood pressure (DBP) were recorded at resting, during (every 10 minutes) and until 50 minutes of recovery. Results: AS, RS, TS e YS showed significant increase in HR compared to resting.AS at 10, 30 e 50 minutes in relation to RS, TS e YS. The RS in relation to TS and YS at 10, 30 and 50 minutes. No significant difference between TS and YS. SBP was significantly increased in AS, RS, TS e YS at 10, 30 e 50 minutes during the session, in relation to rest. AS was significantly higher at 30 e 50 minutes than RS and higher than TS and YS at 10, 30 e 50 minutes. No significant difference in DBP. For PEH, AS, RS and TS significantly reduced at 10, 30 and 50 minutes. YS reduced at 50 minutes. No significant diastolic PEH. Conclusion: TS and YS showed as safe alternatives of exercising in the normotensive young adult woman, despite having lower values, they promote similar hemodynamic behavior to AS and RS.

Cardiovascular effects of human recombinant interleukin-1 beta in conscious rats

1994 ◽  
Vol 266 (4) ◽  
pp. R1148-R1153 ◽  
Author(s):  
A. Bataillard ◽  
J. Sassard
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Interleukin 1 ◽  
Renin Angiotensin System ◽  
Cardiovascular Effects ◽  
Interleukin 1 Beta ◽  
Pronounced Increase ◽  
Arterial Blood

Cardiovascular effects of human recombinant interleukin-1 beta (hrIL-1 beta) were investigated in normotensive rats using a computerized analysis of arterial blood pressure in conscious, unrestrained animals. Intravenous injection of hrIL-1 beta induced a rapid and short-lasting rise in blood pressure associated with a first slight tachycardia followed by a second sustained and pronounced increase in heart rate. These effects occurred in a dose-related manner. Pretreatment with a converting-enzyme inhibitor (perindopril) did not modify the hrIL-1 beta-induced increase in blood pressure. Blockade of beta 1-adrenoceptors (atenolol) prevented the tachycardia, but did not significantly affect the pressor response to hrIL-1 beta. On the contrary, the hrIL-1 beta-induced increase in blood pressure was inhibited by an alpha 1-adrenoceptor antagonist (prazosin), whereas the tachycardia was untouched. Finally, pretreatment with a cyclooxygenase inhibitor (indomethacin) completely abolished the cardiovascular response to hrIL-1 beta. These results suggest that the hrIL-1 beta-induced pressor response and associated tachycardia require the synthesis of prostaglandins and involve a sympathetic nervous system activation but do not depend on the renin-angiotensin system.

Evidence that centrally released arginine vasopressin is involved in central pressor action of angiotensin II

1996 ◽  
Vol 270 (1) ◽  
pp. H167-H173 ◽  
Author(s):  
S. Lon ◽  
E. Szczepanska-Sadowska ◽  
M. Szczypaczewska
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Pressor Effect ◽  
Ang Ii ◽  
Central Administration ◽  
Hypotensive Action ◽  
Series Of Experiments

Five series of experiments were performed on conscious trained dogs to find out whether intracranially released arginine vasopressin (AVP) is involved in mediation of central cardiovascular effects of angiotensin II (ANG II). The dogs were implanted with guide tubes leading to the third cerebral ventricle (ICV) and implanted with the intra-arterial catheters. Blood pressure and heart rate were continuously monitored during intracerebroventricular administration of 1) ANG II alone (250 ng), 2) AVP alone (0.01 ng/min during 10 min), 3) ANG II together with AVP, 4) AVP together with AVP V1-receptor antagonist 1(1-mercapto-4-methylcyclohexaneacetic acid)-8-AVP [MeCAAVP, V1ANT,100 ng/min], and 5) ANG II together with V1ANT. The results revealed that 1) ANG II and AVP applied separately elicited significant, long-lasting increases of blood pressure; 2) the maximum pressor effect after ANG II and AVP applied together did not differ from that after separate application of either of these peptides, but the duration of the pressor response was significantly shorter; 3) pretreatment with V1ANT effectively prevented blood pressure increases elicited by central administration of AVP and ANG II; and 4) after blockade of V1 receptors administration of AVP resulted in a significantly delayed decrease of blood pressure below baseline. The results strongly suggest that 1) centrally released AVP mediates the pressor effect of intracerebroventricularly applied ANG II by means of V1 receptors; 2) intracerebroventricularly applied ANG II and AVP interact to activate the mechanism involved in extinction of their pressor effect; and 3) blockade of central V1 receptors uncovers the hypotensive action of centrally applied AVP.

Influence of apnea on cardiovascular responses to neck suction during exercise

1996 ◽  
Vol 271 (4) ◽  
pp. H1370-H1374 ◽  
Author(s):  
P. Sundblad ◽  
D. Linnarsson
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Isometric Exercise ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Voluntary Contraction ◽  
Dynamic Exercise ◽  
Residual Capacity ◽  
Leg Exercise ◽  
Blood Pressure Responses

Short-lasting neck suction (NS) is a common method to assess the carotid-cardiac baroreflex, and NS is usually applied during apnea to avoid breath-synchronous variations of heart rate (HR) and blood pressure. We hypothesized that the apnea might provoke cardiovascular effects that could confound the HR and blood pressure responses to NS. HR and blood pressure responses to 10-s trains of 50-mmHg pulses of NS were studied in six male subjects during supine rest, upright rest, isometric arm exercise at 30% of maximal voluntary contraction, and dynamic leg exercise at 100 W in the sitting position. Repeated NS sequences were performed during apnea preceded by a relaxed expiration to functional residual capacity and during eupnea. Initial HR responses to NS were similar during eupnea and apnea in all conditions. However, during isometric and dynamic exercise, recordings made under eupneic and apneic conditions differed during the second half of the NS period. During apneic isometric arm contraction, the elevation of mean carotid distending pressure (MCDP) (arterial pressure at carotid level minus NS pressure) was maintained at a 25-35% higher level than during eupneic isometric exercise over the last half of the NS period. In dynamic exercise, mean arterial pressure and MCDP started to increase after 3-5 s of apneic NS, whereas they were maintained during eupnea. One to three seconds later, HR started to drop markedly in apneic subjects, reaching values 20 beats/min lower than those in eupneic subjects at the end of the NS. We conclude that cardiovascular effects of apnea may appear after only 8 s of apnea in dynamic exercise and therefore could confound responses to NS.

Cardiovascular responses during feeding in newborn lambs

1989 ◽  
Vol 257 (3) ◽  
pp. R568-R573
Author(s):  
B. L. Langille ◽  
S. L. Adamson ◽  
S. A. Jones
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Gastrointestinal Tract ◽  
Pressor Response ◽  
Sympathetic Innervation ◽  
Cardiovascular Responses ◽  
Bottle Feeding ◽  
Chemical Sympathectomy ◽  
Thyroid Glands ◽  
6 Hydroxydopamine

We examined the cardiovascular responses to bottle feeding in newborn lambs. Feeding induced a persistent rise in blood pressure, from 76.3 +/- 1.9 mmHg to 114 +/- 3.8 mmHg, that lasted for the duration of the feeding episode. This was accompanied by a transient tachycardia that lasted for approximately 10 s at the beginning of each feeding episode. Vasoconstriction of the hindlimb circulation, the gastrointestinal tract, kidneys, and adrenal and thyroid glands contributed to the pressor response, whereas changes in skeletal muscle resistance were not statistically significant. Of tissues assessed, only those actively involved in feeding (tongue and esophagus) vasodilated. Feeding tachycardia was greatly inhibited or abolished by the beta-blocker propranolol but the alpha-blocker phentolamine caused only moderate inhibition of the pressor response. Furthermore, chemical sympathectomy with 6-hydroxydopamine delayed the onset of the pressor response but did not abolish the ultimate rise in pressure. These findings indicate that feeding causes a significant pressor response in newborn lambs that is only partially mediated by sympathetic innervation.

scholarly journals Cardiovascular Responses to Repetitive McKenzie Lumbar Spine Exercises

2001 ◽  
Vol 81 (9) ◽  
pp. 1524-1533 ◽  
Author(s):  
Saud Al-Obaidi ◽  
Joseph Anthony ◽  
Elizabeth Dean ◽  
Nadia Al-Shuwai
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Low Back Pain ◽  
Back Pain ◽  
Lumbar Spine ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Low Back ◽  
Pulmonary Risk ◽  
Flexion And Extension

Abstract Background and Purpose. Repetitive exercises of the type recommended by McKenzie for the lumbar spine, such as flexion and extension exercises in standing (FIS and EIS) and lying positions (FIL and EIL), have been used in the management of low back pain for over 20 years. The cardiovascular effects of exercises that involve postural stabilization and the arms and of exercises performed in a lying position are well known. Therefore, the purpose of this study was to examine the cardiovascular effects of 4 exercises used in the McKenzie system. Subjects and Methods. One hundred subjects without cardiovascular or cardiopulmonary disease (mean age=31 years, SD=6.1, range=22–44) and who were representative of people susceptible to low back pain were studied. Subjects were randomly assigned to 1 of 4 exercise groups (ie, FIS, EIS, FIL, and EIL). Subjects performed sets of 10, 15, and 20 repetitions of the assigned exercise, with a 15-minute rest between sets. Heart rate, blood pressure, and rate-pressure product (an index of myocardial work) were recorded before and after each set of repetitions. Results. After 10 repetitions, flexion and extension in lying were more hemodynamically demanding than in standing. This trend persisted for 15 and 20 repetitions; however, at 20 repetitions, the hemodynamic demands were different across exercise groups (ie, FIL>EIL>FIS>EIS). Discussion and Conclusion. Repetitive exercises of the type suggested by McKenzie for the lumbar spine can have cardiovascular effects in people with no cardiovascular or cardiopulmonary conditions. These effects may be important with respect to cardiac work, and patients for whom these exercises are indicated should have a cardiac and pulmonary risk factor assessment to determine whether heart rate and blood pressure should be monitored.

Cardiovascular responses to hypoxia and hypercapnia in barodenervated rats

1990 ◽  
Vol 68 (2) ◽  
pp. 678-686 ◽  
Author(s):  
B. R. Walker ◽  
B. L. Brizzee
Keyword(s):  
Blood Pressure ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Arterial Baroreflex ◽  
Conscious Rat ◽  
Hypercapnic Hypoxia ◽  
Intact Rats

Experiments were performed to examine the role of the arterial baroreceptors in the cardiovascular responses to acute hypoxia and hypercapnia in conscious rats chronically instrumented to monitor systemic hemodynamics. One group of rats remained intact, whereas a second group was barodenervated. Both groups of rats retained arterial chemoreceptive function as demonstrated by augmented ventilation in response to hypoxia. The cardiovascular effects to varying inspired levels of O2 and CO2 were examined and compared between intact and barodenervated rats. No differences between groups were noted in response to mild hypercapnia (5% CO2); however, the bradycardia and reduction in cardiac output observed in intact rats breathing 10% CO2 were eliminated by barodenervation. In addition, hypocapnic hypoxia caused a marked fall in blood pressure and total peripheral resistance (TPR) in barodenervated rats compared with controls. Similar differences in TPR were observed between the groups in response to isocapnic and hypercapnic hypoxia as well. It is concluded that the arterial baroreflex is an important component of the overall cardiovascular responses to both hypercapnic and hypoxic stimuli in the conscious rat.

The Brain as a Possible Site for the Cardiovascular Effects of β-Adrenoceptor Blocking Agents in Cats

1974 ◽  
Vol 48 (s2) ◽  
pp. 269s-272s
Author(s):  
M. D. Day ◽  
A. G. Roach
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Effects ◽  
Intracerebroventricular Administration ◽  
Blocking Agents ◽  
Intracerebroventricular Infusion ◽  
Pressor Responses ◽  
Maximum Inhibition ◽  
The Brain

1. dl-Propranolol, l-propranolol, dl-alprenolol, pindolol (LB46), practolol, ICI 66082, sotalol and oxprenolol all produced prolonged falls in blood pressure and heart rate after intracerebroventricular administration in conscious normotensive cats. 2. Transient initial pressor responses and tachycardias were observed after intracerebroventricular infusions of all the β-adrenoceptor antagonists used, except ICI 66082. 3. d-Propranolol, d-alprenolol, procaine and lignocaine all produced initial increases in blood pressure and heart rate but did not subsequently cause any reduction in either blood pressure or heart rate. 4. The time of maximum hypotension and bradycardia after intracerebroventricular infusion of β-adrenoceptor antagonists coincided with the maximum inhibition of the centrally mediated tachycardia observed after intracerebroventricular isoprenaline.

Spinai cord serotonin receptors in cardiovascular regulation and potentiation of the pressor response to intrathecal substance P after serotonin depletion

1993 ◽  
Vol 71 (7) ◽  
pp. 453-464 ◽  
Author(s):  
Haroutioun Hasséssian ◽  
Philippe Poulat ◽  
Edith Hamel ◽  
Tomás A. Reader ◽  
Réjean Couture
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Cardiovascular Regulation ◽  
Cardiac Effect ◽  
Receptor Subtypes ◽  
Dependent Manner ◽  
Arterial Blood

The aim of this study was to characterize, in conscious rats, the spinal cord 5-hydroxytryptamine (5-HT) receptors involved in mean arterial pressure (MAP) and heart rate (HR) regulation as well as to examine the influence of bulbospinal 5-HT fibers on cardiovascular responses to intrathecal (i.t.) substance P (SP). The i.t. injection of 5-HT or 5-carboxamidotryptamine (5-CT) (5-HT1A, 1B, 1D agonist) reduced MAP and increased HR in a dose-dependent manner. In contrast, the agonists 8-hydroxy-2-(di-n-propylamino)tetraiin (8-OH-DPAT, 5-HT1A agonist) and α-CH3-5-HT (5-HT1C and 5-HT2) only caused a decrease in HR, while the agonist 2-CH3-5-HT (5-HT3) was devoid of cardiovascular effects. The vasodepressor response to 5-CT was antagonized by methiothepin but not affected by mesulergine, ketanserin, propranolol, or yohimbine. However, all five antagonists reduced the HR increase to 5-CT. Ketanserin, propranolol, mesulergine, yohimbine, and methysergide were without effect on resting MAP, while methiothepin reduced MAP. Methiothepin, ketanserin, and methysergide increased resting HR, yet the other antagonists had no effect on this parameter. Rats treated with p-chlorophenylalanine or 5,7-dihydroxytryptamine, but not with 6-hydroxydopamine, exhibited higher resting HR than that of control rats. Although the resting MAP was unaffected, the pressor response to i.t. SP was significantly enhanced by either 5-HT toxin. The results suggest that the receptor mediating the depressor response to 5-HT and 5-CT conforms with the broad pharmacological profile of a 5-HT1-like receptor and is unlikely to be of the 5-HT2 or 5-HT3 subtype. Since the HR response evoked by 5-CT was blocked by antagonists that exhibit affinities for various 5-HT receptor subtypes, it is suggested that a nonspecific blockade or, alternatively, that more than one receptor contributes to this cardiac effect. In addition, the results raise the possibility that a spinal 5-HT input, likely mediated by 5-HT2 receptors, tonically inhibits HR. Hence, an antagonistic interaction between 5-HT and SP is proposed to play a role in the control of arterial blood pressure in the spinal cord.Key words: 5-hydroxytryptamine, 5-HT receptors, substance P, spinal cord, cardiovascular regulation.

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