Pressor effects of systemic administration of methionine and leucine enkephalin in the conscious rat

1986 ◽  
Vol 64 (11) ◽  
pp. 1353-1360 ◽  
Author(s):  
J. A. Thornhill ◽  
M. Ewen ◽  
A. A. Wilfong ◽  
L. Gregor ◽  
W. S. Saunders
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptor ◽  
Low Dose ◽  
Pressor Response ◽  
Peripheral Vasculature ◽  
Conscious Rat ◽  
Pressor Responses ◽  
Receptor Blockers ◽  
Change In Mean ◽  
Mean Heart Rate

Experiments were designed using conscious Spargue–Dawley rats to determine the blood pressure (BP) and heart rate (HR) responses to intravenous doses of (1) the adrenal catecholamines noradrenaline (NA) and adrenaline (A), (2) adrenal pentapeptides methionine enkephalin (ME) and leucine enkephaline (LE), (3) combination (i.v.) injections of both ME or LE with NA or A that modulate the hemodynamic responses when the adrenal catecholamines were given alone, and (4) the possible receptor mechanisms mediating the resultant BP and HR response to i.v. pentapeptide administration. NA (0.48 and 2.4 nmol) and A (0.3 and 1.5 nmol) given i.v. evoked potent, dose-related pressor responses associated with reflex bradycardia. ME and LE (1.6 – 48 nmol) elicited transient (10–20 s) increases in mean arterial pressure (MAP), which was associated either with no change in mean heart rate (MHR), such as ME, or with slight bradycardia (i.e., LE). Combining ME or LE (16 nmol) with NA (2.4 nmol) or A (0.3 or 1.5 nmol) did not change MAP and MHR from when these respective doses of NA or A were given alone. However, 16 nmol of ME or LE with a low dose of NA (0.48 nmol) increased the pressor response compared with NA (0.48 nmol) given alone. Other experiments whereby specific receptor blockers (naloxone, diprenorphine, atropine, propranolol, phentolamine or quanethidine) were given i.v. 5 min before subsequent i.v. administration of LE or ME (16 nmol) indicated that only phentolamine or quanethidine could completely suppress the pressor responses of LE and ME. Naloxone and diprenorphine pretreatment attenuated the pressor response of LE but did not affect the BP response to ME. The results suggest that i.v. LE or ME injections to conscious rats evoke an α-adrenergic receptor-mediated pressor response which is not associated with tachycardia and that is likely due to vasoconstriction of the peripheral vasculature.

Baroreflex buffering of pressor response to vasopressin is mediated by V1, not V2, receptors in conscious rats

1993 ◽  
Vol 264 (2) ◽  
pp. R345-R349
Author(s):  
K. Shimizu ◽  
J. Schwartz ◽  
B. P. McGrath
Keyword(s):  
Heart Rate ◽  
Receptor Agonist ◽  
Pressor Response ◽  
Conscious Rat ◽  
Conscious Rats ◽  
Pressor Responses ◽  
Autonomic Blockade ◽  
V2 Receptor ◽  
Intact Rats

Arginine vasopressin (AVP) enhances reflex buffering of its own pressor response, thus attenuating its vasoconstrictor potential in vivo. To investigate the extent to which this effect of AVP is mediated by V1 or V2 receptors, mean arterial pressure (MAP) and heart rate (HR) changes were examined in response to graded injections of AVP or [Phe2,Orn8]oxytocin, a potent, selective V1-receptor agonist, in the absence and presence of infusion of [Val4,D-Arg8]VP, a selective V2-receptor agonist. Responses were compared in intact and autonomically blocked conscious rats. During autonomic blockade with methscopolamine and hexamethonium, the pressor sensitivities to AVP and [Phe2,Orn8]oxytocin were similarly increased. Infusion of the V2-receptor agonist had no effect by itself on MAP or HR in conscious intact rats. It also did not alter the pressor responses to the V1 agonist, in either intact or autonomically blocked rats. In the presence of the V2 agonist, the decrease in heart rate induced by the V1 agonist was enhanced. These results indicate that reflex buffering of the pressor response to AVP in the conscious rat is mediated by V1 and not V2 receptors. However, V2 receptors may be involved in modulating the heart rate response to AVP.

Neurocirculatory consequences of abrupt change in sleep state in humans

1996 ◽  
Vol 80 (5) ◽  
pp. 1627-1636 ◽  
Author(s):  
B. J. Morgan ◽  
D. C. Crabtree ◽  
D. S. Puleo ◽  
M. S. Badr ◽  
F. Toiber ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Intrathoracic Pressure ◽  
Nrem Sleep ◽  
Auditory Stimuli ◽  
Sleep State ◽  
Healthy Humans ◽  
Pressor Responses

The arterial pressure elevations that accompany sleep apneas may be caused by chemoreflex stimulation, negative intrathoracic pressure, and/or arousal. To assess the neurocirculatory effects of arousal alone, we applied graded auditory stimuli during non-rapid-eye-movement (NREM) sleep in eight healthy humans. We measured muscle sympathetic nerve activity (intraneural microelectrodes), electroencephalogram (EEG; C4/A1 and O1/A2), arterial pressure (photoelectric plethysmography), heart rate (electrocardiogram), and stroke volume (impedance cardiography). Auditory stimuli caused abrupt increases in systolic and diastolic pressures (21 +/- 2 and 15 +/- 1 mmHg) and heart rate (11 +/- 2 beats/min). Cardiac output decreased (-10%). Stimuli that produced EEG evidence of arousal evoked one to two large bursts of sympathetic activity (316 +/- 46% of baseline amplitude). Stimuli that did not alter EEG frequency produced smaller but consistent pressor responses even though no sympathetic activation was observed. We conclude that arousal from NREM sleep evokes a pressor response caused by increased peripheral vascular resistance. Increased sympathetic outflow to skeletal muscle may contribute to, but is not required for, this vasoconstriction. The neurocirculatory effects of arousal may augment those caused by asphyxia during episodes of sleep-disordered breathing.

Kainic acid lesions of the median preoptic nucleus: effects on angiotensin II induced drinking and pressor responses in the conscious rat

1988 ◽  
Vol 66 (8) ◽  
pp. 1082-1086 ◽  
Author(s):  
D. L. Jones
Keyword(s):  
Angiotensin Ii ◽  
Kainic Acid ◽  
Pressor Response ◽  
Cerebral Ventricle ◽  
Central Administration ◽  
Preoptic Region ◽  
Conscious Rat ◽  
Drinking Response ◽  
Pressor Responses ◽  
Lateral Cerebral Ventricle

Input to the nucleus medianus of the preoptic region has been suggested to be involved in both the drinking and pressor responses elicited by the central administration of angiotensin II. Evidence in support of this suggestion has been gained principally from electrical lesion experiments. This lesion procedure does not differentiate between the cells of the region and fibers coursing through the region. To test the hypothesis that cells in this region are involved in both the pressor and drinking responses elicited by central administration of angiotensin II, injections of kainic acid were made to induce lesions of the cells, while sparing fibers of passage. Drinking and blood pressure responses were determined pre- and post-lesion in the chronically instrumented awake rat. Injections of 50 ng angiotensin II in a 2-μL volume into a lateral cerebral ventricle of the conscious rat elicited pronounced drinking and pressor responses with a latency of 3–5 min. Lesions of the median preoptic region produced by injecting 1.0 μg of kainic acid in 0.25 μL for 15 s attenuated or blocked the drinking response and increased the latency to drink induced by central injections of angiotensin II. However, kainic acid lesions did not significantly alter the pressor responses produced by angiotensin II administration. These results suggest that cells in the median preoptic region are involved in the drinking response but do not participate in the pressor response elicited by angiotensin II administration into a lateral cerebral ventricle of the conscious rat.

Cluster Headache: Heart Rate and Blood Pressure Changes During Spontaneous Attacks

Cephalalgia ◽  
1982 ◽  
Vol 2 (2) ◽  
pp. 61-70 ◽  
Author(s):  
David Russell ◽  
Are von der Lippe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cluster Headache ◽  
Diastolic Blood Pressure ◽  
Head Pain ◽  
The Mean ◽  
Significant Change ◽  
Pressure Changes ◽  
Change In Mean ◽  
Mean Heart Rate

The ECG findings before, during and following 81 spontaneous attacks of cluster headache in 24 patients have been recorded using a Holter cardiography system. No significant change in mean heart rate was found during attacks, when all attacks were considered as a group. Attacks which began when patients were awake differed from those which began during sleep as regards changes in mean heart rate. The mean heart rate decreased during the majority (61%) of attacks which began when patients were awake, whereas it remained unchanged or increased during the majority (67.5%) of attacks which began during sleep. The attacks which began when patients were awake also had higher absolute mean heart rate values before, during and following attacks compared to similar values for those attacks which began during sleep. Blood pressure was measured during 11 attacks and showed a significant increase in both systolic and diastolic blood pressure. The heart rate and blood pressure in six patients usually increased during induced head pain.

scholarly journals A New Understanding for Preoperative Management in a Patient with Blunt Brachiocephalic Trunk Injury

2021 ◽  
Vol 24 (2) ◽  
pp. E376-E378
Author(s):  
Lei Wang ◽  
Hong-mei Wang ◽  
Dai-peng Zhou ◽  
Yan-fei Xia ◽  
Kai Kang
Keyword(s):  
Adrenergic Receptor ◽  
Low Dose ◽  
Vital Signs ◽  
Preoperative Preparation ◽  
Preoperative Management ◽  
Physiological Factors ◽  
Brachiocephalic Trunk ◽  
Preparation Period ◽  
Receptor Blockers ◽  
Adrenergic Receptor Agonist

We report a case of a 24-year-old male patient with blunt brachiocephalic trunk injury, who was given low-dose dexmedetomidine (DEX) for 2 weeks to help smoothly pass the preparation period before the recanalization operation. Because the patient’s vital signs were stable after the injury, the surgeon did not perform emergency surgery. Taking into account the characteristics of blunt brachiocephalic trunk injury, it is necessary to avoid damage to or even rupture of brachiocephalic trunk resulting from irritability and high blood pressure. Patients should be sedated to avoid hemodynamic fluctuations that may be caused by cerebral ischemia and restlessness, and based on the patient’s neurological symptoms, prevention or treatment of perioperative neurocognitive disorders (PNDs) cannot be ignored. Therefore, the choice of drugs for bridging the preoperative preparation stage is crucial. DEX is an α2-adrenergic receptor agonist with antianxiety, analgesic, and sedative effects. It can also stabilize hemodynamics, regulate neuroinflammation, and provide neuroprotection. Instead of using either β-adrenergic receptor antagonists or sedatives, the patient received only low-dose DEX during preoperative preparation. DEX achieved the effects of β-adrenergic receptor blockers, vasodilators, and other sedatives, and it also had certain benefits for the patient’s PND. In short, based on our understanding of the relevant physiological factors, risk factors of brachiocephalic trunk injury, and the effects of DEX, low-dose DEX provides a good option for preoperative management in a patient with blunt brachiocephalic trunk injury.

scholarly journals Habitual cigarette smoking raises pressor responses to spontaneous bursts of muscle sympathetic nerve activity

2019 ◽  
Vol 317 (2) ◽  
pp. R280-R288 ◽  
Author(s):  
Jian Cui ◽  
Rachel C. Drew ◽  
Matthew D. Muller ◽  
Cheryl Blaha ◽  
Virginia Gonzalez ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Activity ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Pressor Responses ◽  
Averaging Techniques

Smoking is a risk factor for cardiovascular diseases. Prior reports showed a transient increase in blood pressure (BP) following a spontaneous burst of muscle sympathetic nerve activity (MSNA). We hypothesized that this pressor response would be accentuated in smokers. Using signal-averaging techniques, we examined the BP (Finometer) response to MSNA in 18 otherwise healthy smokers and 42 healthy nonsmokers during resting conditions. The sensitivities of baroreflex control of MSNA and heart rate were also assessed. The mean resting MSNA, heart rate, and mean arterial pressure (MAP) were higher in smokers than nonsmokers. The MAP increase following a burst of MSNA was significantly greater in smokers than nonsmokers (Δ3.4 ± 0.3 vs. Δ1.6 ± 0.1 mmHg, P < 0.001). The baroreflex sensitivity (BRS) of burst incidence, burst area, or total activity was not different between the two groups. However, cardiac BRS was lower in smokers than nonsmokers (14.6 ± 1.7 vs. 24.6 ± 1.5 ms/mmHg, P < 0.001). Moreover, the MAP increase following a burst was negatively correlated with the cardiac BRS. These observations suggest that habitual smoking in otherwise healthy individuals raises the MAP increase following spontaneous MSNA and that the attenuated cardiac BRS in the smokers was a contributing factor. We speculate that the accentuated pressor increase in response to spontaneous MSNA may contribute to the elevated resting BP in the smokers.

Commissural NTS contributes to pressor responses to glutamate injected into the medial NTS of awake rats

1996 ◽  
Vol 270 (6) ◽  
pp. R1220-R1225 ◽  
Author(s):  
E. Colombari ◽  
J. V. Menani ◽  
W. T. Talman
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Baroreceptor Reflex ◽  
Electrolytic Lesion ◽  
Conscious Rats ◽  
Reflex Pathways ◽  
Pressor Responses ◽  
Reflex Activation ◽  
Change In Mean ◽  
Awake Rats

In the present study we investigated whether interruption of the chemoreceptor reflex by an electrolytic lesion of the commissural subnucleus of the nucleus tractus solitarii (commNTS) influenced pressor and bradycardic responses induced by microinjection of L-glutamate (L-Glu) into the medial NTS (mNTS) of conscious rats. Seven days after sham lesions, seven rats demonstrated significant pressor [change in mean arterial pressure (MAP) = +33 +/- 3 mmHg] and bradycardic [change in heart rate (HR) = -74 +/- 8 beats/min (bpm)] responses to chemoreceptor reflex activation by intravenous injection of KCN. Likewise, L-Glu (1 nmol in 100 nl) injected into the mNTS in sham rats induced pressor (+29 +/- 2 mmHg) and bradycardic responses (-90 +/- 8 bpm). However, in 11 rats with lesions in commNTS, pressor and bradycardic chemoreceptor reflex responses were abolished, and injection of L-Glu into the mNTS decreased MAP (-14 +/- 6 mmHg) and HR (-59 +/- 16 bpm) as is reported in anesthetized control rats. We conclude that pressor responses induced by L-Glu microinjected into the baroreceptor reflex region of mNTS in conscious rats depend on the integrity of the commNTS, which plays an important role in central chemoreceptor reflex pathways.

Pressor response buffering by beta-adrenergic and cholinergic vasodilation in tranquilized dogs

1979 ◽  
Vol 236 (1) ◽  
pp. H165-H173 ◽  
Author(s):  
J. M. Evans ◽  
C. F. Knapp ◽  
T. R. Lowery
Keyword(s):  
Heart Rate ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Beta Blockade ◽  
Lower Heart Rate ◽  
Beta Adrenergic ◽  
Intravenous Injections ◽  
Pressor Responses ◽  
Control State

Buffering of alpha-receptor-mediated pressor responses by beta-adrenergic or cholinergic vasodilation in tranquilized, chronically instrumented gos was investigated. Increases in aortic pressure were produced in the same animal by intravenous injections of phenylephrine in the control state and in three successive experimental states by 1) pacing the heart to remove the reflex capability to lower heart rate, 2) pacing the heart and beta-blockade to remove beta-adrenergic vascular buffering, and 3) beta-blockade plus atropine to also remove cholinergic vascular buffering. The pressor response in each experimental state was greater than that in the state preceding it. With the combined beta-adrenergic and cholinergic blockade, the pressor response to an alpha-receptor stimulation was three times greater than that of the control state. From an analysis of the components of the pressor response, cardiac output, and peripheral resistance, it is suggested that normal buffering of an alpha-mediated pressor response may include beta-adrenergic and cholinergic vascular dilation in addition to a decrease in heart rate.

Cardiovascular actions of vasopressin: baroreflex modulation in the conscious rat

1986 ◽  
Vol 251 (6) ◽  
pp. H1244-H1251 ◽  
Author(s):  
R. L. Webb ◽  
J. W. Osborn ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Base Line ◽  
Ang Ii ◽  
Response Curves ◽  
Conscious Rat ◽  
Cardiovascular Actions ◽  
Pressor Responses ◽  
Baroreceptor Reflexes

Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were recorded during graded infusions of arginine vasopressin (AVP), angiotensin II (ANG II), and phenylephrine (PE) in conscious, unrestrained, sinoaortic-denervated (SAD) and normal rats. Base-line MAP, CO, and TPR values before infusion were not different between groups. HR values were significantly higher in SAD rats. Dose-response curves indicated that there was a similar enhancement in pressor sensitivity to AVP, ANG II, and PE in the absence of the baroreceptors. Pressor responses to AVP were buffered by offsetting decreases of CO. Similar elevations in MAP evoked a 50% greater reduction in CO with AVP, and HR decreased 1.5 times as much with AVP than with ANG II or PE. The dose of AVP required to raise MAP by 25 mmHg in control rats resulted in similar falls of CO in SAD rats, whereas HR responses to AVP were attenuated significantly in SAD rats. We conclude that baroreceptor buffering of AVP-induced pressor responses is due principally to reflex reduction of TPR. Furthermore, CO suppression was not baroreflex-mediated, whereas bradycardia was reflex dependent. Finally, in rats, AVP does not appear to interact with the baroreceptor reflexes in a manner unique from other vasoconstrictor agents to buffer MAP.

Intravenous morphine infusion (IMF) to drug-naive, conscious rats evokes bradycardic, hypotensive effects, but pressor actions are elicited after IMF to rats previously given morphine

1989 ◽  
Vol 67 (3) ◽  
pp. 213-222 ◽  
Author(s):  
J. A. Thornhill ◽  
C. Townsend ◽  
L. Gregor
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Infusion Pump ◽  
Morphine Sulphate ◽  
Vagal Activity ◽  
Chronic Morphine ◽  
Morphine Infusion ◽  
Drug Naïve ◽  
Mean Heart Rate

Hemodynamic (blood pressure and heart rate) responses of conscious drug-naive rats were studied following intravenous (i. v.) infusion of sterile saline, morphine sulphate, and then naloxone hydrochloride, as well as of other groups previously injected with morphine sulphate. Those groups chronically given morphine sulphate received twice daily injections of morphine sulphate (5 mg/kg, s.c. per injection) for 3 or 6 days before testing with the i. v. infusion of morphine sulphate. Drugs were infused (135 μL/min) through an indwelling femoral venous catheter via a Harvard infusion pump, and blood pressure was recorded from the abdominal aorta via a femoral arterial catheter. Other pretreatment studies were done to determine the receptor mechanisms mediating the blood pressure responses of drug-naive and chronic morphine-treated rats, whereby equimolar doses (0.32 μmol) of specific receptor antagonists were given as a bolus i.v. injection 5 min after saline but before subsequent infusion with morphine sulphate. Intravenous infusion of morphine sulphate (7.5 mg/kg total over 15 min) to drug-naive rats caused a transient but precipitous fall in mean arterial pressure and mean heart rate with an associated rise in mean pulse pressure; these effects were blocked in other groups pretreated with atropine. Interestingly, however, rats chronically injected with morphine sulphate for 3 days previously evoked a transient pressor response when subsequently infused i.v. with morphine sulphate, actions that were blocked in other groups when pretreated i.v. with 0.32 μmol of phentolamine, yohimbine, prazosin, or guanethidine. A greater and persistent pressor response occurred following morphine infusion to groups of rats previously injected over 6 days with morphine sulphate, which was associated with tachycardia during the later stages of the 15-min morphine sulphate infusion period. The prolonged pressor and tachycardic responses of this 6-day chronically injected group were completely blocked in another group pretreated i.v. with both phentolamine and propranolol (0.32 μmol). The results suggest that morphine sulphate infusion to conscious, drug-naive rats evokes classical hypotensive effects due to decreases in mean heart rate caused by activation of parasympathetic vagal activity. With 3 or 6 days of chronic morphine sulphate administration beforehand, subsequent i.v. infusion of morphine sulphate evoked pressor actions felt to be caused by a progressive activation of the sympathetic nervous system. These events cause vasoconstriction of peripheral vasculature and, with time, increased cardiac frequency, actions that can be blocked by pretreatment with specific α- and β-adrenergic receptor blockers.Key words: drug-naive rats, morphine-pretreated rats, acute hypotension, bradycardia, chronic pressor responses, opiate and non-opiate receptor blockade.

Sign in / Sign up

Export Citation Format

Share Document