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.

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.

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.

Stress and cocaine elicit similar cardiac output responses in individual rats

1993 ◽  
Vol 265 (2) ◽  
pp. H779-H782 ◽  
Author(s):  
M. M. Knuepfer ◽  
C. A. Branch ◽  
P. J. Mueller ◽  
Q. Gan
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Cardiovascular Responses ◽  
Aortic Blood Flow ◽  
Conscious Rats ◽  
Air Jet ◽  
Behavioral Stress ◽  
Pressor Responses ◽  
Output Only

Cocaine use and behavioral stress elicit variable cardiovascular responses in individuals. In the present study, we examined the effects of cocaine or stress on arterial pressure, heart rate, and cardiac output in conscious rats. Rats were instrumented for determination of ascending aortic blood flow as an index of cardiac output using pulsed Doppler flow-metry. Cocaine administration elicited consistent decreases in cardiac output in some rats, whereas others had increases. In contrast, the pressor and heart rate responses were similar in these two groups of animals. Air jet stress also elicited a decrease in cardiac output only in a subset of conscious rats, yet produced equivalent pressor responses in all rats. Cardiac output responses to cocaine and air jet stress were closely correlated in individual rats, indicating that these stimuli evoke similar hemodynamic responses in individual rats. These observations suggest that the rat may provide a model for understanding differential cardiovascular sensitivity to cocaine and/or stress in humans.

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.

Effect of Intraventricular Perfusion of Angiotensin II in Conscious Normal Rats and in Rats with Hereditary Hypothalamic Diabetes Insipidus

1976 ◽  
Vol 51 (s3) ◽  
pp. 391s-394s
Author(s):  
J. S. Hutchinson ◽  
P. Schelling ◽  
J. Möhring ◽  
D. Ganten
Keyword(s):  
Angiotensin Ii ◽  
Diabetes Insipidus ◽  
Pressor Response ◽  
Cerebral Ventricles ◽  
Basal Secretion ◽  
Artificial Cerebrospinal Fluid ◽  
Pressor Responses ◽  
Long Evans ◽  
Hereditary Hypothalamic Diabetes Insipidus ◽  
Intact Rats

1. Artificial cerebrospinal fluid was perfused through the cerebral ventricles of conscious rats. A basal secretion rate of 16 ± 3 × 10—15 mol of immunoreactive angiotensin 11/min was calculated for intact rats. 2. Most of the immunoreactive angiotensin II consisted probably of the heptapeptide or pentapeptide angiotensin II fragments. 3. The pressor responses to intraventricular perfusions of angiotensin II were normal in Long—Evans rats, virtually absent in rats homozygous for hereditary hypothalamic diabetes insipidus, irrespective of whether they were injected with vasopressin tannate or not, and intermediate in rats heterozygous for hypothalamic diabetes insipidus. 4. The results suggest that the pressor response to intraventricular angiotensin II is related to the release of vasopressin.

Systemic arterial pressor responses induced by potassium in dogfish, Squalus acanthias

1981 ◽  
Vol 241 (3) ◽  
pp. R228-R232
Author(s):  
D. F. Opdyke ◽  
R. G. Carroll ◽  
N. E. Keller
Keyword(s):  
Pressor Response ◽  
Muscle Tension ◽  
Plasma Catecholamines ◽  
Blocking Agent ◽  
Adrenergic Stimulation ◽  
Direct Exposure ◽  
Pressor Responses ◽  
Before And After ◽  
K Concentration

Intravascular injection of small doses of potassium (0.025-0.5 meq) into dogfish results in dose-related dorsal aortic pressor responses. The responses are blocked by phentolamine, an alpha-adrenergic blocking agent. Assays of plasma catecholamines before and after injection of potassium (K+) showed that plasma levels of epinephrine (E) and norepinephrine (NE) had increased significantly (E, 314%; NE, 233%) 1 min after injection. The pressor responses were initiated 40-90 s after K+ injection at which time plasma E and NE levels were already significantly elevated. Experiments on isolated dogfish arterial strips showed that phentolamine cannot block the increase in vascular smooth muscle tension that occurs after direct exposure to small increases (0.003 meq/ml) in K+ concentration. Because phentolamine effectively blocks the pressor response to even higher doses of K+ in vivo, it is thought that, in addition to any direct vasoconstrictor effect or K+, the adrenergic stimulation provided by catecholamine release is required to produce the observed pressor response.

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.

Stereoselective actions of S-nitrosocysteine in central nervous system of conscious rats

1997 ◽  
Vol 272 (5) ◽  
pp. H2361-H2368 ◽  
Author(s):  
R. L. Davisson ◽  
M. D. Travis ◽  
J. N. Bates ◽  
A. K. Johnson ◽  
S. J. Lewis
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Intracerebroventricular Injection ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Recognition Sites ◽  
Pressor Responses ◽  
The Central Nervous System ◽  
Intracerebroventricular Injections

This study examined whether the stereoselective actions of S-nitrosocysteine (SNC) in the central nervous system involves the activation of stereoselective SNC recognition sites. We examined the effects produced by intracerebroventricular injection of the L- and D-isomers of SNC (L- and D-SNC) on mean arterial blood pressure, heart rate, and vascular resistances in conscious rats. We also examined the hemodynamic effects produced by intracerebroventricular injections of 1) L-cystine, the major non-nitric oxide (NO) decomposition product of L-SNC, 2) the parent thiols L- and D-cysteine, and 3) the bulky S-nitrosothiol L-S-nitroso-gamma-glutamylcysteinylglycine [L-S-nitrosoglutathione, (L-SNOG)]. Finally, we examined the decomposition of L- and D-SNC and L-SNOG to NO on their addition to brain homogenates. The intracerebroventricular injection of L-SNC (250-1,000 nmol) produced falls in mean arterial pressure, increases in heart rate, and a dose-dependent pattern of changes in hindquarter, renal, and mesenteric vascular resistances. The intracerebroventricular injections of D-SNC, L-cystine, and L-SNOG produced only minor effects. The intracerebroventricular injection of L-cysteine produced pressor responses and tachycardia, whereas D-cysteine was inactive. L- and D-SNC decomposed equally to NO on addition to brain homogenates. L-SNOG decomposed to similar amounts of NO as L- and D-SNC. These results suggest that SNC may activate stereoselective SNC recognition sites on brain neurons and that S-nitrosothiols of substantially different structure do not stimulate these sites. These recognition sites may be stereoselective membrane-bound receptors for which L-SNC is the unique ligand.

Acute effects of ethanol on baroreceptor reflex control of heart rate and on pressor and depressor responsiveness in rats

1987 ◽  
Vol 65 (5) ◽  
pp. 834-841 ◽  
Author(s):  
A-R. A. Abdel-Rahman ◽  
Roy Russ ◽  
J. A. Strickland ◽  
W. R. Wooles
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Baroreflex Sensitivity ◽  
Pressor Response ◽  
Base Line ◽  
Response Curves ◽  
Baroreflex Control ◽  
Conscious Rats ◽  
Upward Shift ◽  
The Right

In rats anesthetized with α-chloralose, doses of 0.1, 0.5, and 1 g/kg of ethanol produced an upward shift of baroreflex curves constructed by plotting the heart rate response against mean arterial pressure following evoked rises in mean arterial pressures by phenylephrine or angiotensin II. Whereas the upward shift of baroreceptor curves may be related, at least in part, to a higher base-line heart rate after ethanol, the data showed that the 1 g/kg dose of ethanol significantly depressed baroreflex sensitivity, suggesting that higher doses of ethanol impair baroreflex-mediated bradycardia. The phenylephrine, but not the angiotensin II or the nitroprusside, dose–response curves were shifted to the right after ethanol, indicating a decreased pressor responsiveness and suggesting that ethanol may have α-adrenergic blocking activity. This effect was also obtained in conscious rats. That this effect was not influenced by changes in baroreflex sensitivity was supported by the finding that a similar shift of the phenylephrine pressor–response curve was obtained in bilaterally vagotomized and hexamethonium-treated rats. Whether this effect of ethanol on baroreflex control of heart rate was influenced by anesthesia was investigated in conscious rats; the 1 g/kg dose of ethanol that produced the most significant decrease in baroreflex sensitivity was used in these experiments. Ethanol was still able to significantly inhibit baroreflex sensitivity in conscious rats, but the upward shift of the baroreflex curve and the elevated base-line heart rate no longer occurred. On the other hand, none of the three doses of ethanol had any significant effect on baroreflex-mediated tachycardia (in response to nitroprusside-evoked hypotension). The data suggest that high doses of ethanol selectively inhibit baroreflex-mediated bradycardia and that ethanol has an α-blocking-like activity in conscious and anesthetized rats.

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.

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