scholarly journals Evaluation for roles of nitric oxide generated in the anteroventral third ventricular region in controlling vasopressin secretion and cardiovascular system of conscious rats

2000 ◽  
pp. 523-533 ◽  
Author(s):  
K Yamaguchi ◽  
K Watanabe ◽  
K Yamaya
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Cardiovascular System ◽  
Plasma Osmolality ◽  
Cardiovascular Responses ◽  
Prostaglandin E ◽  
Adjacent Area ◽  
Conscious Rats ◽  
Cardiovascular Variables

OBJECTIVE: To examine local actions of nitric oxide (NO) on the neural mechanisms controlling the release of vasopressin (AVP) and the cardiovascular system in the anteroventral third ventricular region (AV3V), a pivotal area for autonomic functions, and to pursue the problem of whether it may have any role in the AVP and cardiovascular responses evoked by plasma hypertonicity or by increased prostaglandin E(2) (PGE(2)) in the AV3V - one possible factor implicated in osmotic responses. METHODS: We infused NO-related agents into the AV3V, its adjacent area, the nucleus of the vertical limb of the diagonal band (VDB), or into the lateral cerebral ventricle of conscious rats, monitoring effects on plasma AVP, osmolality, sodium, potassium and chloride, arterial pressure and heart rate in the presence or absence of an osmotic or PGE(2) stimulus. The infusion sites were determined histologically. RESULTS: Infusion of L-arginine, the substrate of NO synthase (NOS), into the AV3V structures such as the median preoptic nucleus and periventricular nucleus produced dose-related increases in plasma AVP, arterial pressure and heart rate 5 or 15 min later, whereas infusion of D-arginine (which is not a substrate for NO synthesis) was without significant effect on these variables. Plasma osmolality or electrolytes were not changed by these treatments. The AV3V infusion of sodium nitroprusside (SNP), a spontaneous releaser of NO, also induced dose-dependent augmentations of plasma AVP, without evoking remarkable alteration in the cardiovascular parameters. The infusion of L- or D-arginine into the VDB affected none of the variables significantly. When applied intracerebroventricularly, L-arginine caused only increases in plasma AVP, whereas SNP caused only reductions in arterial pressure, leaving other variables at stable values. The effects of AV3V L-arginine on plasma AVP and the cardiovascular variables were abolished by N(G)-nitro-L-arginine methyl ester (L-NAME), a potent inhibitor of NOS, applied 15 min before. In contrast, infusion of L-NAME to the AV3V did not exert a significant effect on the responses of plasma AVP or cardiovascular variables to AV3V application of PGE(2) or i.v. infusion of hypertonic NaCl. The infusion of L-NAME alone did not affect plasma variables including AVP, although it tended to increase basal arterial pressure and heart rate. CONCLUSION: These results suggest that NO generated in or near the AV3V may act to enhance AVP release, arterial pressure and heart rate, but it may not play an essential role in eliciting the responses of these variables to osmotic or PGE(2) stimuli.

Cardiovascular responses attenuate with repeated NO synthesis inhibition in conscious fetal sheep

1998 ◽  
Vol 274 (5) ◽  
pp. H1472-H1480 ◽  
Author(s):  
A. Chlorakos ◽  
B. L. Langille ◽  
S. L. Adamson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
High Heart Rate ◽  
Synthesis Inhibitor ◽  
Fetal Sheep ◽  
Synthesis Inhibition ◽  
Near Term ◽  
Cardiovascular Variables

The cardiovascular effects of repeated administration of the nitric oxide (NO) synthesis inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) were assessed daily for 3 days in fetal sheep near term (124–126 days gestation) beginning 4 days after surgery ( n = 7). In the first hour on day 1, fetal infusion ofl-NAME (30 mg bolus, 6 mg/min infusion iv for 3 h) significantly increased fetal arterial pressure from 41 ± 2 to 58 ± 3 mmHg, decreased heart rate from 173 ± 5 to 134 ± 3 beats/min, increased umbilicoplacental resistance from 0.16 ± 0.02 to 0.28 ± 0.07 mmHg ⋅ ml−1 ⋅ min, and inhibited the hypotensive response to acetylcholine (ACh; 2 μg iv bolus). All changes were sustained except for arterial pressure, which decreased significantly to 50 ± 3 mmHg in the third hour. Within 17 h, all cardiovascular variables returned to control.l-NAME readministered on days 2 and 3 had no effect on cardiovascular variables. l-NAME did not potentiate the pressor response to angiotensin II on day 2 and caused a surprising attenuation of the pressor response to endothelin-1 on day 3. We conclude that, whereas NO normally contributes to low arterial pressure, high heart rate, and low umbilicoplacental vascular resistance in fetal sheep near term, the role of NO in these functions is replaced by an alternate mechanism within 17 h after NO synthesis inhibition withl-NAME.

scholarly journals Plasma hyperosmolality and arterial pressure regulation during heating in dehydrated and awake rats

1998 ◽  
Vol 275 (5) ◽  
pp. R1703-R1711 ◽  
Author(s):  
Yasufumi Nakajima ◽  
Hiroshi Nose ◽  
Akira Takamata
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Skin Blood Flow ◽  
Plasma Osmolality ◽  
Cardiovascular Responses ◽  
Pressure Regulation ◽  
Highly Correlated ◽  
Arterial Pressure Regulation

To gain better insights into the effect of dehydration on thermal and cardiovascular regulation during hyperthermia, we examined these regulatory responses during body heating in rats under isosmotic hypovolemia and hyperosmotic hypovolemia. Rats were divided into four groups: normovolemic and isosmotic (C), hypovolemic and isosmotic [L, plasma volume loss (ΔPV) = −20% of control], hypovolemic and less hyperosmotic [HL1, increase in plasma osmolality (ΔPosm) = 23 mosmol/kgH2O, ΔPV = −16%], and hypovolemic and more hyperosmotic (HL2, ΔPosm = 52 mosmol/kgH2O, ΔPV = −17%). Hyperosmolality was attained by subcutaneous injection of hypertonic saline and hypovolemia by intra-arterial injection of furosemide before heating. Then rats were placed in a thermocontrolled box (35°C air temperature, ∼20% relative humidity) for 1–2 h until rectal temperatures (Tre) reached 40.0°C. Mean arterial pressure in L decreased with rise in Tre( P < 0.001), whereas mean arterial pressure remained constant in the other groups. Maximal tail skin blood flow in L, HL1, and HL2 was decreased to ∼30% of that in C ( P < 0.001). Tre threshold for tail skin vasodilation (TVD) was not changed in L, whereas the threshold shifted higher in the HL groups. Trethreshold for TVD was highly correlated with Posm( r = 0.94, P < 0.001). Heart rate in the HL groups increased with rise in Tre( P < 0.001), whereas it remained unchanged in C and L. Cardiovascular responses to heating were not influenced by V1 antagonist in C, L, and HL2. Thus isotonic hypovolemia attenuates maximal tail skin blood flow, whereas hypertonic hypovolemia causes an upward shift of Tre threshold for TVD and an increase in heart rate during hyperthermia. These results suggest that plasma hyperosmolality stimulates pressor responses in the hypovolemic condition that subsequently contribute to arterial pressure regulation during heat stress.

Electrical stimulation of the carotid sinus lowers arterial pressure and improves heart rate variability in l-NAME hypertensive conscious rats

2020 ◽  
Vol 43 (10) ◽  
pp. 1057-1067 ◽  
Author(s):  
Gean Domingos-Souza ◽  
Fernanda Machado Santos-Almeida ◽  
César Arruda Meschiari ◽  
Nathanne S. Ferreira ◽  
Camila A. Pereira ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Conscious Rats ◽  
Stimulation Of

Cardiovascular Responses to Muscle Stretching: A Systematic Review and Meta-analysis

2021 ◽  
Author(s):  
Ewan Thomas ◽  
Marianna Bellafiore ◽  
Ambra Gentile ◽  
Antonio Paoli ◽  
Antonio Palma ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular System ◽  
Vascular Function ◽  
Meta Analysis ◽  
Random Effect ◽  
Cardiovascular Responses ◽  
Qualitative Description ◽  
Cross Sectional ◽  
Quantitative Synthesis

AbstractThe aim of this study will be to review the current body of literature to understand the effects of stretching on the responses of the cardiovascular system. A literature search was performed using the following databases: Scopus, NLM Pubmed and ScienceDirect. Studies regarding the effects of stretching on responses of the cardiovascular system were investigated. Outcomes regarded heart rate(HR), blood pressure, pulse wave velocity (PWV of which baPWV for brachial-ankle and cfPWV for carotid-femoral waveforms), heart rate variability and endothelial vascular function. Subsequently, the effects of each outcome were quantitatively synthetized using meta-analytic synthesis with random-effect models. A total of 16 studies were considered eligible and included in the quantitative synthesis. Groups were also stratified according to cross-sectional or longitudinal stretching interventions. Quality assessment through the NHLBI tools observed a “fair-to-good” quality of the studies. The meta-analytic synthesis showed a significant effect of d=0.38 concerning HR, d=2.04 regarding baPWV and d=0.46 for cfPWV. Stretching significantly reduces arterial stiffness and HR. The qualitative description of the studies was also supported by the meta-analytic synthesis. No adverse effects were reported, after stretching, in patients affected by cardiovascular disease on blood pressure. There is a lack of studies regarding vascular adaptations to stretching.

Cardiovascular responses to head-stand posture

1963 ◽  
Vol 18 (5) ◽  
pp. 987-990 ◽  
Author(s):  
Shanker Rao
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
High Pressure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Skin Temperature ◽  
Cardiovascular Responses ◽  
Posterior Tibial Artery ◽  
Nervous Control ◽  
Posterior Tibial

Reports of cardiovascular responses to head-stand posture are lacking in literature. The results of the various responses, respectively, to the supine, erect, and head-stand posture, are as follows: heart rate/min 67, 84, and 69; brachial arterial pressure mm Hg 92, 90, and 108; posterior tibial arterial pressure mm Hg 98, 196, and 10; finger blood flow ml/100 ml min 4.5, 4.4, and 5.2; toe blood flow ml/100 ml min 7.1, 8.1, and 3.4; forehead skin temperature C 34.4, 34.0 and 34.3; dorsum foot skin temperature C 28.6, 28.2, and 28.2. It is inferred that the high-pressure-capacity vessels between the heart level and posterior tibial artery have little nervous control. The high-pressure baroreceptors take active part in postural adjustments of circulation. The blood pressure equating mechanism is not as efficient when vital tissues are pooled with blood as when blood supply to them is reduced. man; heart rate; blood flow; skin temperature Submitted on January 3, 1963

Rebound cardiovascular responses following stimulation of canine vagosympathetic complexes or cardiopulmonary nerves

1985 ◽  
Vol 63 (9) ◽  
pp. 1122-1132 ◽  
Author(s):  
J. A. Armour ◽  
W. C. Randall
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Cardiovascular System ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Cardiac Responses ◽  
Stimulation Of

Electrical stimulation of a canine vagosympathetic complex or a cardiopulmonary nerve can elicit a variety of negative chronotropic and inotropic cardiac responses, with or without alterations in systemic arterial pressure. In the period immediately following cessation of such a stimulation "rebound" tachycardia, increased inotropism above control values in one or more regions of the heart, and (or) elevation in systemic arterial pressure can occur. These "rebound" phenomena are abolished by propranolol or ipsilateral chronic sympathectomy. It is proposed that "vagal" poststimulation "rebound" of the canine cardiovascular system is primarily the result of activation of sympathetic neural elements present in the vagosympathetic complexes or cardiopulmonary nerves.

Respiratory and cardiovascular responses to static handgrip exercise in humans

1993 ◽  
Vol 75 (6) ◽  
pp. 2789-2796 ◽  
Author(s):  
G. A. Fontana ◽  
T. Pantaleo ◽  
F. Bongianni ◽  
F. Cresci ◽  
R. Manconi ◽  
...  
Keyword(s):  
Heart Rate ◽  
Time Course ◽  
Minute Ventilation ◽  
Muscle Tension ◽  
Maximum Voluntary Contraction ◽  
Cardiovascular Responses ◽  
Inspiratory Flow ◽  
Electromyographic Activity ◽  
Handgrip Exercise ◽  
Cardiovascular Variables

We studied the time course of respiratory and cardiovascular responses by evaluating changes in the breathing pattern, mean blood pressure (MBP), and heart rate elicited by 3 min of static handgrip at 15, 25, and 30% of the maximum voluntary contraction (MVC) in 15 healthy volunteers. Muscle tension and integrated electromyographic activity remained fairly constant during each trial. During 15% MVC bouts, initially only mean inspiratory flow increased; then, tidal volume and minute ventilation (VI) also rose progressively. No significant changes in MBP and heart rate were observed. During 25 and 30% MVC bouts, not only did mean inspiratory flow, VT, and VI increase but MBP and heart rate increased as well. A slight and delayed rise in respiratory rate was also observed. Unlike 15 and 25% MVC handgrip, 30% MVC handgrip caused a small decrease in end-tidal PCO2. Changes in the pattern of breathing occurred more promptly than those in cardiovascular variables in the majority of subjects. Furthermore, we found a positive correlation between changes in VI and those in cardiovascular variables at the end of 25 and 30% MVC trials. This study indicates that respiratory and cardiovascular responses to static handgrip exercise are controlled independently.

scholarly journals Role of nitric oxide-containing factors in the ventilatory and cardiovascular responses elicited by hypoxic challenge in isoflurane-anesthetized rats

2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vital Role ◽  
Initial Increase ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Before And After

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.

scholarly journals Regulation of arterial pressure by the paraventricular nucleus in conscious rats: interactions among glutamate, GABA, and nitric oxide

2013 ◽  
Vol 3 ◽  
Author(s):  
Marli C. Martins-Pinge ◽  
Patrick J. Mueller ◽  
C. Michael Foley ◽  
Cheryl M. Heesch ◽  
Eileen M. Hasser
Keyword(s):  
Nitric Oxide ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Conscious Rats

Glycine microinjected into nucleus tractus solitarii of rat acts through cholinergic mechanisms

1991 ◽  
Vol 260 (4) ◽  
pp. H1326-H1331 ◽  
Author(s):  
W. T. Talman ◽  
J. M. Colling ◽  
S. C. Robertson
Keyword(s):  
Heart Rate ◽  
Nmda Receptor ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Cardiovascular Regulation ◽  
Nucleus Tractus Solitarii ◽  
Receptor Blockade ◽  
Receptor Complex ◽  
Cholinergic Mechanisms ◽  
Nmda Receptor Complex

Previous studies have demonstrated the release of glycine from neurotransmitter pools in the region of the nucleus tractus solitarii (NTS) where cardiovascular afferents terminate. Microinjection of glycine into NTS elicits decreases in arterial pressure and heart rate; these effects are also produced by glutamate or acetylcholine. As glycine may act both at the N-methyl-D-aspartate (NMDA)-receptor complex and centrally to release acetylcholine, we have sought to determine whether the cardiovascular responses to exogenous glycine are mediated through glutamatergic or cholinergic mechanisms. Responses to glycine microinjected into the NTS of anesthetized rats were not affected by blockade of the NMDA receptor complex but, like acetylcholine, were blocked by muscarinic receptor blockade. Physostigmine prolonged responses to glycine. Subthreshold doses of glycine, which augmented responses to acetylcholine microinjected into NTS, either decreased or had no effect on glutamate or NMDA. This study supports a role for glycine in cardiovascular regulation by the NTS and suggests that the actions of glycine may be effected, at least in part, through cholinergic mechanisms.

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