scholarly journals Voltage-Sensitive K+ Channels Inhibit Parasympathetic Ganglion Transmission and Vagal Control of Heart Rate in Hypertensive Rats

2015 ◽  
Vol 6 ◽  
Author(s):  
Torill Berg
Keyword(s):  
Heart Rate ◽  
Hypertensive Rats ◽  
K Channels ◽  
Vagal Control ◽  
Parasympathetic Ganglion

Ruta montana evokes antihypertensive activity through increase of prosta-glandins release in L-NAME-induced hypertensive rats

2020 ◽  
Vol 20 ◽  
Author(s):  
El-Ouady Fadwa ◽  
Mohamed Eddouks
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Aqueous Extract ◽  
Antihypertensive Effect ◽  
Antihypertensive Activity ◽  
Computer Assisted ◽  
Hypertensive Rats ◽  
Vasorelaxant Effect ◽  
Vasorelaxant Activity ◽  
Ruta Montana

Aims: The aim of the study was to investigate experimentally the antihypertensive effect of Ruta Montana. Background: Ruta montana L. is traditionally used in Moroccan herbal medicine to treat hypertension. This study aimed to evaluate experimentally the hypotensive and vasoactive properties of this plant. Objective: The objective of the study was to evaluate the effect of the aqueous extract of Ruta Montana on blood pressure parameters in LNAME-induced hypertensive rats and to determine the vasorelaxant activity of this aqueous extract. Methods: The antihypertensive effect of the aqueous extract obtained from Ruta montana aerial parts (RMAPAE) (200 mg/kg) was evaluated in normal and anesthetized hypertensive rats. Blood pressure parameters (systolic blood pressure (SBP), mean blood pressure (MBP) and diastolic blood pressure (DBP)) and heart rate were measured using a tail-cuff and a computer-assisted monitoring device. The acute and chronic effect of RMAPAE was recorded during 6 hours for the acute experiment and during 7 days for the sub-chronic test. In the other set, the vasorelaxant effect of RMAPAE on the contractile response was undertaken in isolated thoracic aorta. Results: The results indicated that RMAPAE extract significantly decreased SBP, MBP, DBP and heart rate in L-NAMEinduced hypertensive rats. Furthermore, RMAPAE was demonstrated to induce a dose dependent relaxation in the aorta precontracted with Epinephrine or KCl. More interestingly, this vasorelaxant activity of RMAPAE seems to be probably mediated through the prostaglandins pathway. Conclusion: The present study illustrates the beneficial action of Ruta montana on hypertension and supports then its use as an antihypertensive agent.

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 Role of Ca+-dependent K-channels in the membrane potential and contractility of aorta from spontaneously hypertensive rats

1994 ◽  
Vol 113 (3) ◽  
pp. 1022-1028 ◽  
Author(s):  
Eneida G. Silva ◽  
Eugenio Frediani-Neto ◽  
Alice T. Ferreira ◽  
Antonio CM. Paiva ◽  
Therezinha B. Paiva
Keyword(s):  
Membrane Potential ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
K Channels

Assessment of parasympathetic control of heart rate by a noninvasive method

1984 ◽  
Vol 246 (6) ◽  
pp. H838-H842 ◽  
Author(s):  
F. M. Fouad ◽  
R. C. Tarazi ◽  
C. M. Ferrario ◽  
S. Fighaly ◽  
C. Alicandri
Keyword(s):  
Heart Rate ◽  
Respiratory Sinus Arrhythmia ◽  
Separate Group ◽  
Noninvasive Method ◽  
Sinus Arrhythmia ◽  
Beta Adrenergic ◽  
Normal Volunteers ◽  
Vagal Control ◽  
Parasympathetic Control ◽  
The Relationship

The degree of parasympathetic control of heart rate was assessed by the abolition of respiratory sinus arrhythmia with atropine. Peak-to-peak variations in heart periods (VHP) before atropine injection correlated significantly (r = 0.90, P less than 0.001) with parasympathetic control, indicating that VHP alone may be used as a noninvasive indicator of the parasympathetic control of heart rate. Pharmacologic blockade of beta-adrenergic supply in a separate group of normal volunteers did not alter the relationship between VHP and parasympathetic control, indicating that the condition of the experiment (complete rest in a quiet atmosphere) allows the use of VHP alone without pharmacologic interventions to characterize the vagal control of heart rate in humans.

Cardiac enkephalins attenuate vagal bradycardia: interactions with NOS-1-cGMP systems in canine sinoatrial node

2003 ◽  
Vol 285 (5) ◽  
pp. H2001-H2012 ◽  
Author(s):  
Martin Farias ◽  
Keith Jackson ◽  
Michael Johnson ◽  
James L. Caffrey
Keyword(s):  
Heart Rate ◽  
Phosphodiesterase Inhibitor ◽  
Endogenous Opioids ◽  
Muscarinic Agonist ◽  
No Donor ◽  
Parasympathetic Nerve ◽  
Sa Node ◽  
Vagal Control ◽  
Nos Inhibitors ◽  
Vagal Bradycardia

Endogenous opioids and nitric oxide (NO) are recognized modulators of cardiac function. Enkephalins and inhibitors of NO synthase (NOS) both produce similar interruptions in the vagal control of heart rate. This study was conducted to test the hypothesis that NO systems within the canine sinoatrial (SA) node facilitate local vagal transmission and that the endogenous enkephalin methionine-enkephalin-arginine-phenylalanine (MEAP) attenuates vagal bradycardia by interrupting the NOS-cGMP pathway. Microdialysis probes were inserted into the SA node, and they were perfused with nonselective ( Nω-nitro-l-arginine methyl ester) and neuronal (7-nitroindazole) NOS inhibitors. The right vagus nerve was stimulated and both inhibitors gradually attenuated the resulting vagal bradycardia. The specificity of these inhibitions was verified by an equally gradual reversal of the inhibition with an excess of the NOS substrate l-arginine. Introduction of MEAP into the nodal interstitium produced a quickly developing but quantitatively similar interruption of vagal bradycardia that was also slowly reversed by the addition of l-arginine and not by d-arginine. Additional support for convergence of opioid and NO pathways was provided when the vagolytic effects of MEAP were also reversed by the addition of the NO donor S-nitroso- N-acetyl-penicillamine, the protein kinase G activator 8-bromo-cGMP, or the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. MEAP and 7-nitroindazole were individually combined with the direct acting muscarinic agonist methacholine to evaluate potential interactions with muscarinic receptors within the SA node. MEAP and 7-nitroindazole were unable to overcome the bradycardia produced by methacholine. These data suggest that NO and enkephalins moderate the vagal control of heart rate via interaction with converging systems that involve the regulation of cAMP within nodal parasympathetic nerve terminals.

Chronic isolation of carotid sinus baroreceptor region in conscious normotensive and hypertensive rats

1998 ◽  
Vol 275 (1) ◽  
pp. H322-H329 ◽  
Author(s):  
Kelly P. McKeown ◽  
Artin A. Shoukas
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Baroreceptor Reflex ◽  
Hypertensive Rats ◽  
Conscious Rat ◽  
Sd Rats ◽  
The Right ◽  
Reflex System

We have developed a chronic technique to isolate the carotid sinus baroreceptor region in the conscious rat model. Our technique, when used in conjunction with other methods, allows for the study of the control of arterial pressure, heart rate, and cardiac output by the carotid sinus baroreceptor reflex in conscious, unrestrained rats. The performance of our technique was evaluated in two strains: normotensive Sprague-Dawley (SD) rats and spontaneously hypertensive rats (SHR). Each rat was instrumented with an aortic flow probe and a catheter placed in the right femoral artery to monitor cardiac output and arterial pressure, respectively. The cervical sympathetic trunk and aortic depressor nerve were ligated and cut bilaterally, leaving vagus nerves intact. The right and left carotid sinuses were isolated using our new technique. We tested the open-loop function of the carotid sinus baroreceptor reflex system in the conscious rat after recovery from the isolation surgery. We found that changes in nonpulsatile carotid sinus pressure caused significant changes in arterial pressure, heart rate, and total peripheral resistance in both rat strains. However, the cardiac output responses differed dramatically between strains. Significant changes were seen in the cardiac output response of SHR, whereas no significant changes were observed in normotensive SD rats. We have found this technique to be a highly reliable tool for the study of the carotid sinus baroreceptor reflex system in the conscious rat.

Antihypertensive Effect of Prolonged Blockade of Angiotensin Formation in Benign and Malignant, one- and two-Kidney Goldblatt Hypertensive Rats

1979 ◽  
Vol 57 (1) ◽  
pp. 53-62 ◽  
Author(s):  
R. G. Bengis ◽  
T. G. Coleman
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Normal Pressure ◽  
Hypertensive Rats ◽  
Physiological Basis ◽  
Excretory Function ◽  
Contralateral Kidney ◽  
The One

1. The effect of chronic inhibition of angiotensin II formation was investigated in four groups of hypertensive rats. Benign hypertension was produced by placing a 0·25 mm-diameter silver clip on the renal artery; a 0·20 mm clip was used to create malignant hypertension. A two-kidney model had a clip plus intact contralateral kidney and a one-kidney model had a clip plus contralateral nephrectomy. Benign and malignant groups were prepared in both the one-kidney and two-kidney variations. Converting enzyme inhibitor (SQ 14.225) was given to these four groups for 1 week in drinking water and average intake ranged from 33 to 77 mg/day. 2. The two malignant groups had the highest plasma renin activities and they showed a precipitous fall in arterial pressure in the first 24 h of inhibition of angiotensin formation. All groups showed an additional slow decline in pressure during the remaining 6 days of inhibition. Changes in heart rate and sodium excretion were variable but, in general, heart rate decreased during inhibition. 3. Arterial pressure did not become normal with inhibition in either of the one-kidney models: decreases to 126 and 132 mmHg were observed in the benign and malignant groups respectively. Three of the malignant one-kidney animals became uraemic with inhibition and one died before inhibition was discontinued. 4. Arterial pressure was reduced to normal pressure (95 mmHg) after 1 week of inhibition in both the benign and malignant two-kidney models. 5. It appears that normal pressure was restored in the two-kidney model but not in the one-kidney model because of the presence of the intact contralateral kidney. The physiological basis for this difference is not known but changes in renal excretory function may be involved.

Arterial baroreflex resetting mediates postexercise reductions in arterial pressure and heart rate

1998 ◽  
Vol 275 (5) ◽  
pp. H1627-H1634 ◽  
Author(s):  
Margaret P. Chandler ◽  
David W. Rodenbaugh ◽  
Stephen E. DiCarlo
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Acute Exercise ◽  
Operating Point ◽  
Arterial Baroreflex ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Single Bout ◽  
Before And After ◽  
The Relationship

We tested the hypothesis that postexercise reductions in arterial pressure and heart rate (HR) are mediated by a lowering of the operating point and a reduction in the gain of the arterial baroreflex. To test this hypothesis, spontaneous changes in arterial pressure and the reflex responses of HR were examined before and after a single bout of mild to moderate dynamic exercise in 19 spontaneously hypertensive rats (SHR, 10 male and 9 female). Eleven SHR subjected to sinoaortic denervation (SAD) (6 male, 5 female) were also studied. All rats were instrumented with an arterial catheter for the measurement of arterial pressure and HR. After exercise, arterial pressure and HR were reduced below preexercise levels. Furthermore, the operating point and spontaneous gain (G) of the arterial baroreflex were reduced. Specifically, after exercise, the spontaneous range of HR (P1, 50%), the pressure at the midpoint of the pressure range (P3, 13%) and the HR at the midpoint of the HR range (H3, 10%), the spontaneous minimum HR (P4, 8%) and maximum HR (10%), and G (76%) were significantly attenuated. SAD significantly attenuated the relationship between arterial pressure and HR by reducing G (males 94%, females 95%). These results demonstrate that acute exercise resulted in a postexercise resetting of the operating point and a reduction in the gain of the arterial baroreflex. Furthermore, these data suggest that postexercise reductions in arterial pressure and HR are mediated by a lowering of the operating point of the arterial baroreflex.

scholarly journals The Diagnostic Value of Cardiac Deceleration Capacity in Vasovagal Syncope

2020 ◽  
Vol 13 (12) ◽  
Author(s):  
Lihui Zheng ◽  
Wei Sun ◽  
Shangyu Liu ◽  
Erpeng Liang ◽  
Zhongpeng Du ◽  
...  
Keyword(s):  
Heart Rate ◽  
Vasovagal Syncope ◽  
Diagnostic Value ◽  
Control Group ◽  
Vagal Activity ◽  
Tilt Table Test ◽  
Tilt Table ◽  
Good Tool ◽  
Deceleration Capacity ◽  
Vagal Control

Background: Increased parasympathetic activity is thought to play important roles in syncope events of patients with vasovagal syncope (VVS). However, direct measurements of the vagal control are difficult. The novel deceleration capacity (DC) of heart rate measure has been used to characterize the vagal modulation. This study aimed to assess vagal control in patients with VVS and evaluate the diagnostic value of the DC in VVS. Methods: Altogether, 161 consecutive patients with VVS (43±15 years; 62 males) were enrolled. Tilt table test was positive in 101 and negative in 60 patients. Sixty-five healthy subjects were enrolled as controls. DC and heart rate variability in 24-hour ECG, echocardiogram, and biochemical examinations were compared between the syncope and control groups. Results: DC was significantly higher in the syncope group than in the control group (9.6±3.3 versus 6.5±2.0 ms, P <0.001). DC was similarly increased in patients with VVS with a positive and negative tilt table test (9.7±3.5 and 9.4±2.9 ms, P =0.614). In multivariable logistic regression analyses, DC was independently associated with syncope (odds ratio=1.518 [95% CI, 1.301–1.770]; P =0.0001). For the prediction of syncope, the area under curve analysis showed similar values when comparing single DC and combined DC with other risk factors ( P =0.1147). From the receiver operator characteristic curves for syncope discrimination, the optimal cutoff value for the DC was 7.12 ms. Conclusions: DC>7.5 ms may serve as a good tool to monitor cardiac vagal activity and discriminate VVS, particularly in those with negative tilt table test.

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