Impaired an Arterial Baroreflex Function in Prehypertensive and Hypertensive Spontaneously Hypertensive Rats

The aim of the present study was to determine the receptor subtype involved in arginine vasopressin (AVP)-induced modulation of baroreflex function in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats using novel nonpeptide AVP V1- and V2-receptor antagonists. Baroreceptor heart rate (HR) reflex was investigated in both SHR and WKY rats which were intravenously administered the selective V1- and V2-receptor antagonists OPC-21268 and OPC-31260, respectively. Baroreflex function was assessed by obtaining alternate pressor and depressor responses to phenylephrine and sodium nitroprusside, respectively, to construct baroreflex curves. In both SHR and WKY rats baroreflex activity was tested before and after intravenous administration of vehicle (20% DMSO), OPC-21268 (10 mg/kg), and OPC-31260 (1 and 10 mg/kg). Vehicle did not significantly alter basal mean arterial pressure (MAP) and HR values or baroreflex function in SHR or WKY rats. The V1-receptor antagonist had no significant effect on resting MAP or HR values or on baroreflex parameters in both groups of rats, although this dose was shown to significantly inhibit the pressor response to AVP (5 ng iv; ANOVA, P < 0.05). In SHR but not WKY rats the V2-receptor antagonist significantly attenuated the gain (or slope) of the baroreflex curve (to 73 ± 3 and 79 ± 7% of control for 1 and 10 mg/kg, respectively), although AVP-induced pressor responses were also attenuated with the higher dose of the V2-receptor antagonist. These findings suggest that AVP tonically enhances baroreflex function through a V2 receptor in the SHR.

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α2-Adrenergic receptors in NTS facilitate baroreflex function in adult spontaneously hypertensive rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00167.2001 ◽

2002 ◽

Vol 282 (6) ◽

pp. H2336-H2345 ◽

Cited By ~ 16

Author(s):

Linda F. Hayward ◽

Alecia P. Riley ◽

Robert B. Felder

Keyword(s):

Arterial Pressure ◽

Spontaneously Hypertensive Rats ◽

Hypertensive Rats ◽

Baroreflex Control ◽

Renal Sympathetic Nerve Activity ◽

Spontaneously Hypertensive ◽

Aortic Depressor Nerve ◽

Baroreflex Function ◽

Wistar Kyoto ◽

Renal Sympathetic

We examined the effect of α2-adrenoreceptor blockade in the nucleus of the solitary tract (NTS) on baroreflex responses elicited by electrical stimulation of the left aortic depressor nerve (ADN) in urethane-anesthetized spontaneously hypertensive rats (SHR, n = 11) and normotensive Wistar-Kyoto rats (WKY, n = 11). ADN stimulation produced a frequency-dependent decrease in mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate (HR). In SHR, unilateral microinjection of idazoxan into the NTS markedly reduced baroreflex control of MAP, RSNA, and HR and had a disproportionately greater influence on baroreflex control of MAP than of RSNA. In WKY, idazoxan microinjections did not significantly alter baroreflex function relative to control vehicle injections. These results suggest that baroreflex regulation of arterial pressure in SHR is highly dependent on NTS adrenergic mechanisms. The reflex regulation of sympathetic outflow to the kidney is less influenced by the altered α2-adrenoreceptor mechanisms in SHR.

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Ketanserin improves cardiac performance after myocardial infarction in spontaneously hypertensive rats partially through restoration of baroreflex function

Acta Pharmacologica Sinica ◽

10.1038/aps.2013.147 ◽

2013 ◽

Vol 34 (12) ◽

pp. 1508-1514 ◽

Cited By ~ 6

Author(s):

Jian-guang Yu ◽

En-hui Zhang ◽

Ai-jun Liu ◽

Jian-guo Liu ◽

Guo-jun Cai ◽

...

Keyword(s):

Myocardial Infarction ◽

Spontaneously Hypertensive Rats ◽

Cardiac Performance ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Baroreflex Function

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Involvement of arterial baroreflex and nicotinic acetylcholine receptor α7 subunit pathway in the protection of metformin against stroke in stroke-prone spontaneously hypertensive rats

European Journal of Pharmacology ◽

10.1016/j.ejphar.2017.01.035 ◽

2017 ◽

Vol 798 ◽

pp. 1-8 ◽

Cited By ~ 6

Author(s):

Jin-Min Guo ◽

Li Zhang ◽

Xue-Cai Niu ◽

He Shu ◽

Lei Wang ◽

...

Keyword(s):

Acetylcholine Receptor ◽

Nicotinic Acetylcholine Receptor ◽

Spontaneously Hypertensive Rats ◽

Arterial Baroreflex ◽

Hypertensive Rats ◽

Nicotinic Acetylcholine ◽

Spontaneously Hypertensive ◽

Α7 Subunit

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Central administration of a specific angiotensin II receptor antagonist on baroreflex function in spontaneously hypertensive rats

Journal of Hypertension ◽

10.1097/00004872-199104000-00009 ◽

1991 ◽

Vol 9 (4) ◽

pp. 365-371 ◽

Cited By ~ 30

Author(s):

Kathleen H. Berecek ◽

Joel D. Robertson ◽

M Hernandez Thorstad

Keyword(s):

Angiotensin Ii ◽

Receptor Antagonist ◽

Spontaneously Hypertensive Rats ◽

Central Administration ◽

Angiotensin Ii Receptor ◽

Hypertensive Rats ◽

Angiotensin Ii Receptor Antagonist ◽

Spontaneously Hypertensive ◽

Baroreflex Function

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Exercise Training Improves the Depressed Sensitivity of the Baroreceptors in Spontaneously Hypertensive Rats

Hypertension ◽

10.1161/hyp.36.suppl_1.700-d ◽

2000 ◽

Vol 36 (suppl_1) ◽

pp. 700-701

Author(s):

Gustavo J J Silva ◽

Edson D Moreira ◽

Carlos E Negrao ◽

Patricia C Brum ◽

Eduardo M Krieger

Keyword(s):

Blood Pressure ◽

Arterial Pressure ◽

Spontaneously Hypertensive Rats ◽

Systolic Arterial Pressure ◽

Arterial Baroreflex ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Baroreceptor Function ◽

Low Intensity Exercise ◽

The Relationship

P43 We have previously demonstrated that low-intensity exercise traning (ET) diminishes blood pressure and partially restores the sensitivity of the baroreflex bradycardia and tachycardia that are depressed in spontaneously hypertensive rats (SHR). Presently, the influence of the exercise trainig (ET) on the afferent part of the baroreflex (baroreceptor function curve) and its implication on the baroreflex was analysed in SHR and in normal control rats (NCR). NCR and SHR were subdivided in sedentary (S) and ET groups: SHR-S (n=8) and SHR-ET (n=6), and NCR-S (n=8) and NCR-ET (n=8). ET was performed on treadmill, during 60 min, 5 days/wk, at 50% of VO 2 max, for 12 wk. Arterial baroreflex sensitivity was evaluated by bradycardiac responses to phenylephrine (0.5;1;2;4;8 and 16 μg/ml, i.v.) and tachycardiac responses to sodium nitroprusside (0.5;1;2;4;8 and 16 μg/ml, i.v.). Aortic baroreceptor function curve was evaluated under pentobarbital anesthesia (40 mg/kg) during rapid variations of arterial pressure (AT/CODAS, 3kHz per channel). The relationship between changes in baroreceptor discharge (0-100%) and systolic arterial pressure was analysed using a sigmoidal regression. Mean arterial pressure was reduced in SHR-ET compared to SHR-S group (165±7 vs. 183±4 mmHg) but remained inaltared in NCR-ET compared to NCR-S (112±3 vs. 115±3 mmHg). In SHR, ET increased the sensitivity of baroreflex bradycardia (1.9±0.1 vs. 0.7±0.1 bpm.mmHg -1 ) and tachycardia (2.9±0.1 vs. 1.8±0.2 bpm.mmHg -1 ) which were depressed. In NCR-ET baroreflex bradycardia was decreased (1.4±0.1 vs. 1.7±0.1 bpm.mmHg -1 ) but baroreflex tachycardia was increased (4.6±0.5 vs. 3.0±0.2 bpm.mmHg -1 ). ET increased the aortic baroreceptor gaing-sensitivity in both groups: SHR (0.9±0.1 vs. 0.7±0.1 %.mmHg -1 ) and NCR (2.1±0.1 vs. 1.4±0.1 %.mm Hg -1 ). Conclusion:1. ET increases aortic baroreceptor gain-sensitivity in NCR as well in SHR; 2. The improvement of the baroreflex produced by ET in SHR is partially explainedd by the recovery of the baroreceptor sensitivity, which may also participate in the reduction of high blood pressure.

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