Depressor Response to Endothelin in Normotensive and Hypertensive Rats

2015 ◽  
pp. 104-109
Author(s):  
Raymond J. Winquist ◽  
Patricia B. Bunting ◽  
Patricia K. Lumma ◽  
Victor M. Garsky ◽  
Ann L. Scott ◽  
...  
Keyword(s):  
Hypertensive Rats ◽  
Depressor Response

Abstract 13102: Brain Angiotensin II Type1 Receptor Blockade Ameliorates the Development of Atrial Fibrillation via Sympathoinhibition Independent of Depressor Response in Hypertensive Rats

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Tomomi Nagayama ◽  
Yoshitaka Hirooka ◽  
Takuya Kishi ◽  
Yasushi Mukai ◽  
Shujiro Inoue ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Renin Angiotensin System ◽  
Atrial Fibrosis ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Depressor Response ◽  
Intracerebroventricular Infusion ◽  
Echocardiographic Parameters ◽  
Wistar Kyoto

Background: Previous studies demonstrated that the pathophysiology of atrial fibrillation (AF) with hypertension is associated with sympathoexcitation or the renin-angiotensin system. Conventional therapies, however, do not sufficiently prevent the development of AF. We reported that sympathoexcitation via brain angiotensin type1 receptors (AT1R) plays an important role in hypertension. Here we examined the hypothesis that brain AT1R-induced sympathoexcitation contributes to the development of AF in hypertension. Methods and Results: Sixteen-week-old male stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar Kyoto rats (WKY) were divided into 4 groups and administered treatment for 2 weeks, as follows: 1) SHRSP treated with intracerebroventricular infusion (ICV) of vehicle, S-VEH; 2) SHRSP treated with ICV of the AT1R blocker, losartan (1 mg/kg/day), S-LOS; 3) SHRSP treated with oral administration of hydralazine (100 mg/L in drinking water), S-HYD; 4) WKY treated with ICV of vehicle, W-VEH. Systolic blood pressure was significantly lower in both S-LOS and S-HYD than in S-VEH (201.0±1.7 and 172.4±4.0 vs. 233.0±3.5 mmHg, n=7-8/group, respectively, P<0.05). Urinary norepinephrine excretion for 24 hours as an indicator of sympathoexcitation was significantly reduced in S-LOS, but increased in S-HYD despite the larger depressor response. The induction rates of AF by transesophageal burst pacing were higher in S-VEH and S-HYD than in S-LOS and W-VEH (96±2% and 92±4% vs. 74±6% and 71±9%, n=7-8/group, respectively, p<0.05). AF duration was markedly inhibited in S-LOS, but not in S-HYD (Figure). Interstitial atrial fibrosis and echocardiographic parameters did not differ among SHRSP groups. Conclusions: Blockade of brain AT1R lowered the inducibility and sustainability of AF via sympathoinhibition independent of depressor response in hypertensive rats. We conclude that brain AT1R is a potential target of treatment for AF with hypertension.

NITRIC OXIDE IN vPAG MEDIATES THE DEPRESSOR RESPONSE TO ACUPUNCTURE IN STRESS-INDUCED HYPERTENSIVE RATS

2001 ◽  
Vol 26 (3) ◽  
pp. 165-170 ◽  
Author(s):  
Li Li ◽  
Yin-Xiang Cao ◽  
Hong Xue ◽  
Peng Li ◽  
Da-Nian Zhu
Keyword(s):  
Nitric Oxide ◽  
Hypertensive Rats ◽  
Depressor Response

Prominent depressor response to endothelin in spontaneously hypertensive rats

1989 ◽  
Vol 163 (1) ◽  
pp. 199-203 ◽  
Author(s):  
Raymond J. Winquist ◽  
Patricia B. Bunting ◽  
Victor M. Garsky ◽  
Patricia K. Lumma ◽  
Timothy L. Schofield
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Depressor Response

scholarly journals Microchannel Electrode Stimulation of Deep Peroneal Nerve Fascicles Induced Mean Arterial Depressor Response in Hypertensive Rats

2015 ◽  
Vol 2 (1) ◽  
pp. 55-62 ◽  
Author(s):  
Young-tae Kim ◽  
Aswini Kanneganti ◽  
Caleb Nothnagle ◽  
Ryan Landrith ◽  
Masaki Mizuno ◽  
...  
Keyword(s):  
Peroneal Nerve ◽  
Deep Peroneal Nerve ◽  
Hypertensive Rats ◽  
Depressor Response ◽  
Electrode Stimulation ◽  
Stimulation Of

Abstract MP23: Arterial Depressor Responses Induced By Neuromodulation Of Deep Peroneal Nerve In Spontaneously Hypertensive Rats

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Maria A Gonzalez-Gonzalez ◽  
John Beitter ◽  
Kevin Romero ◽  
Danny Lam ◽  
Ana G Hernandez-Reynoso ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Peroneal Nerve ◽  
Spontaneously Hypertensive Rats ◽  
Pressure Control ◽  
Deep Peroneal Nerve ◽  
Hypertensive Rats ◽  
Renal Nerve ◽  
Spontaneously Hypertensive ◽  
Depressor Response ◽  
Renal Nerve Activity

Hypertension affects nearly half of the US population but only 43% achieved blood pressure control with medication alone. Medical devices for hypertension include implantable lead electrodes that stimulate the carotid baroreceptors with promising results, albeit with significant adverse complications. To address these limitations, we have proposed the use of deep peroneal nerve stimulation (DPNS), which elicited a depressor response in anesthetized, breathing supported, spontaneously hypertensive rats (SHR). In this study, we further define the electrical stimulation parameters that optimize the DPNS depressor response, and demonstrated that increasing the pulse duration from 0.15 ms to 1ms, of 1.0 mA pulses at 2 Hz for 10 sec, significantly reduced the mean arterial pressure (MAP) by 8±4 mmHg (p<0.005; n=4) in this animal model. DPNS also caused an immediate increase in renal nerve activity (RNA; p< 0.004, n=5), which may represent afferent sensory axons from the kidney, although this possibility needs to be further investigated. In a separate cohort of anesthetized SHR animals, breathing spontaneously, we demonstrated that optimal DPNS stimulation reduced the MAP from 121±3 to 108±4; p=0.02; n=10). To confirm if DPNS is able to evoke a depressor response in fully awake SHR animals, we developed a novel miniaturized wireless microchannel electrode (w-μCE) with a L-shaped microchannel, through which the DPN slides and locks into a recording/stimulation chamber, causing no discomfort to the animal during locomotion. Two weeks after implantation of the w-μCE neural stimulation device, animals were movement-retrained to received wireless DPNS for 10 min daily for 2 weeks. Blood pressure was measured by tail-cuff at baseline, 10 days after device implantation, and 1 and 2-hr 15 days after DPNS. After two weeks of DPNS, the acute neuromodulation treatment reduced the initial systolic BP of 154±20 mmHg to 127±7 and 119±2 mmHg at 1 and 2 hr; respectively (p< 0.001, n=15-19 measurements; n=2 animals). These results provide evidence of the effectiveness and reliability of DPN neuromodulation as a possible treatment for drug-resistant hypertension.

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