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  • 1
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    The Ninth J. A. F. Stevenson Memorial Lecture The many roles of the kidney in arterial pressure control and hypertension
    Canadian Science Publishing ; 1981
    In:  Canadian Journal of Physiology and Pharmacology Vol. 59, No. 6 ( 1981-06-01), p. 513-519
    Details
    In: Canadian Journal of Physiology and Pharmacology, Canadian Science Publishing, Vol. 59, No. 6 ( 1981-06-01), p. 513-519
    Type of Medium: Online Resource
    ISSN: 0008-4212 , 1205-7541
    URL: Article
    DOI: 10.1139/y81-077
    Language: English
    Publisher: Canadian Science Publishing
    Publication Date: 1981
    detail.hit.zdb_id: 2004356-9
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  • 2
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    Sustained Activation of the Central Baroreceptor Pathway in Angiotensin Hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2002
    In:  Hypertension Vol. 39, No. 2 ( 2002-02), p. 550-556
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 39, No. 2 ( 2002-02), p. 550-556
    Abstract: Recent studies indicate that renal sympathetic nerve activity is chronically suppressed in angiotensin (Ang II) hypertension and that baroreflexes play a critical role in mediating this response. To support these findings, we determined whether the hypertension associated with chronic infusion of Ang II at 4.8 pmol/kg per minute (5ng/kg per minute) produces sustained activation of medullary neurons that participate in the central baroreceptor reflex pathway. We used Fos-like (Fos-Li) protein immunohistochemical methods to determine activation of neurons in the nucleus tractus solitarius (NTS), caudal ventrolateral medulla (CVLM), and rostral ventrolateral medulla (RVLM). Results were compared in three groups of chronically instrumented dogs subjected to infusion of: 1) saline (control); 2) Ang II-2 hours (acute); and 3) Ang II-5 days (chronic). Mean arterial pressure increased 22±3 and 35±3 mm Hg during acute and chronic Ang II infusion, respectively. There was little Fos-Li immunoreactivity in medullary neurons in control dogs. In contrast, during acute Ang II infusion there was a 2- to 3-fold increase in Fos-Li staining in the NTS and CVLM, but no increase in staining in RVLM neurons. As baroreceptor suppression of sympathoexcitatory cells in the RVLM is mediated by activation of neurons in the NTS and CVLM, these results were expected. More importantly, this same pattern of central neuronal activation was observed during chronic Ang II hypertension. Therefore, these results support recent findings indicating that baroreflex suppression of renal sympathetic nerve activity is a long-term compensatory response in Ang II hypertension.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hy0202.103003
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2002
    detail.hit.zdb_id: 2094210-2
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  • 3
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    Sustained influence of the renal nerves to attenuate sodium retention in angiotensin hypertension
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 281, No. 2 ( 2001-08-01), p. R434-R443
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 281, No. 2 ( 2001-08-01), p. R434-R443
    Abstract: Recent studies indicate that baroreflex suppression of renal sympathetic nerve activity is sustained for up to 5 days of ANG II infusion; however, steady-state conditions are not associated with ANG II hypertension of this short duration. Thus the major goal of this study was to determine whether neurally induced increments in renal excretory function during chronic intravenous infusion of ANG II are sustained under more chronic conditions when hypertension is stable and sodium balance is achieved. Experiments were conducted in five conscious dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders to allow separate 24-h urine collection from denervated (Den) and innervated (Inn) kidneys. ANG II was infused after control measurements for 10 days at a rate of 5 ng · kg −1 · min −1 . Twenty-four-hour control values for mean arterial pressure (MAP) and the ratio for urinary sodium excretion from Den and Inn kidneys (Den/Inn) were 92 ± 4 mmHg and 0.99 ± 0.05, respectively. On days 8–10 of ANG II infusion, MAP was stable (+30 ± 3 mmHg) and sodium balance was achieved. Whereas equal amounts of sodium were excreted from the kidneys during the control period, throughout ANG II infusion there was a greater rate of sodium excretion from Inn vs. Den kidneys ( day 10 Den/Inn sodium = 0.56 ± 0.05), indicating chronic suppression of renal sympathetic nerve activity. The greater rate of sodium excretion in Inn vs. Den kidneys during renal sympathoinhibition also revealed a latent impairment in sodium excretion from Den kidneys. Although the Den/Inn for sodium and the major metabolites of nitric oxide (NO) decreased in parallel during ANG II hypertension, the Den/Inn for cGMP, a second messenger of NO, remained at control levels throughout this study. This disparity fails to support the notion that a deficiency in NO production and action in Den kidneys accounts for the impaired sodium excretion. Most importantly, these results support the contention that baroreflex suppression of renal sympathetic nerve activity is sustained during chronic ANG II hypertension, a response that may play an important role in attenuating the rise in arterial pressure.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.2001.281.2.R434
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 4
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    Baroreflexes Prevent Neurally Induced Sodium Retention in Angiotensin Hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 36, No. suppl_1 ( 2000-10), p. 680-680
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2000-10), p. 680-680
    Abstract: 14 Recent studies indicate that renal sympathetic nerve activity is chronically supressed during angiotensin (ANG II) hypertension. To determine whether cardiopulmonary reflexes and/or arterial baroreflexes mediate this chronic renal sympathoinhibition, experiments were conducted in 5 conscious dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders to allow separate 24-h urine collection from denervated (DEN) and innervated (INN) kidneys. Dogs were studied before and after deafferentation of cardiopulmonary receptors and arterial baroreceptors (CPD + SAD). After control measurements, ANG II was infused for 5 days at a rate of 5 ng/kg/min; this was followed by a 5-day recovery period. In the intact state, 24-h control values for mean arterial pressure (MAP) and the ratio for urinary sodium excretion from DEN and INN kidneys (DEN/INN) were 98±4 mm Hg and 1.04±0.04 respectively. As expected, sodium retention occurred for several days during ANG II infusion before sodium balance was achieved at an increase in MAP of 30-35 mm Hg. Throughout ANG II infusion, there was a substantially greater rate of sodium excretion from INN versus DEN kidneys (day 5 DEN/INN-sodium = 0.51±0.05), indicating chronic suppression of renal sympathetic nerve activity. CPD + SAD did not influence baseline values for either MAP or the DEN/INN-sodium, nor did it alter the severity of ANG II hypertension. However, after CPD + SAD there was an appreciably lower, rather than a greater, rate of sodium excretion from INN versus DEN kidneys during ANG II hypertension (day 5 DEN/INN-sodium = 2.02±0.14). These data indicate that cardiac and/or arterial baroreflexes chronically inhibit renal sympathetic nerve activity during ANG II hypertension and that in the absence of these reflexes, ANG II has sustained renal sympathoexcitatory effects that promote sodium retention.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.36.suppl_1.680-b
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 2094210-2
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  • 5
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    Baroreflexes prevent neurally induced sodium retention in angiotensin hypertension
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 279, No. 4 ( 2000-10-01), p. R1437-R1448
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 279, No. 4 ( 2000-10-01), p. R1437-R1448
    Abstract: Recent studies indicate that renal sympathetic nerve activity is chronically suppressed during ANG II hypertension. To determine whether cardiopulmonary reflexes and/or arterial baroreflexes mediate this chronic renal sympathoinhibition, experiments were conducted in conscious dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders to allow separate 24-h urine collection from denervated (Den) and innervated (Inn) kidneys. Dogs were studied 1) intact, 2) after thoracic vagal stripping to eliminate afferents from cardiopulmonary and aortic receptors [cardiopulmonary denervation (CPD)], and 3) after subsequent denervation of the carotid sinuses to achieve CPD plus complete sinoaortic denervation (CPD + SAD). After control measurements, ANG II was infused for 5 days at a rate of 5 ng · kg −1 · min −1 . In the intact state, 24-h control values for mean arterial pressure (MAP) and the ratio for urinary sodium excretion from Den and Inn kidneys (Den/Inn) were 98 ± 4 mmHg and 1.04 ± 0.04, respectively. ANG II caused sodium retention and a sustained increase in MAP of 30–35 mmHg. Throughout ANG II infusion, there was a greater rate of sodium excretion from Inn vs. Den kidneys ( day 5 Den/Inn sodium = 0.51 ± 0.05), indicating chronic suppression of renal sympathetic nerve activity. CPD and CPD + SAD had little or no influence on baseline values for either MAP or the Den/Inn sodium, nor did they alter the severity of ANG II hypertension. However, CPD totally abolished the fall in the Den/Inn sodium in response to ANG II. Furthermore, after CPD + SAD, there was a lower, rather than a higher, rate of sodium excretion from Inn vs. Den kidneys during ANG II infusion ( day 5 Den/Inn sodium = 2.02 ± 0.14). These data suggest that cardiac and/or arterial baroreflexes chronically inhibit renal sympathetic nerve activity during ANG II hypertension and that in the absence of these reflexes, ANG II has sustained renal sympathoexcitatory effects.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.2000.279.4.R1437
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 6
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    Renal Denervation Update From the International Sympathetic Nervous System Summit
    Elsevier BV ; 2019
    In:  Journal of the American College of Cardiology Vol. 73, No. 23 ( 2019-06), p. 3006-3017
    Details
    In: Journal of the American College of Cardiology, Elsevier BV, Vol. 73, No. 23 ( 2019-06), p. 3006-3017
    Type of Medium: Online Resource
    ISSN: 0735-1097
    URL: Article
    DOI: 10.1016/j.jacc.2019.04.015
    RVK:
    XA 17760
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 1468327-1
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  • 7
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    Recent insights into the interactions between the baroreflex and the kidneys in hypertension
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 288, No. 4 ( 2005-04), p. R828-R836
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 288, No. 4 ( 2005-04), p. R828-R836
    Abstract: Recent findings in chronically instrumented animals challenge the classic concept that baroreflexes do not play a role in the chronic regulation of arterial pressure. As alterations in renal excretory function are of paramount importance in the chronic regulation of arterial pressure, several of these recent studies have focused on the long-term interactions between the baroreflex and the kidneys during chronic perturbations in arterial pressure and body fluid volumes. An emerging body of evidence indicates that the baroreflex is chronically activated in several experimental models of hypertension, but in most cases, the duration of these studies has not exceeded 2 wk. Although these studies suggest that the baroreflex may play a compensatory role in attenuating the severity of the hypertension, possibly even in primary hypertension with uncertain causes of sympathetic activation, there has been only limited assessment of the quantitative importance of this interaction in the regulation of arterial pressure. In experimental models of secondary hypertension, baroreflex suppression of renal sympathetic nerve activity is sustained and chronically promotes sodium excretion. This raises the possibility that the renal nerves may be the critical efferent link for baroreceptor-induced suppression of central sympathetic output through which long-term compensatory reductions in arterial pressure are produced. This contention is supported by strong theoretical evidence but must be corroborated by experimental studies. Finally, although it is now clear that pressure-induced increases in baroreflex activity persist for longer periods of time than previously suggested, studies using new tools and novel approaches and extending beyond 2 wk of hypertension are needed to elucidate the true role of the baroreflex in the pathogenesis of clinical hypertension.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00591.2004
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 8
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    Sustained Activation of the Central Baroreceptor Pathway in Obesity Hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Hypertension Vol. 42, No. 1 ( 2003-07), p. 96-102
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 42, No. 1 ( 2003-07), p. 96-102
    Abstract: The major goal of this study was to determine whether there is increased activation of medullary neurons that participate in the central baroreceptor reflex pathway in dogs with obesity-induced hypertension, a model of hypertension that is associated with increased sympathetic activity. We used Fos-like (Fos-Li) protein immunohistochemical methods to determine activation of neurons in the nucleus tractus solitarius (NTS), caudal ventrolateral medulla (CVLM), and rostral ventrolateral medulla (RVLM). Dogs were fed either a regular diet or an identical diet with the addition of 0.5 to 0.9 kg of cooked beef fat. After ≈6 weeks of the high fat diet, body weight (36.3±0.4 vs 21.5±0.5 kg), mean arterial pressure (105±4 vs 91±3 mm Hg), and heart rate (97±4 vs 70±3 bpm) were significantly greater in obese than in control dogs, respectively. There was little Fos-Li immunoreactivity in medullary neurons of control dogs but marked reactivity in obese dogs. Specifically, the number of Fos-Li–positive cells in the NTS and CVLM was 3 to 5 times greater in obese than in control dogs. Furthermore, despite sustained activation of these baroreceptor-sensitive neurons, there was a significantly greater number of Fos-Li positive cells in the RVLM of dogs fed the high fat diet. As baroreceptor suppression of sympathoexcitatory cells in the RVLM is mediated by activation of neurons in the NTS and CVLM, these results support recent findings indicating that baroreflex suppression of sympathetic activity is a long-term compensatory response in hypertension. However, sympathoexcitatory inputs onto RVLM neurons would appear to predominate over the inhibitory effects of the baroreflex in obesity hypertension.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.0000076092.10923.FD
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 2094210-2
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  • 9
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    Device-Based Neuromodulation for Resistant Hypertension Therapy : Too Early for Prime Time?
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Circulation Research Vol. 124, No. 7 ( 2019-03-29), p. 1071-1093
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 124, No. 7 ( 2019-03-29), p. 1071-1093
    Abstract: Despite availability of effective drugs for hypertension therapy, significant numbers of hypertensive patients fail to achieve recommended blood pressure levels on ≥3 antihypertensive drugs of different classes. These individuals have a high prevalence of adverse cardiovascular events and are defined as having resistant hypertension (RHT) although nonadherence to prescribed antihypertensive medications is common in patients with apparent RHT. Furthermore, apparent and true RHT often display increased sympathetic activity. Based on these findings, technology was developed to treat RHT by suppressing sympathetic activity with electrical stimulation of the carotid baroreflex and catheter-based renal denervation (RDN). Over the last 15 years, experimental and clinical studies have provided better understanding of the physiological mechanisms that account for blood pressure lowering with baroreflex activation and RDN and, in so doing, have provided insight into which patients in this heterogeneous hypertensive population are most likely to respond favorably to these device-based therapies. Experimental studies have also played a role in modifying device technology after early clinical trials failed to meet key endpoints for safety and efficacy. At the same time, these studies have exposed potential differences between baroreflex activation and RDN and common challenges that will likely impact antihypertensive treatment and clinical outcomes in patients with RHT. In this review, we emphasize physiological studies that provide mechanistic insights into blood pressure lowering with baroreflex activation and RDN in the context of progression of clinical studies, which are now at a critical point in determining their fate in RHT management.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.118.313221
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 1467838-X
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  • 10
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    Proceedings from the Society of Interventional Radiology Foundation Research Consensus Panel on Renal Sympathetic Denervation
    Elsevier BV ; 2014
    In:  Journal of Vascular and Interventional Radiology Vol. 25, No. 4 ( 2014-04), p. 497-509
    Details
    In: Journal of Vascular and Interventional Radiology, Elsevier BV, Vol. 25, No. 4 ( 2014-04), p. 497-509
    Type of Medium: Online Resource
    ISSN: 1051-0443
    URL: Article
    DOI: 10.1016/j.jvir.2013.12.572
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2014
    detail.hit.zdb_id: 2041331-2
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