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  • 1
    Online Resource
    Online Resource
    Abstract 351: Temperature Dependency of Blood Pressure and Heart Rate in Norepinephrine-Deficient Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Hypertension Vol. 60, No. suppl_1 ( 2012-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 60, No. suppl_1 ( 2012-09)
    Abstract: Dopamine beta-hydroxylase (Dbh) knockout mice lack the sympathetic neurotransmitter, norepinephrine, but have intact sympathetic neurons and adrenergic receptors. These mice offer an excellent model for assessing the role of the sympathetic nervous system in physiological and pathophysiological processes. Mouse blood pressure (BP) and heart rate (HR) increase as ambient temperature drops below the thermoneutral temperature (30° C), apparently due to sympathetic nervous system activation. The present study tested the hypothesis that BP and HR are not sensitive to changes in ambient temperature in Dbh knockout (KO) mice lacking sympathetic function. BP, HR and activity data were obtained at least one week after BP telemeters were implanted in the carotid artery. Eight Dbh wild type (WT) and 7 KO mice were initially maintained at 23° C, singly housed in temperature-controlled brooders with a 12-hour light-dark cycle. With 3° C temperature changes every 3-4 days, chambers were warmed to 32° C, followed by cooling back to 23° C. Twenty-four hour averaged BP and HR were significantly lower in KO than WT mice at all temperatures, although activity levels were no different. HR, averaged over 24hr, were significantly higher at 23° C after cooling from 32° C for both genotypes (mean±SD; KO: 376±24 to 462±53 beats/min, P=0.016; WT: 411±22 to 542±46 beats/min, P=0.008). In contrast, BP increased with the drop in temperature only in the WT mice (KO: 83±7 to 87±10 mmHg, P=0.109; WT: 94±9 to 107±9 mmHg, P=0.008), and BP differences between 32° and 23° C were greater in WT mice (delta BP 23 ° -32 ° averaged 12.2±5.4 mmHg for WT and 4.2±5.0 mmHg for KO, P=0.011). Activity did not change as ambient temperature was lowered. These data indicate that effects of ambient temperature on HR occur independently of sympathetic activation, but our results confirm that an intact sympathetic nervous system is required for the pressor effect of a cooler environmental temperature.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.60.suppl_1.A351
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2094210-2
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  • 2
    Online Resource
    Online Resource
    Modulatory effects of adenosine on baroreflex activation in the brainstem of normotensive rats
    Elsevier BV ; 1989
    In:  European Journal of Pharmacology Vol. 174, No. 1 ( 1989-12), p. 119-122
    Details
    In: European Journal of Pharmacology, Elsevier BV, Vol. 174, No. 1 ( 1989-12), p. 119-122
    Type of Medium: Online Resource
    ISSN: 0014-2999
    URL: Article
    DOI: 10.1016/0014-2999(89)90882-0
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1989
    detail.hit.zdb_id: 1483526-5
    SSG: 15,3
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  • 3
    Online Resource
    Online Resource
    Tachycardia, reduced vagal capacity, and age-dependent ventricular dysfunction arising from diminished expression of the presynaptic choline transporter
    American Physiological Society ; 2010
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 299, No. 3 ( 2010-09), p. H799-H810
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 299, No. 3 ( 2010-09), p. H799-H810
    Abstract: Healthy cardiovascular function relies on a balanced and responsive integration of noradrenergic and cholinergic innervation of the heart. High-affinity choline uptake by cholinergic terminals is pivotal for efficient ACh production and release. To date, the cardiovascular impact of diminished choline transporter (CHT) expression has not been directly examined, largely due to the transporter's inaccessibility in vivo. Here, we describe findings from cardiovascular experiments using transgenic mice that bear a CHT genetic deficiency. Whereas CHT knockout (CHT −/− ) mice exhibit early postnatal lethality, CHT heterozygous (CHT +/− ) mice survive, grow, and reproduce normally and exhibit normal spontaneous behaviors. However, the CHT +/− mouse heart displays significantly reduced levels of high-affinity choline uptake accompanied by significantly reduced levels of ACh. Telemeterized recordings of cardiovascular function in these mice revealed tachycardia and hypertension at rest. After treadmill exercise, CHT +/− mice exhibited slower heart rate recovery, consistent with a diminished cholinergic reserve, a contention validated through direct vagal nerve stimulation. Echocardiographic and histological experiments revealed an age-dependent decrease in fractional shortening, increased left ventricular dimensions, and increased ventricular fibrosis, consistent with ventricular dysfunction. These cardiovascular phenotypes of CHT +/− mice encourage an evaluation of humans bearing reduced CHT expression for their resiliency in maintaining proper heart function as well as risk for cardiovascular disease.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00170.2010
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Smoking and mechanisms of cardiovascular control
    Elsevier BV ; 1988
    In:  American Heart Journal Vol. 115, No. 1 ( 1988-01), p. 258-263
    Details
    In: American Heart Journal, Elsevier BV, Vol. 115, No. 1 ( 1988-01), p. 258-263
    Type of Medium: Online Resource
    ISSN: 0002-8703
    URL: Article
    DOI: 10.1016/0002-8703(88)90646-1
    RVK:
    XA 18100
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1988
    detail.hit.zdb_id: 2003210-9
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  • 5
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    Online Resource
    Norepinephrine transporter variant A457P knock-in mice display key features of human postural orthostatic tachycardia syndrome
    The Company of Biologists ; 2013
    In:  Disease Models & Mechanisms
    Details
    In: Disease Models & Mechanisms, The Company of Biologists
    Abstract: Postural orthostatic tachycardia syndrome (POTS) is a common autonomic disorder of largely unknown etiology that presents with sustained tachycardia on standing, syncope and elevated norepinephrine spillover. Some individuals with POTS experience anxiety, depression and cognitive dysfunction. Previously, we identified a mutation, A457P, in the norepinephrine (NE; also known as noradrenaline) transporter (NET; encoded by SLC6A2) in POTS patients. NET is expressed at presynaptic sites in NE neurons and plays a crucial role in regulating NE signaling and homeostasis through NE reuptake into noradrenergic nerve terminals. Our in vitro studies demonstrate that A457P reduces both NET surface trafficking and NE transport and exerts a dominant-negative impact on wild-type NET proteins. Here we report the generation and characterization of NET A457P mice, demonstrating the ability of A457P to drive the POTS phenotype and behaviors that are consistent with reported comorbidities. Mice carrying one A457P allele (NET+/P) exhibited reduced brain and sympathetic NE transport levels compared with wild-type (NET+/+) mice, whereas transport activity in mice carrying two A457P alleles (NETP/P) was nearly abolished. NET+/P and NETP/P mice exhibited elevations in plasma and urine NE levels, reduced dihydroxyphenylglycine (DHPG), and reduced DHPG:NE ratios, consistent with a decrease in sympathetic nerve terminal NE reuptake. Radiotelemetry in unanesthetized mice revealed tachycardia in NET+/P mice without a change in blood pressure or baroreceptor sensitivity, consistent with studies of human NET A457P carriers. NET+/P mice also demonstrated behavioral changes consistent with CNS NET dysfunction. Our findings support that NET dysfunction is sufficient to produce a POTS phenotype and introduces the first genetic model suitable for more detailed mechanistic studies of the disorder and its comorbidities.
    Type of Medium: Online Resource
    ISSN: 1754-8411 , 1754-8403
    URL: Article
    DOI: 10.1242/dmm.012203
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2013
    detail.hit.zdb_id: 2451104-3
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  • 6
    Online Resource
    Online Resource
    Portal Osmopressor Mechanism Linked to Transient Receptor Potential Vanilloid 4 and Blood Pressure Control
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Hypertension Vol. 55, No. 6 ( 2010-06), p. 1438-1443
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 55, No. 6 ( 2010-06), p. 1438-1443
    Abstract: Human subjects with impaired baroreflex function cannot buffer rises or falls in blood pressure (BP), thus allowing BP effects of endogenous or environmental stimuli that previously escaped detection to emerge dramatically. Studies in these patients led us to discover that water ingestion induced a robust increase in BP and vascular resistance. Here, using a mouse model of baroreflex impairment, we show that the increase in blood pressure after water ingestion is mediated through sympathetic nervous system activation and that the osmosensitive transient receptor potential vanilloid 4 channel ( Trpv4 ) is an essential component of the response. Although portal osmolality decreases after water ingestion in both wild-type and Trpv4 −/− mice, only the wild-type animals show a pressor response. The same volume of physiological saline does not elicit an increase in BP, suggesting osmolality as the stimulus. The osmopressor response to water, and Trpv4 thus represent new factors now implicated in the physiology of BP regulation.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.110.151860
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 2094210-2
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  • 7
    Online Resource
    Online Resource
    Wavelet Methods for Spike Detection in Mouse Renal Sympathetic Nerve Activity
    Institute of Electrical and Electronics Engineers (IEEE) ; 2007
    In:  IEEE Transactions on Biomedical Engineering Vol. 54, No. 1 ( 2007-01), p. 82-93
    Details
    In: IEEE Transactions on Biomedical Engineering, Institute of Electrical and Electronics Engineers (IEEE), Vol. 54, No. 1 ( 2007-01), p. 82-93
    Type of Medium: Online Resource
    ISSN: 0018-9294
    URL: Article
    DOI: 10.1109/TBME.2006.883830
    RVK:
    XA 48665
    Language: Unknown
    Publisher: Institute of Electrical and Electronics Engineers (IEEE)
    Publication Date: 2007
    detail.hit.zdb_id: 2021742-0
    detail.hit.zdb_id: 2571926-9
    detail.hit.zdb_id: 2561637-7
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  • 8
    Online Resource
    Online Resource
    Norepinephrine Transporter–Deficient Mice Exhibit Excessive Tachycardia and Elevated Blood Pressure With Wakefulness and Activity
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Circulation Vol. 110, No. 10 ( 2004-09-07), p. 1191-1196
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 110, No. 10 ( 2004-09-07), p. 1191-1196
    Abstract: Background— Norepinephrine (NE) is a primary neurotransmitter of central autonomic regulation and sympathetic nerve conduction, and the norepinephrine transporter (NET) is crucial in limiting catecholaminergic signaling. NET is sensitive to antidepressants, cocaine, and amphetamine. NET blockade often is associated with cardiovascular side effects, and NET deficiency is linked to tachycardia in familial orthostatic intolerance. Methods and Results— We telemetrically monitored NET-deficient (NET −/− ) mice to determine the cardiovascular effects of reduced NE reuptake. Mean arterial pressure was elevated in resting NET −/− mice compared with NET +/+ controls (103±0.6 versus 99±0.4 mm Hg; P 〈 0.01), and corresponding pressures increased to 122±0.3 and 116±0.3 mm Hg ( P 〈 0.0001) with activity. Heart rate was also greater in resting NET −/− mice (565±5 versus 551±3 bpm; P 〈 0.05), and genotypic differences were highly significant during the active phase (640±5 versus 607±3 bpm; P 〈 0.0001). Conversely, the respiratory rate of resting NET −/− mice was dramatically reduced, whereas increases after the day/night shift surpassed those of controls. Plasma catecholamines in NET −/− and NET +/+ mice were as follows: NE, 69±8 and 32±7; dihydroxyphenylglycol, 2+0.4 and 17±3; epinephrine, 15±3 and 4±0.6; and dopamine, 13±4 and 4±1 pmol/mL. Catechols in urine, brain, and heart also were determined. Conclusions— Resting mean arterial pressure and heart rate are maintained at nearly normal levels in NET-deficient mice, most likely as a result of increased central sympathoinhibition. However, sympathetic activation with wakefulness and activity apparently overwhelms central modulation, amplifying peripheral catecholaminergic signaling, particularly in the heart.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.0000141804.90845.E6
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 1466401-X
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  • 9
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    Online Resource
    Animal Model of Neuropathic Tachycardia Syndrome
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Hypertension Vol. 37, No. 6 ( 2001-06), p. 1357-1361
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 37, No. 6 ( 2001-06), p. 1357-1361
    Abstract: Abstract —Clinically relevant autonomic dysfunction can result from either complete or partial loss of sympathetic outflow to effector organs. Reported animal models of autonomic neuropathy have aimed to achieve complete lesions of sympathetic nerves, but incomplete lesions might be more relevant to certain clinical entities. We hypothesized that loss of sympathetic innervation would result in a predicted decrease in arterial pressure and a compensatory increase in heart rate. Increased heart rate due to loss of sympathetic innervation is seemingly paradoxical, but it provides a mechanistic explanation for clinical autonomic syndromes such as neuropathic postural tachycardia syndrome. Partially dysautonomic animals were generated by selectively lesioning postganglionic sympathetic neurons with 150 mg/kg 6-hydroxydopamine hydrobromide in male Sprague-Dawley rats. Blood pressure and heart rate were monitored using radiotelemetry. Systolic blood pressure decreased within hours postlesion (Δ 〉 20 mm Hg). Within 4 days postlesion, heart rate rose and remained elevated above control levels. The severity of the lesion was determined functionally and pharmacologically by spectral analysis and responsiveness to tyramine. Low-frequency spectral power of systolic blood pressure was reduced postlesion and correlated with the diminished tyramine responsiveness ( r =0.9572, P =0.0053). The tachycardia was abolished by treatment with the β-antagonist propranolol, demonstrating that it was mediated by catecholamines acting on cardiac β-receptors. Partial lesions of the autonomic nervous system have been hypothesized to underlie many disorders, including neuropathic postural tachycardia syndrome. This animal model may help us better understand the pathophysiology of autonomic dysfunction and lead to development of therapeutic interventions.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.37.6.1357
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
    detail.hit.zdb_id: 2094210-2
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  • 10
    Online Resource
    Online Resource
    The pressor effect of water: mechanism and location of action
    Wiley ; 2009
    In:  The FASEB Journal Vol. 23, No. S1 ( 2009-04)
    Details
    In: The FASEB Journal, Wiley, Vol. 23, No. S1 ( 2009-04)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v23.S1
    DOI: 10.1096/fasebj.23.1_supplement.1019.26
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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