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  • 1
    Electronic Resource
    Electronic Resource
    Evidence for a Selective Localization of Voltage-Sensitive Ca2+ Channels in Nerve Cell Bodies of Corpus Striatum (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 47 (1986), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract Specific binding sites for [3H]nitrendipine, an organic Ca2+ channel antagonist, were abolished in crude syn-aptosomal membranes of kainic acid-lesioned caudate nuclei. In contrast, specific lesions of dopaminergic or serotonergic axon terminals in caudate nuclei failed to alter the density or the affinity of [3H]nitrendipine binding sites. In addition, the basal and veratridine-stimulated 45Ca2+ accumulations were greatly impaired in slices prepared from kainic acid-lesioned caudate nuclei. The veratridine-elicited accumulation of 45Ca2+ in control slices was attenuated by addition of tetrodotoxin in the incubation medium. The present data provide evidence that most of the [3H]nitrendipine binding sites and the voltage-dependent Ca2+ channels are located in intrinsic neurons or interneurons in caudate nucleus. In contrast, destruction of dopaminergic or serotonergic nerve terminals emanating from other brain areas and innervating the caudate nucleus failed to change the apparent Bmax value for [3H]nitrendipine binding.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1986.tb00794.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    ACTIONS OF TETRAHYDROPAPAVEROLINE ON THE CARDIOVASCULAR SYSTEM AND SKELETAL MUSCLES OF THE ANAESTHETIZED CAT AND ON GUINEA-PIG SOLEUS MUSCLE IN VITRO (1978)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 5 (1978), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1978.tb00680.x
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  • 3
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    Exposure to a High-Fat Diet During Development Alters Leptin and Ghrelin Sensitivity and Elevates Renal Sympathetic Nerve Activity and Arterial Pressure in Rabbits [Nervous System] (2014)
    American Heart Association (AHA)
    Details
    Publication Date: 2014-01-09
    Description: Exposure to maternal obesity or a maternal diet rich in fat during development may have adverse outcomes in offspring, such as the development of obesity and hypertension. The present study examined the effect of a maternal high-fat diet (m-HFD) on offspring blood pressure and renal sympathetic nerve activity, responses to stress, and sensitivity to central administration of leptin and ghrelin. Offspring of New Zealand white rabbits fed a 13% HFD were slightly heavier than offspring from mothers fed a 4% maternal normal fat diet ( P 〈0.05) but had 64% greater fat pad mass ( P =0.015). Mean arterial pressure, heart rate, and renal sympathetic nerve activity at 4 months of age were 7%, 7%, and 24% greater, respectively ( P 〈0.001), in m-HFD compared with maternal normal fat diet rabbits, and the renal sympathetic nerve activity response to airjet stress was enhanced in the m-HFD group. m-HFD offspring had markedly elevated pressor and renal sympathetic nerve activity responses to intracerebroventricular leptin (5–100 µg) and enhanced sympathetic responses to intracerebroventricular ghrelin (1–5 nmol). In contrast, there was resistance to the anorexic effects of intracerebroventricular leptin and less neuronal activation as detected by Fos immunohistochemistry in the arcuate (–57%; P 〈0.001) and paraventricular (–37%; P 〈0.05) nuclei of the hypothalamus in m-HFD offspring compared with maternal normal fat diet rabbits. We conclude that offspring from mothers consuming an HFD exhibit an adverse cardiovascular profile in adulthood because of altered central hypothalamic sensitivity to leptin and ghrelin.
    Print ISSN: 0194-911X
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 4
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    Cardiovascular role of angiotensin type1A receptors in the nucleus of the solitary tract of mice (2013)
    Oxford University Press
    Details
    Publication Date: 2013-10-17
    Description: Aims The nucleus of the solitary tract (NTS) is important for cardiovascular regulation and contains angiotensin type 1A (AT 1A ) receptors. To assess its function, we examined the effect of expressing in AT 1A receptors in the NTS of mice lacking these receptors. Methods and results Bilateral microinjections of lentivirus expressing AT 1A receptors (AT 1A v mice, n = 6) or green fluorescent protein (GFPv, n = 8, control) under the control of the PRSx8 promotor were made into the NTS of AT 1A receptors null mice (AT 1A –/– ). Telemetry devices recorded blood pressure (BP), heart rate (HR), and locomotor activity. Expression of AT 1A receptors in the NTS increased BP by 11.2 ± 4 mmHg ( P 〈 0.05) at 2 and 3 weeks, whereas GFPv mice remained at pre-injection BP. Ganglion blockade reduced BP to similar levels pre- and post-transfection in GFPv and AT 1A v mice. Greater pressor responses to cage-switch stress were observed following AT 1A receptors expression (+18 ± 2 mmHg pre- to +24 ± 2 mmHg post-virus, P 〈 0.05) with similar stress-induced pressor responses pre- and post-virus in GFPv mice. Pressor responses to restraint stress pre- and post-virus were similar in AT 1A v but were 20% less post-GFPv ( P 〈 0.001). The lack of attenuation in BP to restraint was associated with four-fold greater Fos-expression in AT 1A receptors mice. AT 1A receptors expression in the NTS did not alter baroreflex gain differently between groups. Conclusion The results suggest that transfection of AT 1A receptors on neurons in the NTS elevates BP independent of the SNS and pressor responses to aversive stimuli are associated with greater Fos-expression in forebrain regions. This study suggests a novel mechanism by which the NTS may modulate MAP in the long-term via AT 1A receptors.
    Print ISSN: 0008-6363
    Electronic ISSN: 1755-3245
    Topics: Medicine
    Published by Oxford University Press
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  • 5
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    Major Contribution of the Medial Amygdala to Hypertension in BPH/2J Genetically Hypertensive Mice [Nervous System] (2014)
    American Heart Association (AHA)
    Details
    Publication Date: 2014-03-13
    Description: BPH/2J mice are recognized as a neurogenic model of hypertension primarily based on overactivity of the sympathetic nervous system and greater neuronal activity in key autonomic cardiovascular regulatory brain regions. The medial amygdala (MeAm) is a forebrain region that integrates the autonomic response to stress and is the only region found to have greater Fos during the night and daytime in BPH/2J compared with BPN/3J mice. To determine the contribution of the MeAm to hypertension, the effect of neuronal ablation on blood pressure (BP) was assessed in BPH/2J (n=7) and normotensive BPN/3J mice (n=7). Mice were preimplanted with radiotelemetry devices to measure 24-hour BP and cardiovascular responses to stress, before and 1 to 3 weeks after bilateral lesions of the MeAm. Baseline BP was 121±4 mm Hg in BPH/2J and 101±2 mm Hg in BPN/3J mice ( P strain 〈0.001). MeAm lesions reduced BP by 11±2 mm Hg in BPH/2J mice ( P lesion 〈0.001) but had no effect in BPN/3J mice. The hypotensive effect of lesions in BPH/2J mice was similar during both day and night, suggesting that the MeAm has tonic effects on BP, but the pressor response to stress was maintained in both strains. Midfrequency BP power was attenuated in both strains ( P lesion 〈0.05) and the depressor responses to pentolinium after enalaprilat pretreatment was attenuated after lesions in BPH/2J mice ( P lesion 〈0.001; n=3). These findings indicate that the MeAm provides a tonic contribution to hypertension in BPH/2J mice, which is independent of its role in stress reactivity or circadian BP influences.
    Keywords: Animal models of human disease, Other hypertension, Other etiology
    Print ISSN: 0194-911X
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 6
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    Stimulation of Angiotensin Type 1A Receptors on Catecholaminergic Cells Contributes to Angiotensin-Dependent Hypertension [Renin-Angiotensin System] (2013)
    American Heart Association (AHA)
    Details
    Publication Date: 2013-10-17
    Description: Hypertension contributes to multiple forms of cardiovascular disease and thus morbidity and mortality. The mechanisms inducing hypertension remain unclear although the involvement of homeostatic systems, such as the renin–angiotensin and sympathetic nervous systems, is established. A pivotal role of the angiotensin type 1 receptor in the proximal tubule of the kidney for the development of experimental hypertension is established. Yet, other systems are involved. This study tests whether the expression of angiotensin type 1A receptors in catecholaminergic cells contributes to hypertension development. Using a Cre-lox approach, we deleted the angiotensin type 1A receptor from all catecholaminergic cells. This deletion did not alter basal metabolism or blood pressure but delayed the onset of angiotensin-dependent hypertension and reduced the maximal response. Cardiac hypertrophy was also reduced. The knockout mice showed attenuated activation of the sympathetic nervous system during angiotensin II infusion as measured by spectral analysis of the blood pressure. Increased reactive oxygen species production was observed in forebrain regions, including the subfornical organ, of the knockout mouse but was markedly reduced in the rostral ventrolateral medulla. These studies demonstrate that stimulation of the angiotensin type 1A receptor on catecholaminergic cells is required for the full development of angiotensin-dependent hypertension and support an important role for the sympathetic nervous system in this model.
    Keywords: Other hypertension
    Print ISSN: 0194-911X
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 7
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    Blood Pressure Variability and Prediction of Target Organ Damage in Patients With Uncomplicated Hypertension (2016)
    Oxford University Press
    Details
    Publication Date: 2016-08-10
    Description: BACKGROUND The average of multiple blood pressure (BP) readings (mean BP) independently predicts target organ damage (TOD). Observational studies have also shown an independent relationship between BP variability (BPV) and TOD, but there is limited longitudinal data. This study aimed to determine the effects of changes in mean BP levels compared with BPV on left ventricular mass index (LVMI) and aortic pulse wave velocity (aPWV). METHODS Mean BP levels (research-protocol clinic BP (clinic BP), 24-hour ambulatory BP, and 7-day home BP) and BPV were assessed in 286 patients with uncomplicated hypertension (mean age 64±8 SD years, 53% women) over 12 months. Reading-to-reading BPV (from 24-hour ambulatory BP) and day-to-day BPV (from 7-day home BP) were assessed at baseline and 12 months, and visit-to-visit BPV (clinic BP) was assessed from 5 visits over 12 months. LVMI was measured by 3D echocardiography and aPWV with applanation tonometry. RESULTS The strongest predictors of the changes in LVMI (LVMI) were the changes in mean 24-hour systolic BPs (SBPs) ( P 〈 0.02). Similarly, the strongest predictors of the changes in aPWV (aPWV) were the changes in mean 24-hour ambulatory SBPs ( P 〈 0.01) and the changes in mean clinic SBP ( P 〈 0.001). However, none of the changes in BPV were independently associated with LVMI or aPWV ( P 〉 0.05 for all). CONCLUSIONS Changes in mean BP levels, but not BPV, were most relevant to changes in TOD in patients with uncomplicated hypertension. Thus, from this point of view, BPV appears to have limited clinical utility in this patient population.
    Print ISSN: 0895-7061
    Electronic ISSN: 1879-1905
    Topics: Medicine
    Published by Oxford University Press
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  • 8
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    Say NO to Obesity-Related Hypertension: Role of the L-Arginine-Nitric Oxide Pathway [Brief Reviews] (2016)
    American Heart Association (AHA)
    Details
    Publication Date: 2016-04-14
    Keywords: Endothelium/Vascular Type/Nitric Oxide, Nephrology and Kidney, Oxidant Stress, Hypertension
    Print ISSN: 0194-911X
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 9
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    Origin of Aberrant Blood Pressure and Sympathetic Regulation in Diet-Induced Obesity [Obesity] (2016)
    American Heart Association (AHA)
    Details
    Publication Date: 2016-07-14
    Description: High fat diet (HFD)–induced hypertension in rabbits is neurogenic and caused by the central action of leptin, which is thought to be dependent on activation of α-melanocortin–stimulating hormone (α-MSH) and neuropeptide Y–positive neurons projecting to the dorsomedial hypothalamus (DMH) and ventromedial hypothalamus (VMH). However, leptin may act directly in these nuclei. Here, we assessed the contribution of leptin, α-MSH, and neuropeptide Y signaling in the DMH and VMH to diet-induced hypertension. Male New Zealand white rabbits were instrumented with a cannula for drug injections into the DMH or VMH and a renal sympathetic nerve activity (RSNA) electrode. After 3 weeks of an HFD (13.3% fat; n=19), rabbits exhibited higher RSNA, mean arterial pressure (MAP), and heart rate compared with control diet–fed animals (4.2% fat; n=15). Intra-VMH injections of a leptin receptor antagonist or SHU9119, a melanocortin 3/4 receptor antagonist, decreased MAP, heart rate, and RSNA compared with vehicle in HFD rabbits ( P 〈0.05) but not in control diet–fed animals. By contrast, α-MSH or neuropeptide Y injected into the VMH had no effect on MAP but produced sympathoexcitation in HFD rabbits ( P 〈0.05) but not in control diet–fed rabbits. The effects of the leptin antagonist, α-MSH, or neuropeptide Y injections into the DMH on MAP or RSNA of HFD rabbits were not different from those after vehicle injection. α-MSH into the DMH of control diet–fed animals did increase MAP, heart rate, and RSNA. We conclude that the VMH is the likely origin of leptin-mediated sympathoexcitation and α-MSH hypersensitivity that contribute to obesity-related hypertension.
    Keywords: High Blood Pressure, Hypertension
    Print ISSN: 0194-911X
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 10
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    Contribution of Orexin to the Neurogenic Hypertension in BPH/2J Mice [Nervous System] (2016)
    American Heart Association (AHA)
    Details
    Publication Date: 2016-04-14
    Description: BPH/2J mice are a genetic model of hypertension associated with an overactive sympathetic nervous system. Orexin is a neuropeptide which influences sympathetic activity and blood pressure. Orexin precursor mRNA expression is greater in hypothalamic tissue of BPH/2J compared with normotensive BPN/3J mice. To determine whether enhanced orexinergic signaling contributes to the hypertension, BPH/2J and BPN/3J mice were preimplanted with radiotelemetry probes to compare blood pressure 1 hour before and 5 hours after administration of almorexant, an orexin receptor antagonist. Mid frequency mean arterial pressure power and the depressor response to ganglion blockade were also used as indicators of sympathetic nervous system activity. Administration of almorexant at 100 (IP) and 300 mg/kg (oral) in BPH/2J mice during the dark-active period (2 hours after lights off) markedly reduced blood pressure (–16.1±1.6 and –11.0±1.1 mm Hg, respectively; P 〈0.001 compared with vehicle). However, when almorexant (100 mg/kg, IP) was administered during the light-inactive period (5 hours before lights off) no reduction from baseline was observed ( P =0.64). The same dose of almorexant in BPN/3J mice had no effect on blood pressure during the dark ( P =0.79) or light periods ( P =0.24). Almorexant attenuated the depressor response to ganglion blockade ( P =0.018) and reduced the mid frequency mean arterial pressure power in BPH/2J mice ( P 〈0.001), but not BPN/3J mice ( P =0.70). Immunohistochemical labeling revealed that BPH/2J mice have 29% more orexin neurons than BPN/3J mice which are preferentially located in the lateral hypothalamus. The results suggest that enhanced orexinergic signaling contributes to sympathetic overactivity and hypertension during the dark period in BPH/2J mice.
    Keywords: Animal Models of Human Disease, Basic Science Research, Hypertension
    Print ISSN: 0194-911X
    Topics: Medicine
    Published by American Heart Association (AHA)
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