GLORIA

GEOMAR Library Ocean Research Information Access

You have 0 saved results.
Mark results and click the "Add To Watchlist" link in order to add them to this list.
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 47 (1986), S. 0 
    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
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 5 (1978), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2014-09-13
    Description: BACKGROUND Obesity is associated with elevated cardiovascular mortality, which may be attributed, in part, to sympathetic nervous system (SNS) activation and an associated poor metabolic profile. We examined the effects of laparoscopic adjustable gastric band (LAGB) on SNS activity and cardiovascular profile when the initial weight loss of 10%, corresponding to the recommendation of clinical guidelines, was reached. METHODS Direct muscle sympathetic nerve activity (MSNA, microneurography), baroreflex function, and cardiovascular profile were examined before and after a predetermined weight loss of 10% in 23 severely obese nondiabetic individuals. RESULTS The 10% weight loss was achieved at an average of 7.3±1.4 months (range = 1.3–23.3 months). This was associated with significant improvement in office systolic and diastolic blood pressure (BP) (–12mm Hg and –5mm Hg, respectively), a decrease in MSNA (33±3 to 22±3 bursts per minute), improvement in cardiac (16±3 to 31±4ms/mm Hg) and sympathetic (–2.23±0.39 to –4.30±0.96 bursts/100 heartbeats/mm Hg) baroreflex function, total cholesterol (5.33±0.13 to 4.97±0.16 mmol/L), fasting insulin (29.3±2.4 to 19.6±1.1 mmol/L), and creatinine clearance (172±11 to 142±8ml/min). None of the cardiovascular risk improvement related to the rate of weight loss. The change in systolic and diastolic BP correlated with change in waist circumference ( r = 0.46, P = 0.04; r = 0.50, P = 0.02, respectively). CONCLUSIONS The initial 10% weight loss induced by LAGB was associated with substantial hemodynamic, metabolic, SNS, and renal function improvements. Changes in waist circumference appear to be an important factor contributing to BP adaptation after LAGB surgery.
    Print ISSN: 0895-7061
    Electronic ISSN: 1879-1905
    Topics: Medicine
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 2016-05-03
    Description: One of the main constraints associated with recording sympathetic nerve activity (SNA) in both humans and experimental animals is that microvolt values reflect characteristics of the recording conditions and limit comparisons between different experimental groups. The nasopharyngeal response has been validated for normalizing renal SNA (RSNA) in conscious rabbits, and in humans muscle SNA is normalized to the maximum burst in the resting period. We compared these two methods of normalization to determine whether either could detect elevated RSNA in hypertensive rabbits compared with normotensive controls. We also tested whether either method eliminated differences based only on different recording conditions by separating RSNA of control (sham) rabbits into two groups with low or high microvolts. Hypertension was induced by 5 wk of renal clipping (2K1C), 3 wk of high-fat diet (HFD), or 3 mo infusion of a low dose of angiotensin (ANG II). Normalization to the nasopharyngeal response revealed RSNA that was 88, 51, and 34% greater in 2K1C, HFD, and ANG II rabbits, respectively, than shams ( P 〈 0.05), but normalization to the maximum burst showed no differences. The RSNA baroreflex followed a similar pattern whether RSNA was expressed in microvolts or normalized. Both methods abolished the difference between low and high microvolt RSNA. These results suggest that maximum burst amplitude is a useful technique for minimizing differences between recording conditions but is unable to detect real differences between groups. We conclude that the nasopharyngeal reflex is the superior method for normalizing sympathetic recordings in conscious rabbits.
    Print ISSN: 0363-6135
    Electronic ISSN: 1522-1539
    Topics: Medicine
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 5
    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
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 6
    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
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 7
    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
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 8
    Publication Date: 2016-04-14
    Keywords: Endothelium/Vascular Type/Nitric Oxide, Nephrology and Kidney, Oxidant Stress, Hypertension
    Print ISSN: 0194-911X
    Topics: Medicine
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 9
    Publication Date: 2013-09-12
    Description: Genetically hypertensive mice (BPH/2J) are hypertensive because of an exaggerated contribution of the sympathetic nervous system to blood pressure. We hypothesize that an additional contribution to elevated blood pressure is via sympathetically mediated activation of the intrarenal renin–angiotensin system. Our aim was to determine the contribution of the renin–angiotensin system and sympathetic nervous system to hypertension in BPH/2J mice. BPH/2J and normotensive BPN/3J mice were preimplanted with radiotelemetry devices to measure blood pressure. Depressor responses to ganglion blocker pentolinium (5 mg/kg IP) in mice pretreated with the angiotensin-converting enzyme inhibitor enalaprilat (1.5 mg/kg IP) revealed a 2-fold greater sympathetic contribution to blood pressure in BPH/2J mice during the active and inactive period. However, the depressor response to enalaprilat was 4-fold greater in BPH/2J compared with BPN/3J mice, but only during the active period ( P =0.01). This was associated with 1.6-fold higher renal renin messenger RNA (mRNA; P =0.02) and 0.8-fold lower abundance of micro-RNA-181a ( P =0.03), identified previously as regulating human renin mRNA. Renin mRNA levels correlated positively with depressor responses to pentolinium ( r =0.99; P =0.001), and BPH/2J mice had greater renal sympathetic innervation density as identified by tyrosine hydroxylase staining of cortical tubules. Although there is a major sympathetic contribution to hypertension in BPH/2J mice, the renin–angiotensin system also contributes, doing so to a greater extent during the active period and less during the inactive period. This is the opposite of the normal renin–angiotensin system circadian pattern. We suggest that renal hyperinnervation and enhanced sympathetically induced renin synthesis mediated by lower micro-RNA-181a contributes to hypertension in BPH/2J mice.
    Keywords: Cardiovascular Pharmacology, Animal models of human disease, Other hypertension
    Print ISSN: 0194-911X
    Topics: Medicine
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 10
    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
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...