scholarly journals Is it all in our Heads? The Role of CaMKII in Neurogenic Hypertension

2018 ◽  
Vol 6 (3) ◽  
pp. 129-131
Author(s):  
Nathaniel Edward Hayward ◽  
Paul MacDaragh Ryan ◽  
Ryan Taylor Sless
Keyword(s):  
Neurogenic Hypertension

Abstract MP06: Kinin B1 Receptor Mediates Orexin System Hyperactivity In Salt-sensitive Hypertension

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Rohan U Parekh ◽  
Abdel A Abdel-rahman ◽  
Srinivas Sriramula
Keyword(s):  
Radio Telemetry ◽  
Mrna Levels ◽  
Wild Type ◽  
Salt Treatment ◽  
Neurogenic Hypertension ◽  
B1 Receptor ◽  
Kinin B1 Receptor ◽  
Salt Sensitive Hypertension ◽  
The Brain

Hyperactivity of the orexin system contributes to several animal models of hypertension and enhances arginine vasopressin (AVP) release. We previously reported higher neuronal kinin B1 receptor (B1R) expression and brain AVP levels in hypertensive mice. However, the role of B1R and its interaction with orexin system in neurogenic hypertension have not been studied. In the present study, we tested the hypothesis that kinin B1R contributes to hypertension by upregulation of orexin-AVP signaling in the brain. Deoxycorticosterone acetate (DOCA)-salt treatment (1 mg/g body weight DOCA, 1% saline in drinking water, 3 weeks) of wild-type (WT) male mice produced a significant increase in mean arterial pressure (MAP; radio-telemetry) (138 ±3 mmHg, n=8, p<0.01) that was blunted in B1R knockout mice (121±2 mmHg, P <0.05 vs. WT+DOCA). In WT mice, DOCA-salt, compared to vehicle, increased mRNA levels of orexin receptor 1 (2.5 fold, n=9, p<0.001), orexin receptor 2 (3 fold, n=9, p<0.001) and AVP (3 fold, n=9, p<0.01) in the hypothalamic paraventricular nucleus (PVN), and these DOCA-salt evoked effects were attenuated in B1RKO mice. Similarly, DOCA-salt evoked increases in protein expression of orexin receptor 1 and 2 in the hypothalamic PVN of WT mice were attenuated by 25±5% and 33±5% (p<0.05), respectively, in B1RKO vs WT+DOCA mice. Furthermore, DOCA-salt treatment increased plasma AVP levels in WT mice compared to vehicle treated mice (13.69±1.1 vs. 47.86±8.7 pg/ml, p<0.05), but not in B1RKO mice. Together, these data provide novel evidence that kinin B1R plays an important role in mediating DOCA-salt induced hypertension possibly via upregulating the orexin-AVP signaling in the brain.

scholarly journals A reversal of fate : unravelling the role of central 5-HT in cardiorespiratory control in neonatal and adult rodents

2018 ◽  
Author(s):  
◽  
Jennifer Magnusson
Keyword(s):  
Blood Pressure ◽  
Physiological Role ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Autonomic Tone ◽  
Neurogenic Hypertension ◽  
Cardiorespiratory Control ◽  
Arterial Blood ◽  
Lower Blood

We seek to address the extent to which a specific loss of 5-hydroxytryptamine (5-HT) affects the control of respiration, arterial blood pressure (ABP) and heart rate (HR) across vigilance-states based on existing evidence suggesting that 5-HT defects increase the risk for Sudden Infant Death Syndrome (SIDS) and neurogenic hypertension. SIDS is the leading cause of infant mortality between 1 month and 1 year of age, occurs during sleep, and up to 70% of all SIDS cases have at least one 5-HT system abnormality. Neonatal rodents lacking central 5-HT exhibit severe apneas, and a reduced ABP and HR. Central 5-HT has been implicated in the etiology of neurogenic hypertension, presumably due to projections of 5-HT neurons within the midline raphe to vagal and presympathetic regions of the brain. However, data from studies examining the specific role of central 5-HT function is conflicting or inconclusive. Neurogenic hypertension accounts for more than 90% of all hypertensive cases and the normal fall in ABP that occurs during non-rapid eye movement sleep is absent in some patients with hypertension. Understanding the mechanisms associated with the development of hypertension is critical not only to lower blood pressure, but to lower its associated cardiovascular events. The purpose of this dissertation is to examine the role of central 5-HT in the control of ABP during sleep and reveal, mechanistically, the physiological role of 5-HT in the autonomic control of ABP in neonatal and adult rodents. The overarching hypothesis for this dissertation is that central 5-HT is required for the maintenance of ABP and autonomic tone at rest in both neonatal and adult rodents.

The role of MRI in screening for neurogenic hypertension

2000 ◽  
Vol 42 (2) ◽  
pp. 99-103 ◽  
Author(s):  
D. Johnson ◽  
S. C. Coley ◽  
J. Brown ◽  
I. F. Moseley
Keyword(s):  
Neurogenic Hypertension

Neurogenic hypertension related to basilar impression

1993 ◽  
Vol 79 (6) ◽  
pp. 924-928 ◽  
Author(s):  
Lawrence D. Dickinson ◽  
Stephen M. Papadopoulos ◽  
Julian T. Hoff
Keyword(s):  
Essential Hypertension ◽  
Clinical Evidence ◽  
Basilar Invagination ◽  
Central Regulation ◽  
Basilar Impression ◽  
Neurogenic Hypertension ◽  
Content Type ◽  
Transoral Odontoidectomy ◽  
Fine Print

✓ The authors report the resolution of essential hypertension following transoral odontoidectomy and medullary decompression in a 39-year-old woman with basilar invagination. Current understanding of central regulation of the cardiovascular system is discussed and the pertinent neuroanatomy illustrated. Experimental and clinical evidence supporting the role of neurogenic mechanisms in the pathogenesis of hypertension is reviewed.

Abstract 305: Activation of Central Angiotensin II type 2 Receptors Attenuates Neurogenic Hypertension.

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Sofie Brouwers ◽  
Richard D Wainford ◽  
Ilse Smolders ◽  
Alain G Dupont
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Radio Telemetry ◽  
Treated Group ◽  
Vehicle Group ◽  
Blood Pressure Lowering Effect ◽  
Neurogenic Hypertension ◽  
Lowering Effect

Aim: The role of the angiotensin II type-2 receptor (AT2R) in hypertension is under debate and the expression can be modulated in different pathological states. In hypertension AT2R are upregulated, therefore we hypothesize that central AT2R stimulation will lower blood pressure in conscious spontaneously hypertensive rats (SHR). Methods: SHR were implanted with a radio-telemetry device and an icv cannula connected to a miniosmotic pump delivering saline vehicle, AT2R agonist Compound 21 (C21) (0.002μg/μl/hr) alone or in combination with AT2R antagonist PD123319. MAP was assessed for 21 days: 7 days baseline (saline), 14 days treatment (e.g. C21). To assess the role of the angiotensin II type-1 receptor (AT1R) and NO in these responses, AT1R blocker losartan or NO synthase inhibitor L-NAME were administered centrally with C21. (n=5-7/group). Results: Icv C21-infusion blocked the increase in MAP seen in the vehicle group (MAP (mmHg): baseline: vehicle 153±5 vs C21 157±4; day 21 (D21): vehicle 164±5 vs C21 155±5;p<0.05). PD123319 abolished this blood pressure lowering effect (MAP (mmHg): baseline 154±5; D21 163±5;p<0.05). Co-infusion of C21 and losartan did not reinforce the MAP lowering effect seen with C21 alone (MAP (mmHg): baseline 157±2; D21 153±1;p<0.05). Simultaneous L-NAME administration abolished the effects of C21 (MAP (mmHg): baseline 156±4; D21 190±5;p<0.05). Mechanistically, an improved parasympathetic control of HR was seen in the C21-treated group (change in HR after i.p. propranolol (bpm): vehicle -68.2±2.4 vs C21 -36.3±4.1;p<0.05). Impaired baroreflex sensitivity (BRS) also improved under C21-infusion (BRS (ms/mmHg) D21: vehicle 1.81±0.16 vs C21 3.15±0.07;p<0.05) Conclusion: Selective central AT2R stimulation with C21 attenuates hypertension and corrects autonomic dysfunction in SHR. These effects are mediated through a NO-dependent mechanism. In contrast to an enhanced peripheral AT2R effect following AT1R blockade, concomitant central AT1R blockade did not enhance these responses to central AT2R stimulation. These findings suggest activation of the central AT2R represent a possible new therapeutic target for the treatment of neurogenic hypertension.

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