Neurohumoral Response to Hospitalization in Hypertensive Patients

1981 ◽  
Vol 61 (s7) ◽  
pp. 385s-387s ◽  
Author(s):  
P. W. De Leeuw ◽  
G. A. W. Van Soest ◽  
R. Punt ◽  
R. P. L. M. Hoogma ◽  
A. J. P. M. Smout ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Group 2 ◽  
Reduced Activity ◽  
Hypotensive Response ◽  
Group 1 ◽  
Noradrenaline Levels

1. To investigate whether reduced activity of pressor systems could explain the spontaneous drop in pressure upon hospitalization, 51 subjects with uncomplicated essential hypertension were admitted to hospital. Sodium intake was fixed at 55 mmol/day. 2. Blood samples for noradrenaline, adrenaline, active renin, angiotensin II and aldosterone were drawn on each morning of the first 3 days of hospitalization; blood pressure was measured at 2 h intervals and values were averaged for each day. 3. Subjects were divided in two groups depending on whether they became normotensive (group 1; n = 12) or remained hypertensive (group 2; n = 39). This distinction was thought to reflect mild and more severe hypertensive groups respectively. 4. Although both groups showed a comparable fall in blood pressure during hospitalization, noradrenaline levels fell more consistently in group 1, whereas adrenaline levels fell only in group 2. The components of the renin—angiotensin—aldosterone system rose, but more conspicuously in group 1. 5. It is concluded that withdrawal of sympathetic activity can only partly explain the hypotensive response to hospitalization. The renin—angiotensin system behaves only passively and appears to be counterproductive to alterations in blood pressure.

Abstract 84: Angiotensin II Type 1a Receptor in the Subfornical Organ is Essential for Blood Pressure Regulation and Hydromineral Effects in Mouse Models of Elevated Brain Renin-Angiotensin System Activity.

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Aline Hilzendeger ◽  
Deborah R Davis ◽  
Martin D Cassell ◽  
Allyn L Mark ◽  
Justin L Grobe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Dna Recombination ◽  
Renin Angiotensin System ◽  
Cre Recombinase ◽  
Subfornical Organ ◽  
Specific Expression ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Conditional Allele

Elevated brain renin-angiotensin system (RAS) activity is necessary to increase blood pressure in many animal models of hypertension. We tested the hypothesis that AT1A receptors (AT1AR) within the subfornical organ (SFO) are required for the phenotypes that result from an increased brain RAS. We examined the effect of SFO-targeted Cre-recombinase mediated ablation of AT1A in mice treated with DOCA-salt (deoxycorticosterone acetate, 50 mg s.c. + ad lib 0.15 M NaCl). Mice homozygous for a conditional allele of the endogenous AT1A gene (AT1ARflox) were administered an adenovirus encoding Cre-recombinase and eGFP (AdCre), or eGFP alone (AdGFP) into the lateral cerebral ventricle, then treated for 3 weeks with DOCA-salt. AdCre reduced DOCA-salt hypertension (AdGFP baseline: 108±3 mmHg; AdGFP pre-DOCA: 104±3; AdGFP post-DOCA: 136±6 vs AdCre baseline: 116±2; Adcre pre-DOCA: 109±3, Adre post-DOCA: 118±5; P≤0.01), polydipsia (AdGFP+DOCA: 20.6±2.1 mL/day; AdCre+DOCA: 11.6±1.1, P<0.05), and sodium intake (AdGFP+DOCA: 2.6±0.3 mEq/day; AdCre+DOCA: 1.8±0.2, P<0.05). AdCre reduced AT1AR mRNA in the SFO (0.4±0.3 fold of AdGFP), without significant effect in the paraventricular or arcuate nuclei, or cortex; this was paralleled by SFO-specific AT1AR genomic DNA recombination. AdCre also caused SFO-specific recombination in ROSA-TdTomato reporter mice. Complementing the DOCA-salt model, we also examined the effect of AT1AR ablation in the SFO of double-transgenic sRA mice. sRA mice exhibit life-long brain-specific angiotensin overproduction via expression of human angiotensinogen via its own promoter and neuron-specific expression of human renin via the synapsin promoter. In sRA mice bred onto the AT1A conditional genetic background, AdCre significantly attenuated the polydipsia (AdGFP: -0.2±2; AdCre: -9.7±2.6 mL/day) and sodium intake (AdGFP: +0.2±0.7; AdCre: -1.3±0.4 mEq/day). Blood pressure measures are in progress. Together, these data highlight the involvement of SFO AT1A receptors in blood pressure in DOCA-salt model and additionally in hydromineral balance in two different models of increased brain RAS activity.

Antisense Inhibition of Central, But not Peripheral Renin Angiotensin System Decreased Arterial Pressure in Chronic Phase of Two-Kidney, One Clip Hypertensive Rats

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 729-729
Author(s):  
Shuntaro Kagiyama ◽  
S M Galli ◽  
M. Ian Phillips
Keyword(s):  
Chronic Phase ◽  
Renin Angiotensin System ◽  
Saline Group ◽  
Chronic Hypertension ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Group 2 ◽  
The Brain ◽  
Group 1

P198 Introduction: The systemic renin angiotensin system (RAS) plays an important role in blood pressure (BP) regulation during the development of two-kidney, one clip hypertension (2K1C). Its contributions decrease with time after constriction of the renal artery. During the chronic phase, the peripheral RAS returns to normal, nevertheless for months the hypertension is sustained. We hypothesized that during this phase of 2K1C hypertension, the brain RAS contributes to the maintenance of high BP. Methods: Therefore, we studied in the role of brain RAS by decreasing the synthesis of angiotensinogen (AGT) and angiotensin type 1a receptors (AT1R) with intracerebroventricular (ICV) injection of antisense oligonucleotides (AS-ODN). The response of systolic BP (SBP) to AS-ODN to AGT was studied at 6 mo(Group 1) and the response to AS-ODN to AT1R at 10 mo post clipping (Group 2). Each group was divided into AS-ODN, sense or inverted ODN, and saline subgroups. All groups were implanted with ICV cannulae one week before treatment. SBP was monitored by tail cuff method. Plasma and brain angiotensin II (AngII) content was measured by radioimmunoassay in all treated 2K1C groups and in nonclipped rats. Results: The results show that in Group 1, at 6 mo post clipping, the ICV AS-ODN to AGT (200 μg/kg, n=5) significantly decreased SBP(≈−22±6 mmHg, P<0.05)compared to sense ODN and saline group (n=5). The hypothalamic AngII content in sense ODN and saline groups was significantly (P<0.05) higher than in nonclipped rats. AS-ODN to AGT reduced the elevated hypothalamic AngII level. Plasma AngII was significantly decreased in the clipped group (40±12 pg/ml) compared with nonclipped group (75±8 pg/ml). In Group 2, 10 mo post clipping, the ICV injection of AS-ODN to AT1R (250 μg/kg, n=6) significantly decreased SBP(≈−26±8 mmHg, P<0.05) for 3 days post injection, compared to inverted ODN. In contrast, intravenous AS-ODN to AT1R in dose of 250-500 μg/kg did not affect SBP. Conclusion: These results suggest that the brain RAS plays an important role in maintaining the elevated SBP in chronic hypertension phase.

Rate of activation of renin-angiotensin-aldosterone axis and sodium intake in rats

1989 ◽  
Vol 256 (5) ◽  
pp. H1311-H1315 ◽  
Author(s):  
E. Holtzman ◽  
L. M. Braley ◽  
A. Menachery ◽  
G. H. Williams ◽  
N. K. Hollenberg
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Sodium Intake ◽  
Pressor Response ◽  
Renin Angiotensin System ◽  
Sodium Balance ◽  
Plasma Aldosterone Concentration ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Rate Of Activation

When sodium intake in the rat is reduced abruptly from the typical high level to a very low level (0.02%), sodium excretion falls exponentially, with a half time of 2-3 h. The result is that the rat achieves external sodium balance, in which intake equals excretion, on the new low intake within a few hours. In this study, we assessed the rate of activation of the renin-angiotensin-aldosterone axis and its contribution to blood pressure during that interval. Plasma renin activity and angiotensin II concentration had risen sharply within 8 h and did not change over the next 40 h. Plasma aldosterone concentration, on the other hand, continued to rise over 48 h. Within 8 h, blood pressure dependency on angiotensin II had increased sharply, as assessed by depressor responses to an angiotensin antagonist (Sar1-Ala8-angiotensin II) and to converting-enzyme inhibition (captopril). The depressor response to neither agent changed over the next 40 h. The pressor response to angiotensin II was blunted significantly by 8 h and also did not change over the next 40 h. The findings indicate that the rapid tempo of sodium homeostasis in the rat is matched by an equally rapid tempo of activation of the renin-angiotensin system, although the factors responsible for aldosterone release are probably more complex. Experiments to assess the renin-angiotensin system in the rat must be designed with this rapid tempo in mind.

Terlipressin Versus  Norepinephrine to Correct Refractory Arterial Hypotension after General Anesthesia in Patients Chronically Treated with Renin-Angiotensin System Inhibitors

2003 ◽  
Vol 98 (6) ◽  
pp. 1338-1344 ◽  
Author(s):  
Gilles Boccara ◽  
Alexandre Ouattara ◽  
Gilles Godet ◽  
Eric Dufresne ◽  
Michèle Bertrand ◽  
...  
Keyword(s):  
Blood Pressure ◽  
General Anesthesia ◽  
Arterial Blood Pressure ◽  
Renin Angiotensin System ◽  
Arterial Hypotension ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Long Term Treatment ◽  
Systolic Arterial Blood Pressure

Background Terlipressin, a precursor that is metabolized to lysine-vasopressin, has been proposed as a drug for treatment of intraoperative arterial hypotension refractory to ephedrine in patients who have received long-term treatment with renin-angiotensin system inhibitors. The authors compared the effectiveness of terlipressin and norepinephrine to correct hypotension in these patients. Methods Among 42 patients scheduled for elective carotid endarterectomy, 20 had arterial hypotension following general anesthesia that was refractory to ephedrine. These patients were the basis of the study. After randomization, they received either 1 mg intravenous terlipressin (n = 10) or norepinephrine infusion (n = 10). Beat-by-beat recordings of systolic arterial blood pressure and heart rate were stored on a computer. The intraoperative maximum and minimum values of blood pressure and heart rate, and the time spent with systolic arterial blood pressure below 90 mmHg and above 160 mmHg, were used as indices of hemodynamic stability. Data are expressed as median (95% confidence interval). Results Terlipressin and norepinephrine corrected arterial hypotension in all cases. However, time spent with systolic arterial blood pressure below 90 mmHg was less in the terlipressin group (0 s [0-120 s] vs. 510 s [120-1011 s]; P &lt; 0.001). Nonresponse to treatment (defined as three boluses of terlipressin or three changes in norepinephrine infusion) occurred in zero and eight cases (P &lt; 0.05), respectively. Conclusions In patients who received long-term treatment with renin-angiotensin system inhibitors, intraoperative refractory arterial hypotension was corrected with both terlipressin and norepinephrine. However, terlipressin was more rapidly effective for maintaining normal systolic arterial blood pressure during general anesthesia.

scholarly journals Divergent mechanism regulating fluid intake and metabolism by the brain renin-angiotensin system

2012 ◽  
Vol 302 (3) ◽  
pp. R313-R320 ◽  
Author(s):  
Curt D. Sigmund
Keyword(s):  
Blood Pressure ◽  
Fluid Intake ◽  
Renin Angiotensin System ◽  
Metabolic Effects ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Intracellular Form ◽  
Efferent Pathways ◽  
The Brain ◽  
Pituitary Adrenal Axis

The purpose of this review is two-fold. First, I will highlight recent advances in our understanding of the mechanisms regulating angiotensin II (ANG II) synthesis in the brain, focusing on evidence that renin is expressed in the brain and is expressed in two forms: a secreted form, which may catalyze extracellular ANG I generation from glial or neuronal angiotensinogen (AGT), and an intracellular form, which may generate intracellular ANG in neurons that may act as a neurotransmitter. Second, I will discuss recent studies that advance the concept that the renin-angiotensin system (RAS) in the brain not only is a potent regulator of blood pressure and fluid intake but may also regulate metabolism. The efferent pathways regulating the blood pressure/dipsogenic effects and the metabolic effects of elevated central RAS activity appear different, with the former being dependent upon the hypothalamic-pituitary-adrenal axis, and the latter being dependent upon an interaction between the brain and the systemic (or adipose) RAS.

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