Attenuation of Electroconvulsive Therapy Induced Hypertension with Sublingual Nifedipine

1989 ◽  
Vol 17 (1) ◽  
pp. 31-33 ◽  
Author(s):  
D. G. Wells ◽  
G. G. Davies ◽  
F. Rosewarne
Keyword(s):  
Blood Pressure ◽  
Electroconvulsive Therapy ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Systolic Pressure ◽  
Response To Therapy ◽  
Induced Hypertension ◽  
Sublingual Nifedipine ◽  
History Of ◽  
Significant Attenuation

Five patients known to be previously hypertensive but not currently receiving anti-hypertensive medications were studied for a total of twenty-six administrations of electroconvulsive therapy Patients randomly received sublingual nifedipine 10 mg, 20 minutes prior to half of their treatments, and for the remaining treatments acted as their own controls. The use of nifedipine resulted in significant attenuation of the blood pressure response to therapy. Systolic pressure increase was 24 mmHg (SD 14) versus 62 mmHg (SD 24) (P< 0.01). There was no difference in heart rate between the two groups. It is concluded that nifedipine reduces the pressor response to electroconvulsive therapy in individuals with a history of hypertension.

scholarly journals Hypertension in Prenatally Undernourished Young-Adult Rats Is Maintained by Tonic Reciprocal Paraventricular–Coerulear Excitatory Interactions

Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3568
Author(s):  
Bernardita Cayupe ◽  
Carlos Morgan ◽  
Gustavo Puentes ◽  
Luis Valladares ◽  
Héctor Burgos ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Young Adult ◽  
Binding Sites ◽  
Systolic Pressure ◽  
Adult Rats ◽  
Excitatory Pathways ◽  
Induced Hypertension ◽  
Prenatal Undernutrition ◽  
Number Of Cells

Prenatally malnourished rats develop hypertension in adulthood, in part through increased α1-adrenoceptor-mediated outflow from the paraventricular nucleus (PVN) to the sympathetic system. We studied whether both α1-adrenoceptor-mediated noradrenergic excitatory pathways from the locus coeruleus (LC) to the PVN and their reciprocal excitatory CRFergic connections contribute to prenatal undernutrition-induced hypertension. For that purpose, we microinjected either α1-adrenoceptor or CRH receptor agonists and/or antagonists in the PVN or the LC, respectively. We also determined the α1-adrenoceptor density in whole hypothalamus and the expression levels of α1A-adrenoceptor mRNA in the PVN. The results showed that: (i) agonists microinjection increased systolic blood pressure and heart rate in normotensive eutrophic rats, but not in prenatally malnourished subjects; (ii) antagonists microinjection reduced hypertension and tachycardia in undernourished rats, but not in eutrophic controls; (iii) in undernourished animals, antagonist administration to one nuclei allowed the agonists recover full efficacy in the complementary nucleus, inducing hypertension and tachycardia; (iv) early undernutrition did not modify the number of α1-adrenoceptor binding sites in hypothalamus, but reduced the number of cells expressing α1A-adrenoceptor mRNA in the PVN. These results support the hypothesis that systolic pressure and heart rate are increased by tonic reciprocal paraventricular–coerulear excitatory interactions in prenatally undernourished young-adult rats.

scholarly journals Evaluation of blood pressure in school children aged 12-16 years

2017 ◽  
Vol 4 (4) ◽  
pp. 1218
Author(s):  
Balakrishnan Nadesan ◽  
Mani Madhavan Sachithananthamoorthi ◽  
Sivaraman Thirumalaikumarasamy ◽  
Ezhilarasu Ramalingam
Keyword(s):  
Blood Pressure ◽  
Family History ◽  
Diastolic Blood Pressure ◽  
School Children ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Cross Sectional ◽  
Significant Difference ◽  
History Of ◽  
Family History Of Hypertension

Background: Hypertension is considered as a major health issue in developed as well as developing countries and its possible origin during childhood prompts pediatricians to routinely include measurement of blood pressure (BP) as an integral part of pediatric physical examination. The objectives of the study were to evaluate the normal range of blood pressure in adolescent school going students of 12-16 years, prevalence of hypertension and relationship of BP with variables like age, body mass index (BMI), socioeconomic status and family history of hypertension.Methods: A cross sectional study was undertaken for a period of one year in adolescent school children in age groups between 12-16 years. Detailed clinical examination was done in 1060 adolescent school children and BP was recorded in right upper limb and correlation of BP with BMI, family history of hypertension and diabetes were studied.Results: Mean systolic and diastolic pressure showed linear relationship with age. There was a highly statistically significant difference between mean systolic and diastolic blood pressure between lower and middle socio-economic class. Prevalence of obesity in our study was 1.13%, overweight was 7.83%. Prevalence of hypertension in obese children was 33.33% and in overweight children 18.07%. Family history of hypertension and diabetes carry a significant correlation with elevated systolic and diastolic blood pressure in adolescents.Conclusions: This study revealed that socio economic factors play a significant role in determining the blood pressure of the individual. Children of middle class have significantly elevated mean systolic pressure and mean diastolic pressure than low socio-economic groups. 

Abstract 161: African Ancestry and Blood Pressure Response Among African Americans in the Systolic Blood Pressure Reduction Intervention Trial

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Shreya Rao ◽  
Matthew W Segar ◽  
Kershaw Patel ◽  
Ambarish Pandey
Keyword(s):  
Blood Pressure ◽  
Kidney Function ◽  
Blood Pressure Response ◽  
African Ancestry ◽  
Blood Pressure Reduction ◽  
Response To Therapy ◽  
Mixed Effect ◽  
Cox Models ◽  
Treatment Interaction ◽  
Over Time

Introduction: African ancestry (AA) is associated with higher BP prevalence, however the association of AA with response to intensive BP therapy, kidney function changes, and CV outcomes has not previously been explored. Methods: The study included participants from the SPRINT trial with available AA proportion. AA proportion was estimated using 106 biallelic genotype markers. Participants were stratified into tertiles from lowest (T1) to highest (T3) AA percentage. Time-dependent changes in SBP and eGFR were assessed by linear mixed-effect modeling after adjustment for potential confounders. Multivariable Cox models were constructed to evaluate the association of AA with risk of composite CV events (non-fatal MI, CV death, and HF event). Results: Among 2479 participants (median AA 78% [IQR: 73-87%], age 62 y, 46% female), baseline BP was similar across tertiles. At baseline, the prevalence of average Framingham CV risk (T1 vs. T2 vs. T3: mean 18.2% vs. 17.3% vs. 16.7%, p=0.01) and eGFR decreased (78 vs. 77 vs. 74, p=0.003) across increasing tertiles of AA. In contrast, the burden of DM (1.4% vs. 1.2% vs. 2.7%, p=0.05) and LV hypertrophy by EKG increased across increasing AA tertiles (11.1% vs. 12.0% vs. 15.7%, p=0.02). On follow up, the decline in BP over time was consistent across AA tertiles (mean reduction in SBP: 10 vs. 7 vs. 11 mm Hg, p=0.19) with no treatment interaction by genetic ancestry (p-int=0.60, Fig. A ). However, there was a greater decline in kidney function over time from T3 vs. T1 (mean eGFR decline = 3.8, 3.3, and 5.0 in T1-3) ( Fig. B ). The risk of adverse CV event was not different across AA tertiles [adjusted HR (95% CI): T3 vs. T1 = 0.93 (0.61-1.44); T2 vs T1 = 0.69 (0.42-1.11)]. Conclusions: Genetic AA was not significantly associated with baseline BP level or response to therapy in the SPRINT trial. Higher genetic African ancestry was associated with favorable CV risk profiles with no difference in adverse CV event risk, but greater decline in renal function over time.

Abstract P041: Proximal Tubule-specific Deletion Of Angiotensin Ii Type 1a Receptors In The Kidney Lowers Basal Blood Pressure And Attenuates Angiotensin Ii-induced Hypertension By Increasing Glomerular Filtration And The Pressure-natriuresis Response

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Xiao C Li ◽  
Ana P Leite ◽  
Liang Zhang ◽  
Jia L Zhuo
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Pressor Response ◽  
Control Group ◽  
Ang Ii ◽  
Induced Hypertension ◽  
Basal Blood Pressure ◽  
Pressure Natriuresis ◽  
Specific Deletion

The present study tested the hypothesis that intratubular angiotensin II (Ang II) and AT 1a receptors in the proximal tubules of the kidney plays an important role in basal blood pressure control and in the development of Ang II-induced hypertension. Mutant mice with proximal tubule-specific deletion of AT 1a receptors in the kidney, PT- Agtr1a -/- , were generated to test the hypothesis. Eight groups (n=7-12 per group) of adult male wild-type (WT) and PT- Agtr1a -/- mice were infused with or without Ang II for 2 weeks (1.5 mg/kg, i.p.). Basal systolic, diastolic, and mean arterial pressures were ~13 ± 3 mmHg lower in PT- Agtr1a -/- than WT mice ( P <0.01). Basal glomerular filtration rate (GFR), as measured using transdermal FITC-sinistrin, was significantly higher in PT- Agtr1a -/- mice (WT: 160.4 ± 7.0 μl/min vs. PT- Agtr1a -/- : 186.0 ± 6.0 μl/min, P <0.05). Basal 24 h urinary Na + excretion (U Na V) was significantly higher in PT- Agtr1a -/- than WT mice ( P <0.01). In response to Ang II infusion, both WT and PT- Agtr1a -/- mice developed hypertension, and the magnitude of the pressor response to Ang II was similar in WT (Δ43 ± 3 mmHg, P <0.01) and PT- Agtr1a -/- mice (Δ39 ± 5 mmHg, P <0.01). However, the absolute blood pressure level was still 16 ± 3 mmHg lower in PT- Agtr1a -/- mice ( P <0.01). Ang II significantly decreased GFR to 132.2 ± 7.0 μl/min in WT mice ( P <0.01), and to 129.4 ± 18.6 μl/min in PT- Agtr1a -/- mice ( P <0.01), respectively. In WT mice, U Na V increased from 139.3 ± 22.3 μmol/24 h in the control group to 196.4 ± 29.6 μmol/24 h in the Ang II-infused group ( P <0.01). In PT- Agtr1a -/- mice, U Na V increased from 172.0 ± 10.2 μmol/24 h in the control group to 264.7 ± 35.4 μmol/24 h in the Ang II-infused group ( P <0.01). The pressor response to Ang II was attenuated, while the natriuretic response was augmented by losartan in WT and PT- Agtr1a -/- mice ( P <0.01). Finally, proximal tubule-specific deletion of AT 1a receptors significantly augmented the pressure-natriuresis response and natriuretic responses to acute saline infusion ( P <0.01) or a 2% high salt diet ( P <0.01). We concluded that deletion of AT 1a receptors selectively in the proximal tubules lowers basal blood pressure and attenuates Ang II-induced hypertension by increasing GFR and promoting the natriuretic response in PT- Agtr1a -/- mice.

Mineralocorticoid antagonist inhibits stress-induced blood pressure response after repeated daily warming

1994 ◽  
Vol 267 (6) ◽  
pp. E921-E926 ◽  
Author(s):  
D. T. Van den Berg ◽  
W. de Jong ◽  
E. R. de Kloet
Keyword(s):  
Blood Pressure ◽  
Restraint Stress ◽  
Blood Pressure Response ◽  
Direct Method ◽  
Pressor Response ◽  
Blood Pressure Measurement ◽  
Training Procedure ◽  
Intracerebroventricular Infusion ◽  
Mineralocorticoid Antagonist ◽  
Corticosterone Response

We report here that with a direct method for measurement of cardiovascular parameters in conscious rats, intracerebroventricular administration of the mineralocorticoid receptor (MR) antagonist RU-28318 (100 ng) reduces the blood pressure, heart rate, and the corticosterone response to a brief restraint stress, provided the rats were previously subjected to a daily 30-min exposure to 32 degrees C for 2 wk. The daily exposure to warming and restraint stress are applied identically to the training procedure required for indirect blood pressure measurement using the tail-cuff method. The basal arterial pressure is not affected by the MR antagonist. The effect of the MR antagonist on the stress-induced pressor response develops with a delay of several hours in the normotensive rats. The corticosterone response to daily warming and stress is also attenuated by the intracerebroventricular infusion of MR antagonist but with shorter onset and shorter duration. The findings suggest that conditioning to daily warming and stress imposes mineralocorticoid dependency of the pressor response, which involves MR functioning in brain.

Muscle chemoreflex alters vascular conductance in nonischemic exercising skeletal muscle

1994 ◽  
Vol 77 (6) ◽  
pp. 2761-2766 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
P. S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Response To Exercise ◽  
Muscle Chemoreflex

Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.

scholarly journals Angiotensin II acts through the angiotensin 1a receptor to upregulate pendrin

2011 ◽  
Vol 301 (6) ◽  
pp. F1314-F1325 ◽  
Author(s):  
Jill W. Verlander ◽  
Seongun Hong ◽  
Vladimir Pech ◽  
James L. Bailey ◽  
Diana Agazatian ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Membrane ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Angiotensin Receptors ◽  
Apical Plasma Membrane ◽  
Protein Abundance ◽  
Wild Type ◽  
Induced Hypertension

Pendrin is an anion exchanger expressed in the apical regions of B and non-A, non-B intercalated cells. Since angiotensin II increases pendrin-mediated Cl− absorption in vitro, we asked whether angiotensin II increases pendrin expression in vivo and whether angiotensin-induced hypertension is pendrin dependent. While blood pressure was similar in pendrin null and wild-type mice under basal conditions, following 2 wk of angiotensin II administration blood pressure was 31 mmHg lower in pendrin null than in wild-type mice. Thus pendrin null mice have a blunted pressor response to angiotensin II. Further experiments explored the effect of angiotensin on pendrin expression. Angiotensin II administration shifted pendrin label from the subapical space to the apical plasma membrane, independent of aldosterone. To explore the role of the angiotensin receptors in this response, pendrin abundance and subcellular distribution were examined in wild-type, angiotensin type 1a (Agtr1a) and type 2 receptor (Agtr2) null mice given 7 days of a NaCl-restricted diet (< 0.02% NaCl). Some mice received an Agtr1 inhibitor (candesartan) or vehicle. Both Agtr1a gene ablation and Agtr1 inhibitors shifted pendrin label from the apical plasma membrane to the subapical space, independent of the Agtr2 or nitric oxide (NO). However, Agtr1 ablation reduced pendrin protein abundance through the Agtr2 and NO. Thus angiotensin II-induced hypertension is pendrin dependent. Angiotensin II acts through the Agtr1a to shift pendrin from the subapical space to the apical plasma membrane. This Agtr1 action may be blunted by the Agtr2, which acts through NO to reduce pendrin protein abundance.

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