scholarly journals Hypotensive Effect Induced by Mandibular Extension in Aged, Hypertensive Humans and Rats

Author(s):  
Cristina Del Seppia ◽  
Cristina Del Seppia ◽  
Giuseppe Federighi ◽  
Enza Fommei ◽  
Sergio Ghione ◽  
...  

Objectives: Previous research has shown that submaximal mouth opening by mandibular extension (ME) is followed by a prolonged reduction in blood pressure. This effect was observed in young and adult normotensive and hypertensive rats and in young normotensive human subjects. Methods: We assessed the effects of a ME for 10 minutes obtained with a fixed mouth opener in both hypertensive adult humans (aged 55 years or older) and elderly (6-7 months) anaesthetized, hypertensive rats (SHR). Blood pressure and heart rate were measured every 10 minutes by non-invasive automatic recorders for 30 minutes before and 120 minutes after the procedure. Nine human hypertensive subjects (7 experimental and 2 controls) and seven spontaneously hypertensive rats (5 experimental and 2 controls) were tested. Results: A statistically significant reduction in systolic blood pressure (SBP), mean arterial blood pressure (MABP) and heart rate (HR) was observed after ME in the seven hypertensive human subjects, in whom an average decrease of 15 mmHg for SBP, 10 mmHg for MABP and 7 bpm for HR, was observed. A similar hypotensive effect was recorded in spontaneously hypertensive rats that displayed a statistically significant decrease of SBP, DBP and MABP, amounting to about 40-50 mmHg. Conclusion: This study provides the first evidence that ME has an important and prolonged hypotensive effect when applied to subjects with high blood pressure, making their arterial blood pressure decrease toward normal values for at least two hours.

2015 ◽  
Vol 10 (2) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Omar Estrada ◽  
Juan M. González-Guzmán ◽  
María M. Salazar-Bookman ◽  
Alfonso Cardozo ◽  
Eva Lucena ◽  
...  

The Aspidosperma genus (Apocynaceae) represents one of the largest sources of indole alkaloids widely associated with cardiovascular effects. Aspidosperma fendleri, a plant found mainly in Venezuela, has a single phytochemical report in which is revealed the presence of alkaloids in its seeds. This study explored the cardiovascular effects of an ethanolic extract of A. fendleri leaves (EEAF) in spontaneously hypertensive rats (SHR) and its potential bioactive compounds. Using bioguided fractionation, fractions and pure compounds were intravenously administered to SHR and their effects on mean arterial blood pressure (MABP) and heart rate (HR) monitored over time. EEAF induced hypotensive and bradycardic effects as shown by significant reductions in mean arterial blood pressure (MABP) and heart rate (HR), respectively. Bioactivity-guided fractionation led to the isolation of a mixture of two known isomeric triterpenoid glycosides identified by spectral evidence as quinovic acid 3- O-β-rhamnopyranoside and quinovic acid 3- O-β-fucopyranoside. This mixture of triterpenoid saponins induced reductions in MABP and HR similar to those induced by propranolol. Together, these findings indicate that the two quinovic acid glycosides are responsible for the hypotensive and bradycardic effects which suggest their potential use in cardiovascular therapy.


1990 ◽  
Vol 258 (6) ◽  
pp. F1479-F1489 ◽  
Author(s):  
F. H. Daniels ◽  
W. J. Arendshorst ◽  
R. G. Roberds

Experiments were conducted in 8-wk-old spontaneously hypertensive rats to determine whether tubuloglomerular feedback is essential for the autoregulation of renal blood flow. Autoregulation curves were obtained by measuring mean renal arterial blood pressure and flow during graded aortic occlusion. Renal vascular admittance was calculated from recordings of pulsatile renal arterial blood pressure and flow during induced atrial fibrillation. After a control period, acute ureteral obstruction was used to suppress tubuloglomerular feedback, as confirmed by measuring stop-flow pressure responses to rapid perfusion of Henle's loop. Ureteral obstruction did not impair steady-state autoregulation. During both the control and obstruction periods, the admittance gain was less than 1 at frequencies below 0.2 Hz, indicating dynamic autoregulatory activity. The control admittance contained two gain shoulders and two phase maxima, suggesting the presence of two control systems with response half-times of 1 and 10 s. During ureteral obstruction, the low-frequency shoulder and maximum disappeared, indicating that the slower system was no longer active. However, the high-frequency shoulder and maximum persisted, suggesting continued activity of the faster system. Collectively, these observations indicate the existence of a rapidly acting intrarenal control mechanism, in young spontaneously hypertensive rats, that may provide efficient autoregulation without assistance from tubuloglomerular feedback.


2020 ◽  
Author(s):  
Savannah Barnett ◽  
Ruhong Dong ◽  
Logan Briggs ◽  
Alexander Moushey ◽  
Aihua Li

AbstractIt has been established that an overactive orexin (OX) system is associated with neurogenic hypertension in spontaneously hypertensive rats (SHRs). However, the chronology and mechanism of such association between orexin system and hypertension is unclear. We hypothesized that an aberrant surge of OX neurons in SHRs precedes the aberrant increase of arterial blood pressure (ABP) during postnatal development, which was primarily contributed by the exaggerated postnatal OX neurogenesis. We found that (1) SHRs experienced a greater surge in the number of orexin neurons than normotensive Wistar-Kyoto (WKY) rats before P16, which led to significantly more OX neurons than age-matched controls by P15-16 (3680±219 vs 2407±182, respectively, P=0.002). (2) Exaggerated OX neurogenesis, marked by bromodeoxyuridine (BrdU), was the primary contributor to excessive OX neurons in SHRs during development. (3) In contrast, SHRs and normotensive control rats have similar mean arterial blood pressure (ABP) at P15, and a significantly higher ABP in SHR than WKY emerges at P20 (74.8 ± 2.5 vs 66.9 ± 4.4 mmHg in wakefulness, respectively, P<0.05), a few days following the surge of OX activity. (4) Selectively eliminating excess (∼30%) orexin neurons, via a targeted neurotoxin, in SHRs between P30 and P40 results in a significantly lowered ABP compared to non-lesioned SHRs at P40. We suggest that the postnatal surge of OX neurons, primarily attributed to the exaggerated postnatal OX neurogenesis, may be necessary for the development of higher ABP in SHRs, and modulation of the overactive OX system may have a preventative effect during the pre-hypertensive period.New FindingsWhat is the central question of this study?Excess orexin neurons have been associated with hypertension in spontaneously hypertensive rats, however, the association and mechanism between developing excess orexin neurons and high blood pressure are unknown.What is the main finding and its importance?Using spontaneously hypertensive rats in anatomical and physiological studies, we provided evidence showing that the excess OX neurons, primarily via exaggerated OX neurogenesis, may be necessary in developing a higher ABP in SHRs during development, and modulation of the overactive orexin system may be beneficial in treating hypertension.


2013 ◽  
pp. 237-245 ◽  
Author(s):  
S. ALBARWANI ◽  
S. AL-SIYABI ◽  
M. O. TANIRA

The aim of this work was to investigate the effect of 10 weeks of lisinopril treatment to spontaneously hypertensive rats (SHRs) on day/night variations of blood pressure, heart rate and autonomic cardio-regulation parameters. Male SHR with surgically implanted radio-telemetry implant that provided direct measurements of arterial pressure and electrocardiogram wave were used. Animals were allocated to two groups (n=5 each). The first group was treated with lisinopril (20 mg/kg by gavage) daily for 10 weeks (treated group); whereas the second was gavaged daily with tap water (untreated group). Arterial blood pressure, ECG and other telemetry parameters were recorded at the start and at the end of 10-week treatment. Collected data were analyzed using specialized software and were statistically tested. In addition to the expected lowering of blood pressure, spectral analysis of R-R intervals revealed that lisinopril treatment for 10 weeks significantly caused 2-3 fold increase in heart rate variability (HRV) during both active and inactive periods. However, R-R interval durations demonstrated variable distribution patterns during those periods. The cause of observed distribution pattern of R-R intervals during active and inactive periods may be of significance to better understand HRV changes and warrants further investigations.


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