Creatine kinase inhibition lowers systemic arterial blood pressure in spontaneously hypertensive rats

2016 ◽  
Vol 34 (12) ◽  
pp. 2418-2426 ◽  
Author(s):  
Fares A. Karamat ◽  
Inge Oudman ◽  
Yentl C. Haan ◽  
Andre B.P. van Kuilenburg ◽  
Rene Leen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Creatine Kinase ◽  
Arterial Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Kinase Inhibition ◽  
Spontaneously Hypertensive ◽  
Systemic Arterial Blood Pressure ◽  
Arterial Blood

Tubuloglomerular feedback and autoregulation in spontaneously hypertensive rats

1990 ◽  
Vol 258 (6) ◽  
pp. F1479-F1489 ◽  
Author(s):  
F. H. Daniels ◽  
W. J. Arendshorst ◽  
R. G. Roberds
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Ureteral Obstruction ◽  
Spontaneously Hypertensive Rats ◽  
Control Period ◽  
Tubuloglomerular Feedback ◽  
Hypertensive Rats ◽  
Two Phase ◽  
Spontaneously Hypertensive ◽  
Arterial Blood

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During ureteral obstruction, the low-frequency shoulder and maximum disappeared, indicating that the slower system was no longer active.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.

scholarly journals Hypotensive and Bradycardic Effects of Quinovic Acid Glycosides from Aspidosperma fendleri in Spontaneously Hypertensive Rats

2015 ◽  
Vol 10 (2) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Omar Estrada ◽  
Juan M. González-Guzmán ◽  
María M. Salazar-Bookman ◽  
Alfonso Cardozo ◽  
Eva Lucena ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Triterpenoid Saponins ◽  
Spontaneously Hypertensive ◽  
Arterial Blood

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.

scholarly journals Exaggerated postnatal surge of orexin and the effects of elimination of excess orexin on blood pressure in spontaneously hypertensive rats in postnatal development

2020 ◽  
Author(s):  
Savannah Barnett ◽  
Ruhong Dong ◽  
Logan Briggs ◽  
Alexander Moushey ◽  
Aihua Li
Keyword(s):  
Blood Pressure ◽  
Postnatal Development ◽  
Arterial Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Neurogenic Hypertension ◽  
Spontaneously Hypertensive ◽  
Arterial Blood ◽  
New Findings ◽  
Wistar Kyoto

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.

scholarly journals Antisense Inhibition of Thyrotropin-Releasing Hormone Reduces Arterial Blood Pressure in Spontaneously Hypertensive Rats

Hypertension ◽  
2001 ◽  
Vol 37 (2) ◽  
pp. 365-370 ◽  
Author(s):  
Silvia I. García ◽  
Azucena L. Alvarez ◽  
Patricia I. Porto ◽  
Victoria M. Garfunkel ◽  
Sammuel Finkielman ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Thyrotropin Releasing Hormone ◽  
Antisense Inhibition ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Releasing Hormone ◽  
Arterial Blood
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