scholarly journals Hypotensive effects of diltiazem hydrochloride in the normotensive, spontaneously hypertensive and renal hypertensive rats

1979 ◽  
Vol 75 (2) ◽  
pp. 99-106 ◽  
Author(s):  
Masanori SATO ◽  
Sakae MURATA ◽  
Hiroshi NARITA ◽  
Midori TOMITA ◽  
Keiko YAMASHITA ◽  
...  
Keyword(s):  
Diltiazem Hydrochloride ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Renal Hypertensive Rats

Evidence of Altered Structure of the Erythrocyte Membrane in Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (1) ◽  
pp. 43-45 ◽  
Author(s):  
S. N. Orlov ◽  
P. V. Gulak ◽  
I. S. Litvinov ◽  
YU. V. Postnov
Keyword(s):  
Arterial Hypertension ◽  
Erythrocyte Membrane ◽  
Fluorescent Probes ◽  
Membrane Structure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Hydrophobic Areas ◽  
Renal Hypertensive Rats ◽  
Normotensive Control

1. The membrane structure of erythrocytes of rats with different forms of arterial hypertension was studied by means of two hydrophobic fluorescent probes (diphenylhexatriene and pyrene). 2. Microviscosity of hydrophobic areas of erythrocyte membrane of spontaneously hypertensive rats was found to be increased compared with that of membranes from normotensive control rats. 3. No alterations of membrane structure of erythrocytes of deoxycorticosterone-treated rats and renal hypertensive rats were found.

Biological Evaluation of a Novel Angiotensin II AT1 Receptor Antagonist with Anti-Hypertensive and Anti-Tumor Effects

2013 ◽  
Vol 803 ◽  
pp. 113-117
Author(s):  
Ya Jing Da ◽  
Zhi Long Chen
Keyword(s):  
Angiotensin Ii ◽  
Cancer Cell Line ◽  
Biological Evaluation ◽  
Angiotensin Ii Receptor ◽  
Hypertensive Rats ◽  
Binding Studies ◽  
Spontaneously Hypertensive ◽  
Anti Cancer ◽  
Cancer Agent ◽  
Renal Hypertensive Rats

A novel nonpeptide angiotensin II receptor 1 antagonist, compound 1, N-butyryl-N-[(2'-(2, 5-dihydro-5-oxo-1, 2, 4-oxadiazol-3-yl) biphenyl-4-yl) methy-L-Valine was investigated by receptor-binding studies and vivo experiments in spontaneously hypertensive rats and renal hypertensive rats. Furthermore, treatment with compound 1 significantly inhibited the viability of human breast cancer cell line and promoted apoptosis of the cancer cells. The compound had the effects of anti-hypertension and anti-cancer, which suggested that this new compound could be considered as a candidate for both novel anti-hypertensive and anti-cancer agent.

scholarly journals Loss of cerebrovascular Shaker-type K+ channels: a shared vasodilator defect of genetic and renal hypertensive rats

2009 ◽  
Vol 297 (1) ◽  
pp. H293-H303 ◽  
Author(s):  
Ann A. Tobin ◽  
Biny K. Joseph ◽  
Hamood N. Al-Kindi ◽  
Sulayma Albarwani ◽  
Jane A. Madden ◽  
...  
Keyword(s):  
Cerebral Arteries ◽  
Chronic Hypertension ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Western Blots ◽  
Spontaneously Hypertensive ◽  
Rat Models ◽  
Middle Cerebral Arteries ◽  
Wistar Kyoto ◽  
Renal Hypertensive Rats

The cerebral arteries of hypertensive rats are depolarized and highly myogenic, suggesting a loss of K+ channels in the vascular smooth muscle cells (VSMCs). The present study evaluated whether the dilator function of the prominent Shaker-type voltage-gated K+ (KV1) channels is attenuated in middle cerebral arteries from two rat models of hypertension. Block of KV1 channels by correolide (1 μmol/l) or psora-4 (100 nmol/l) reduced the resting diameter of pressurized (80 mmHg) cerebral arteries from normotensive rats by an average of 28 ± 3% or 26 ± 3%, respectively. In contrast, arteries from spontaneously hypertensive rats (SHR) and aortic-banded (Ao-B) rats with chronic hypertension showed enhanced Ca2+-dependent tone and failed to significantly constrict to correolide or psora-4, implying a loss of KV1 channel-mediated vasodilation. Patch-clamp studies in the VSMCs of SHR confirmed that the peak K+ current density attributed to KV1 channels averaged only 5.47 ± 1.03 pA/pF, compared with 9.58 ± 0.82 pA/pF in VSMCs of control Wistar-Kyoto rats. Subsequently, Western blots revealed a 49 ± 7% to 66 ± 7% loss of the pore-forming α1.2- and α1.5-subunits that compose KV1 channels in cerebral arteries of SHR and Ao-B rats compared with control animals. In each case, the deficiency of KV1 channels was associated with reduced mRNA levels encoding either or both α-subunits. Collectively, these findings demonstrate that a deficit of α1.2- and α1.5-subunits results in a reduced contribution of KV1 channels to the resting diameters of cerebral arteries from two rat models of hypertension that originate from different etiologies.

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