Control of spontaneous and deoxycorticosterone–salt hypertension and polyuria by nitrendipine pellets

1984 ◽  
Vol 62 (4) ◽  
pp. 436-440 ◽  
Author(s):  
Charles E. Hall ◽  
Shirley Hungerford
Keyword(s):  
Cardiac Hypertrophy ◽  
Diabetes Insipidus ◽  
Spontaneously Hypertensive Rats ◽  
Potassium Excretion ◽  
Subcutaneous Implantation ◽  
Hypertensive Rats ◽  
Salt Treatment ◽  
Spontaneously Hypertensive ◽  
Salt Hypertension ◽  
Blood Pressures

Weekly subcutaneous implantation of 25-mg nitrendipine pellets prevented onset of both spontaneous and deoxycorticosterone–salt hypertension in rats. Discontinuance of implantation led to reappearance of hypertension after about 2 weeks in the former and led to rising though still normotensive pressures after about 3 weeks in the latter. A new implant caused blood pressures in both to drop within a day or two to normotensive levels in the case of spontaneously hypertensive rats. Nitrendipine prevented cardiac hypertrophy in steroid hypertensive rats, but not in spontaneous hypertensives. A nitrendipine pellet given 1 day before or a 30 mg/kg injection given 1 h prior to the administration of a water, Na+, and K+ load, prevented the diabetes insipidus-like syndrome resulting from deoxycorticosterone–salt treatment, and lowered sodium but not potassium excretion. Nitrendipine did not affect steroid-induced hypernatremia and hypokalemia.

scholarly journals Continuous Blockade of L-Type Ca2+ Channels Suppresses Activation of Calcineurin and Development of Cardiac Hypertrophy in Spontaneously Hypertensive Rats

2002 ◽  
Vol 25 (1) ◽  
pp. 117-124 ◽  
Author(s):  
Yunzeng ZOU ◽  
Tsutomu YAMAZAKI ◽  
Keiichi NAKAGAWA ◽  
Haruyasu YAMADA ◽  
Norio IRIGUCHI ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Ca2 Channels

Ca2+/calmodulin-dependent protein kinase II increases the susceptibility to the arrhythmogenic action potential alternans in spontaneously hypertensive rats

2014 ◽  
Vol 307 (2) ◽  
pp. H199-H206 ◽  
Author(s):  
Hirofumi Mitsuyama ◽  
Hisashi Yokoshiki ◽  
Masaya Watanabe ◽  
Kazuya Mizukami ◽  
Junichi Shimokawa ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Action Potential ◽  
Cardiac Hypertrophy ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Dependent Protein Kinase ◽  
Spontaneously Hypertensive ◽  
Dependent Protein ◽  
Rapid Pacing ◽  
Increased Susceptibility

Action potential duration alternans (APD-ALT), defined as long-short-long repetitive pattern of APD, potentially leads to lethal ventricular arrhythmia. However, the mechanisms of APD-ALT in the arrhythmogenesis of cardiac hypertrophy remain undetermined. Ca2+/calmodulin-dependent protein kinase II (CaMKII) is known to modulate the function of cardiac sarcoplasmic reticulum and play an important role in Ca2+ cycling. We thus aimed to determine the role of CaMKII in the increased susceptibility to APD-ALT and arrhythmogenesis in the hypertrophied heart. APD was measured by high-resolution optical mapping in left ventricular (LV) anterior wall from normotensive Wistar-Kyoto (WKY; n = 10) and spontaneously hypertensive rats (SHR; n = 10) during rapid ventricular pacing. APD-ALT was evoked at significantly lower pacing rate in SHR compared with WKY (382 ± 43 vs. 465 ± 45 beats/min, P < 0.01). These changes in APD-ALT in SHR were completely reversed by KN-93 (1 μmol/l; n = 5), an inhibitor of CaMKII, but not its inactive analog, KN-92 (1 μmol/l; n = 5). The magnitude of APD-ALT was also significantly greater in SHR than WKY and was completely normalized by KN-93. Ventricular fibrillation (VF) was induced by rapid pacing more frequently in SHR than in WKY (60 vs. 10%; P < 0.05), which was also abolished by KN-93 (0%, P < 0.05). Western blot analyses indicated that the CaMKII autophosphorylation at Thr287 was significantly increased in SHR compared with WKY. The increased susceptibility to APD-ALT and VF during rapid pacing in hypertrophied heart was prevented by KN-93. CaMKII could be an important mechanism of arrhythmogenesis in cardiac hypertrophy.

Effect of chronic NG-nitro-L-arginine methyl ester (L-NAME) on blood pressure and renal function in conscious uninephrectomized spontaneously hypertensive rats

1998 ◽  
Vol 76 (1) ◽  
pp. 63-67 ◽  
Author(s):  
María Reverte ◽  
Olga Flores ◽  
Belén Gallego ◽  
Antonio Lestón ◽  
José Miguel López-Novoa
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Renal Function ◽  
Methyl Ester ◽  
Spontaneously Hypertensive Rats ◽  
Low Dose ◽  
Potassium Excretion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Sodium And Potassium

We have studied during 30 days the effect of a low dose of NG-nitro-L-arginine methyl ester (1 mg ·kg-1 ·day-1 in drinking water) in the presence of D- or L-arginine (1 mg ·kg-1 ·day-1 in drinking water) in comparison with D- or L-arginine alone on blood pressure and renal function in conscious uninephrectomized female spontaneously hypertensive rats. At the end of the study, there was a significant increase in systolic blood pressure in the NG-nitro-L-arginine methyl ester + D-arginine group (307 ± 6 mmHg (1 mmHg = 133.3 Pa), n = 14, p << 0.05) in comparison with NG-nitro-L-arginine methyl ester + L-arginine (281 ± 6 mmHg, n = 14), L-arginine (262 ± 5 mmHg, n = 13), and D-arginine (258 ± 7 mmHg, n = 12) groups. There were no changes in diuresis, proteinuria, or sodium and potassium excretion between differently treated animals during this study. These results suggest that in uninephrectomized female spontaneously hypertensive rats, after 1 month blockade of NO synthesis with a low dose of NG-nitro-L-arginine methyl ester, vasculature is under tonic control by NO and it is not correlated with renal dysfunction.Key words: Key words: NG -nitro-L-arginine methyl ester (L-NAME), kidney, hypertension, spontaneously hypertensive rats, renaldysfunction, uninephrectomy.

Exercise training and incidence of cerebrovascular lesions in stroke-prone spontaneously hypertensive rats

1990 ◽  
Vol 68 (3) ◽  
pp. 1080-1085 ◽  
Author(s):  
C. M. Tipton ◽  
S. McMahon ◽  
J. R. Leininger ◽  
E. L. Pauli ◽  
C. Lauber
Keyword(s):  
Exercise Training ◽  
Spontaneously Hypertensive Rats ◽  
Female Rats ◽  
Moderate Exercise ◽  
Hypertensive Rats ◽  
Cerebrovascular Lesions ◽  
Spontaneously Hypertensive ◽  
Male And Female Rats ◽  
Blood Pressures ◽  
Subjective Evidence

To assess the effects of moderate exercise [40-70% maximal oxygen uptake (VO2max)] on resting blood pressures, the presence of cerebrovascular lesions, and the life spans of stroke-prone hypertensive rats, nontrained and trained male and female rats were assigned to two experimental groups. The first (n = 48) were exercise trained after 38 days of age, whereas the second (n = 44) initiated exercise training when the animals were 134 days of age. To facilitate cerebrovascular lesions, the sodium concentrations in the rat chow and in the drinking solutions were increased. Symptoms utilized to denote the presence of cerebrovascular lesions were irritability, hyperresponsiveness, ataxia, lethargy, unwillingness to run, and combinations thereof. All brains were removed immediately after death, fixed, and evaluated grossly and microscopically for lesions. In the study with the younger animals, training was associated with a 7-9% increase in VO2max that was statistically significant only in animals with no histological evidence of cerebrovascular lesions. For the older animals, a significant 5-8% increase in VO2max was noted for animals with or without lesions. After 42 days of training for both groups, resting blood pressures for the trained groups with histological lesions were significantly lower. However, this trend did not continue, and the older trained rats appeared to have strokes earlier and to die sooner than their nontrained controls. Although 83% of the older animals had subjective evidence for a stroke before they died, the percentage of animals with lesions ranged from 42 to 58%, with the trained groups having higher percentages.(ABSTRACT TRUNCATED AT 250 WORDS)

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