Effects of riboflavin analogues and diuretics on the spontaneously hypertensive rat heart

  title={Effects of riboflavin analogues and diuretics on the spontaneously hypertensive rat heart},
  author={M. Bhaskar and D. Trachewsky and R. Stith and Y. S. Reddy},
  journal={Basic Research in Cardiology},
SummaryThe chronic treatment of spontaneously hypertensive rats (SHR) with 7,8-dimethyl-10-(3-chlorobenzyl) isoalloxazine [CBI], 7,8-diethyl-10-aminol isoalloxazine [DEAI], enduron (methyclothiazide) and amiloride were studied for their effects on blood pressure and cardiac contractile protein ATPasc activities. After 35 weeks of treatment all the above antihypertensive agents showed a decrease in blood pressure in the SHR (p<0.01). Chronic treatment with CBI, DEAI, enduron, and amiloride… 


Antihypertensive effect of riboflavin analogues in spontaneously hypertensive rats.
The effects of CBI on the systolic blood pressure and iliopsoas muscle Na+ and K+ concentrations of age-matched WKY mildly hypertensive control rats were qualitatively similar to the effects on the SHR.
Antihypertensive Effect of Riboflavin Analogs in Rats with Mineralocorticoid‐Induced Hypertension
It appears that the hypotensive actions of FMI or HEI are closely associated with their ability to modify the effects of mineralocorticoids on Na + balance.
Effect of Converting Enzyme Inhibitor (SQ14,225) on Myocardial Hypertrophy in Spontaneously Hypertensive Rats
Data show that prevention of All formation in combination with BP control can prevent and reverse cardiac hypertrophy in SHR, indicating that whether or not CEI acts only through the renin angiotension system is still speculative.
Effects of chronic dobutamine administration on hearts of normal and hypertensive rats.
Chronic dobutamine treatment induces a physiological cardiac hypertrophy in rats that is associated with improved myosin enzymology and normalization of the contractile protein abnormalities associated with hypertension, unlike physical conditioning, which results in improved contractile function as measured in an isolated buffer-perfused heart apparatus.
Central and peripheral indices of sympathetic activity after blood pressure lowering with enalapril (MK-421) or hydralazine in normotensive rats.
Elimination of angiotensin II (AII) by CEI is associated with decreased sympathetic activity in both the brain stem and heart, whereas an equipotent antihypertensive action by smooth muscle relaxation leads to stimulation of both the renin-angiotENSin and the sympathetic systems.
Aldosterone stimulation of riboflavin incorporation into rat renal flavin coenzymes and the effect of inhibition by riboflavin analogues on sodium reabsorption.
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  • Medicine, Chemistry
    The Journal of clinical investigation
  • 1978
Data strongly suggest that the enhanced synthesis of renal FMN and FAD may be a causative factor in the increased reabsorption of Na(+) as a result of aldosterone; and, consequently, riboflavin analogues may function as a novel class of antimineralocorticoids.
Acute Energetic Effects of Daunomycin on Rabbit Heart Muscle
  • C. Gibbs
  • Medicine
    Journal of cardiovascular pharmacology
  • 1985
It is concluded that, in the rabbit, daunomycin in the acute situation increases total calcium delivery to the myofilaments and decreases the “apparent” transduction efficiency.
Anti-hypertensive effect of metoprolol in spontaneously hypertensive rats.
It is concluded that the anti-hypertensive effect of metoprolol in SHR in many respects resembles that observed in patients, and it is suggested that impairment of vasomotor nerve control may contribute to theAnti- Hypertensive Effect of beta-adrenoreceptor antagonists.
Cardiac Impairment in Adrenal Insufficiency in the Cat: Reduced Adenosinetriphosphatase Activity of Myocardial Contractile Proteins
The reduction in cardiac performance in frank adrenal insufficiency may reflect a decrease in the rate of conversion of chemical to mechanical energy by the myocardial contractile proteins.
Regression of cardiac hypertrophy after therapy in animal hypertension.
Reversing of cardiac hypertrophy seems to be mainly related to the reduced LV systolic load, and specific pharmacodynamic effects may only modulate the extent of LV mass reduction along with blood pressure normalization.