Effects of spironolactone in spontaneously hypertensive adult rats subjected to high salt intake

Abstract

OBJECTIVE:To evaluate the effect of spironolactone on ventricular stiffness in spontaneously hypertensive adult rats subjected to high salt intake.INTRODUCTION:High salt intake leads to cardiac hypertrophy, collagen accumulation and diastolic dysfunction. These effects are partially mediated by cardiac activation of the renin-angiotensin-aldosterone system.METHODS:Male spontaneously hypertensive rats (SHRs, 32 weeks) received drinking water (SHR), a 1% NaCl solution (SHR-Salt), or a 1% NaCl solution with a daily subcutaneous injection of spironolactone (80 mg.kg-1) (SHR-Salt-S). Age-matched normotensive Wistar rats were used as a control. Eight weeks later, the animals were anesthetized and catheterized to evaluate left ventricular and arterial blood pressure. After cardiac arrest, a double-lumen catheter was inserted into the left ventricle through the aorta to obtain in situ left ventricular pressure-volume curves.RESULTS:The blood pressures of all the SHR groups were similar to each other but were different from the normotensive controls (Wistar = 109±2; SHR = 118±2; SHR-Salt = 117±2; SHR-Salt-S = 116±2 mmHg; P<0.05). The cardiac hypertrophy observed in the SHR was enhanced by salt overload and abated by spironolactone (Wistar = 2.90±0.06; SHR = 3.44±0.07; SHR-Salt = 3.68±0.07; SHR-Salt-S = 3.46±0.05 mg/g; P<0.05). Myocardial relaxation, as evaluated by left ventricular dP/dt, was impaired by salt overload and improved by spironolactone (Wistar = -3698±92; SHR = -3729±125; SHR-Salt = -3342±80; SHR-Salt-S = -3647±104 mmHg/s; P<0.05). Ventricular stiffness was not altered by salt overload, but spironolactone treatment reduced the ventricular stiffness to levels observed in the normotensive controls (Wistar = 1.40±0.04; SHR = 1.60±0.05; SHR-Salt = 1.67±0.12; SHR-Salt-S = 1.45±0.03 mmHg/ml; P<0.05).CONCLUSION:Spironolactone reduces left ventricular hypertrophy secondary to high salt intake and ventricular stiffness in adult SHRs.

Exercise training prior to myocardial infarction attenuates cardiac deterioration and cardiomyocyte dysfunction in rats

“…Thus, the LV volume at 5 mmHg was compared among groups and provided an estimate of LV dilation (20). As shown in Figure 3, SED-MI animals displayed LV dilation as compared to SHAM animals, which was prevented by prior AET.…”

“…After hemodynamic measurements were collected, each heart was arrested with 3 M KCl (0.2 mL, iv), and a double lumen catheter (P50 inserted into P200) was inserted into the left ventricle through the aorta to determine the in situ left ventricle diastolic pressure-volume relationship, as previously described (20). Briefly, the atrio-ventricular groove was occluded, and a small incision was made in the right ventricular free wall to hinder any compression effect.…”

“…Then, 0.9% NaCl was infused with an infusion pump (Insight Scientific Equipments, Ribeirão Preto, São Paulo, Brazil) at a constant rate of 0.68 mL.min-1 into the P200, and pressure was continuously monitored through the P50. The pressure followed a linear pattern during volume infusion from 0 to 5 mmHg, indicating the passive distention of ventricular wall; therefore, the slope was used to estimate LV dilatation because no stiffness was observed up to 5 mmHg (20). …”

The Antiapoptotic Effect of Granulocyte Colony-stimulating Factor Reduces Infarct Size and Prevents Heart Failure Development in Rats

“…After hemodynamic measurements, the heart was arrested with 3 M KCl, and a double-lumen catheter (P50 inserted into P200) was inserted into the LV through the aorta to determine the in situ LV diastolic pressure-volume relationship to measure the dilation of the chamber [15]. The atrio-ventricular groove was occluded, and a small incision was made in the right ventricular free wall to avoid any compressor effect.…”

“…Three curves were recorded for each heart for approximately ten minutes. LV dilation was obtained through the slope of pressure-volume curve [15].…”