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Effects of spironolactone in spontaneously hypertensive adult rats subjected to high salt intake
Baldo, Marcelo Perim; Zaniqueli, Divanei; Forechi, Ludimila; Machado, Rebeca Caldeira; Rodrigues, Sérgio Lamêgo; Mill, José Geraldo.
Affiliation
  • Baldo, Marcelo Perim; Federal University of Espirito Santo. Department of Physiological Sciences. Vitoria. BR
  • Zaniqueli, Divanei; Federal University of Espirito Santo. Department of Physiological Sciences. Vitoria. BR
  • Forechi, Ludimila; Federal University of Espirito Santo. Department of Physiological Sciences. Vitoria. BR
  • Machado, Rebeca Caldeira; Federal University of Espirito Santo. Department of Physiological Sciences. Vitoria. BR
  • Rodrigues, Sérgio Lamêgo; Federal University of Espirito Santo. Department of Physiological Sciences. Vitoria. BR
  • Mill, José Geraldo; s.af
Clinics ; Clinics;66(3): 477-482, 2011. ilus, tab
Article in En | LILACS | ID: lil-585961
Responsible library: BR1.1
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 percent NaCl solution (SHR-Salt), or a 1 percent NaCl solution with a daily subcutaneous injection of spironolactone (80 mg.kg-1) (SHRSalt- 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 doublelumen catheter was inserted into the left ventricle through the aorta to obtain in situ left ventricular pressurevolume 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.
Subject(s)
Key words

Full text: 1 Index: LILACS Main subject: Spironolactone / Hypertrophy, Left Ventricular / Sodium Chloride, Dietary / Mineralocorticoid Receptor Antagonists / Hypertension Type of study: Etiology_studies / Prognostic_studies Limits: Animals Language: En Journal: Clinics Journal subject: MEDICINA Year: 2011 Type: Article / Project document

Full text: 1 Index: LILACS Main subject: Spironolactone / Hypertrophy, Left Ventricular / Sodium Chloride, Dietary / Mineralocorticoid Receptor Antagonists / Hypertension Type of study: Etiology_studies / Prognostic_studies Limits: Animals Language: En Journal: Clinics Journal subject: MEDICINA Year: 2011 Type: Article / Project document