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Cardiac hypertrophy and brain natriuretic peptide in experimental hypertension
1First Department of Internal Medicine, Osaka City University Medical School, Japan.
Insights
Enalapril and MK-954 reduced blood pressure and ventricular weight in hypertensive rats, decreasing brain natriuretic peptide (BNP) secretion from the ventricle. Hydralazine lowered blood pressure but not BNP levels.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Deoxycorticosterone acetate (DOCA)-salt administration induces malignant hypertension in spontaneously hypertensive rats (SHR).
- Brain natriuretic peptide (BNP) is a hormone released from the heart, particularly the ventricles, in response to cardiac stress and hypertrophy.
Purpose of the Study:
- To investigate the effects of antihypertensive drugs (enalapril, MK-954, hydralazine) on blood pressure, ventricular weight, and plasma BNP levels in DOCA-salt-induced hypertensive rats.
- To determine the source of BNP secretion (ventricle vs. atrium) affected by these treatments.
Main Methods:
- DOCA-salt hypertension was induced in SHR.
- Rats were chronically treated with enalapril, MK-954, or hydralazine.
- Blood pressure, ventricular weight, and plasma BNP concentration were measured.
- BNP secretory rates from isolated ventricles and atria were assessed.
- Acute administration of captopril or MK-954 was also studied.
Main Results:
- Chronic enalapril and MK-954 treatments decreased blood pressure, ventricular weight, and plasma BNP concentration.
- Hydralazine decreased blood pressure but did not affect ventricular weight or plasma BNP.
- BNP secretory rates from the ventricle were significantly reduced by enalapril and MK-954.
- Ventricular BNP secretion correlated positively with ventricular weight.
- Acute administration of captopril or MK-954 did not alter cardiac BNP secretion.
Conclusions:
- The reduction in plasma BNP observed with enalapril and MK-954 is primarily due to decreased secretion from the ventricle, not the atrium.
- This decrease in ventricular BNP secretion is linked to a reduction in ventricular mass.
- Hydralazine's antihypertensive effect does not involve modulation of ventricular BNP secretion.
Abstract:
The blood pressure was decreased after chronic treatment with enalapril, MK-954, and hydralazine in deoxycorticosterone acetate (DOCA)-salt-induced malignant hypertension of spontaneously hypertensive rats (SHR); however, ventricular weight and plasma brain natriuretic peptide (BNP) concentration were decreased after enalapril and MK-954 but not after hydralazine. The BNP secretory rates from the ventricle in enalapril- and MK-954-treated DOCA-salt SHR were decreased to approximately 50% of those in untreated DOCA-salt SHR. The BNP secretory rate from the ventricle was positively correlated with ventricular weight in untreated and treated DOCA-salt SHR. In contrast, acute administration of captopril or MK-954 did not decrease the BNP secretory rate from the heart. Results suggest that the decrease in plasma BNP after enalapril and MK-954 is attributed to a decline in the secretion from the ventricle but not from the atrium. The reduction in ventricular mass appeared to be related to this decline.