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17β‐Oestradiol enhances the acute hypotensive effect of captopril in female ovariectomized spontaneously hypertensive rats
Author(s) -
Giménez José,
García M. Paz,
Serna Mar,
Bonacasa Bárbara,
Carbonell Luis F.,
Quesada Tomás,
Hernández Isabel
Publication year - 2006
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2006.033449
Subject(s) - captopril , ovariectomized rat , bradykinin , endocrinology , medicine , nitric oxide synthase , mean arterial pressure , nitric oxide , blood pressure , angiotensin converting enzyme , hemodynamics , vascular resistance , chemistry , pharmacology , estrogen , receptor , heart rate
The objective of this study was to investigate whether the acute haemodynamic effects of angiotensin‐converting enzyme inhibition with captopril could be enhanced by oestrogen administration, and then to evaluate the mechanisms involved in this enhancement. All experiments were performed in 18‐week‐old female spontaneously hypertensive rats arranged in three experimental groups: intact; ovariectomized (OVX); and ovariectomized plus treatment with 17β‐oestradiol (OVX + E 2 ). These groups were used to evaluate the effects of captopril administration alone, or following bradykinin B2 receptor blockade or nitric oxide synthase inhibition, on a number of haemodynamic parameters (mean arterial pressure, cardiac index, vascular resistance and heart rate). The drop in mean arterial pressure and vascular resistance index in response to captopril was more pronounced in intact and ovariectomized rats treated with 17β‐oestradiol than in ovariectomized animals. Blockade of bradykinin B2 receptors or inhibition of nitric oxide synthesis attenuated the synergy between 17β‐oestradiol and captopril. It is concluded that ovariectomy blunted the blood pressure and vascular resistance index drop observed in intact rats in response to captopril. Treatment with 17β‐oestradiol prevented the blunted response to captopril in ovariectomized rats. Kinins and nitric oxide may be involved in the mechanisms of 17β‐oestradiol potentiation of the haemodynamic effects of captopril.

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