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Cardiovascular effects evoked by central moxonidine in renovascular hypertensive (RH) rats.
Author(s) -
Costa Bruno M,
OliveiraSales Elisabeth B,
Moreira Thiago S,
Bergamaschi Cassia T,
Campos Ruy R,
Menani Jose Vanderlei,
Colombari Eduardo,
Sato Monica Akemi
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a513-a
Subject(s) - moxonidine , medicine , saline , imidazoline receptor , heart rate , mean arterial pressure , anesthesia , bradycardia , blood pressure , renovascular hypertension , endocrinology , agonist , receptor
Moxonidine is an anti‐hypertensive drug that binds on α 2 ‐adrenergic/imidazoline receptors. The main site of action of this drug is the rostroventrolateral medulla that causes fall in mean arterial pressure (MAP) and heart rate (HR) due to a decrease in sympathetic nerve activity. In the present study, we investigated the cardiovascular responses elicited by injections of moxonidine into the 4 th brain ventricle (4 th V) in conscious RH rats. Male Wistar rats (300–350 g, N= 6/group) had the left renal artery partially obstructed with a silver clip (0.2 mm width) 6 weeks prior to the experiments to induce the Goldblatt 2 kidneys‐1 clip hypertension model. Stainless steel guide cannulas were implanted into the 4 th V and polyethelene tubing was inserted into the femoral artery 5 days and 1 day prior to the experiments, respectively. Baseline MAP was 155 ± 4 mmHg and HR was 403 ± 12 bpm. Moxonidine (20 nmol) injected into 4 th V produced a long lasting (more than 30 min) decrease in MAP (−34 ± 4 mmHg, vs. saline 3 ± 4 mmHg, p<0.05) and HR (−99 ± 16 bpm, vs. saline 5 ± 4 bpm, p<0.05). These data suggest that central moxonidine also evokes hypotension and bradycardia in RH rats. Supported by FAPESP, CNPq‐PRONEX, and NEPAS.