The influence of common
salt (NaCl) and a novel
potassium-,
magnesium-, and
L-lysine-enriched
mineral salt on the cardiovascular and renal effects of the selective
imidazoline I1-receptor agonist
moxonidine was examined in spontaneously hypertensive rats (SHR). Common
salt was added at the level of 6% of the dry weight of the chow, and
mineral salt at a 75% higher level of 10.5% thereof to produce the same NaCl concentration of 6% as in the common
salt group. During the control diet an 8-week oral treatment with
moxonidine (117 mg/1000 g of the dry weight of the chow producing an approximate daily dose of 10 mg/kg), lowered blood pressure by 13 mmHg. The common
salt diet alone raised blood pressure by 27 mmHg.
Moxonidine lowered blood pressure by 21 mmHg during the common
salt diet, but the blood pressure remained 19 mmHg higher than in the
moxonidine-treated SHR receiving the control diet (P<0.05). Unlike common
salt,
mineral salt alone did not raise blood pressure nor did it interfere with the
antihypertensive effect of
moxonidine.
Moxonidine showed a kidney-protective effect during the control diet measured as decreased urinary
protein excretion, but it did not affect the development of
left ventricular hypertrophy.
Moxonidine increased plasma
renin activity during the control diet and it raised the serum
aldosterone level both during the control and
mineral salt diets. The vascular relaxation responses of the mesenteric arterial rings to both
acetylcholine (an
indicator of endothelium-dependent vascular relaxation) and
nitroprusside and
nitroprusside (an
indicator of endothelium-independent vascular relaxation) were attenuated by the common
salt diet alone but maintained during the
moxonidine treatment. Our findings are consistent with the concept that
moxonidine is able to improve the excretion of
sodium. This effect might explain the maintenance of normal vascular relaxation during a high intake of common
salt. These effects may partly account for the
antihypertensive effect of
moxonidine.