INFLUENCE OF DIFFERENT DIETARY SALTS ON THE CARDIOVASCULAR AND RENAL EFFECTS OF MOXONIDINE IN SPONTANEOUSLY HYPERTENSIVE RATS

Citation
Ema. Mervaala et al., INFLUENCE OF DIFFERENT DIETARY SALTS ON THE CARDIOVASCULAR AND RENAL EFFECTS OF MOXONIDINE IN SPONTANEOUSLY HYPERTENSIVE RATS, Naunyn-Schmiedeberg's archives of pharmacology, 356(1), 1997, pp. 107-114
Citations number
38
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00281298
Volume
356
Issue
1
Year of publication
1997
Pages
107 - 114
Database
ISI
SICI code
0028-1298(1997)356:1<107:IODDSO>2.0.ZU;2-P
Abstract
The influence of common salt (NaCl) and a novel potassium-, magnesium- , and L-lysine-enriched mineral salt on the cardiovascular and renal e ffects of the selective imidazoline I-1-receptor agonist moxonidine wa s examined in spontaneously hypertensive rats (SHR). Common salt was a dded at the level of 6% of the dry weight of the chow, and mineral sal t at a 75% higher level of 10.5% thereof to produce the same NaCl conc entration of 6% as in the common salt group. During the control diet a n 8-week oral treatment with moxonidine (117 mg/1000 g of the dry weig ht of the chow producing an approximate daily dose of 10mg/kg), lowere d blood pressure by 13 mmHg. The common salt diet alone raised blood p ressure by 27 mmHg. Moxonidine lowered blood pressure by 21 mmHg durin g 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 m easured 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 relaxat ion) and nitroprusside and nitroprusside (an indicator of endothelium- independent vascular relaxation) were attenuated by the common salt di et 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 nor mal vascular relaxation during a high intake of common salt. These eff ects may partly account for the antihypertensive effect of moxonidine.