'Calcium agonist' in salt-dependent hypertension: hints at calcium-mediated blood pressure increase.
To substantiate further the hypothesized importance of increased calcium influx into vascular smooth muscle, salt-sensitive Dahl rats (DS/JR, John Rapp), on either a low or a high salt diet, were treated with 100 or 300 ppm (i.e. mg/kg food) BAY k 8644, a calcium agonist. Simultaneously, salt-resistant Dahl rats (DR/JR) on a high salt diet received 300 ppm BAY k 8644. Blood pressure rose more rapidly in the agonist-treated DS/JR rats than in the untreated DS/JR controls on high salt diet. On the low salt diet, blood pressure was only slightly higher in the agonist-treated DS/JR. Although an increased calcium influx seems to be involved in salt-induced hypertension, the presence of high sodium chloride is apparently essential for its development. In addition, since DR/JR rats remained resistant to the effect of the calcium agonist, calcium per se is not the decisive factor responsible for the sensitivity or resistance of Dahl rats to salt load.
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D002118:Calcium / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D006973:Hypertension / Q000139:chemically induced* / Q000503:physiopathology; D009543:Nifedipine / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride / Q000633:toxicity*; D013997:Time Factors
D012965:Sodium Chloride; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009543:Nifedipine; D002118:Calcium