Salt-Induced Hypertension in Dahl Salt-Sensitive Rats

Cardiac output, blood volume, total peripheral resistance, and renal blood flow were measured in awake salt-sensitive and salt-resistant Dahl rats on normal rat chow (1% NaCl) and on high salt (8% NaCl) diets. Rats were studied after 4, 8, and 46 weeks on a 1% NaCl diet and after 4 and 8 weeks on an 8% NaCl diet Salt-sensitive rats on 8% NaCl for 4 weeks developed systolic hypertension; by 8 weeks they developed greater systolic and also diastolic hypertension. Salt-resistant rats on 8% NaCl remained nonnotensive throughout the studies, although renal resistance decreased (p<0.05). At 4 weeks, hypertension in salt-sensitive rats on 8% NaCl was caused by increased blood volume and cardiac output (p<0.05), with normal total peripheral resistance. At 8 weeks, hypertension was due to increased total peripheral resistance (/><0.05); cardiac output was below normal despite persistent elevation of blood volume (p<0.05). Salt-sensitive rats on 1% NaCl for 46 weeks were hypertensive, with elevated total peripheral resistance (/?<0.05); cardiac output decreased (p<0.05), whereas blood volume remained unchanged. Salt-resistant rats on 1% NaCl remained nonnotensive with no changes in hemodynamics. Salt-sensitive rats on 8% NaCl for 4 weeks had an increase in renal vascular resistance but no significant change in nonrenal resistance or total peripheral resistance. The increased total peripheral resistance in salt-sensitive rats on 8% NaCl for 8 weeks and on 1% NaCl for 46 weeks was a reflection of increases of both renal and nonrenal vascular resistance. Salt-induced hypertension in salt-sensitive rats occurs by two mechanisms: on S% NaCl, hypertension is initiated by increased blood volume and cardiac output but is sustained by increased total peripheral resistance; with prolonged ingestion of a 1% NaCl diet, hypertension results from increased total peripheral resistance without increased blood volume or cardiac output Salt-sensitive rats on a 1% NaCl diet provide another model, probably more appropriate, to study human salt-sensitive hypertension unaccompanied by blood volume expansion. (Hypertension 1991;17:1063-1071)