Dual hemodynamic mechanisms for salt-induced hypertension in Dahl salt-sensitive rats. Hypertension

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. Th