Enhanced depressor effect of centrally administered high-calcium solution in salt-loaded experimental hypertension

The depressor effect by oral calcium supplementation is known to be more pronounced in salt-dependent than in renin-dependent hypertension. This study was conducted to investigate the role of central calcium on two different pathophysiologic subtypes of experimental hypertension; (a) salt-dependent, deoxycorticosterone acetate-salt hypertensive rats (DOCA), and (b) renin-dependent, 2-kidney, 1 clip (2-K, 1C) hypertensive rats. In DOCA (n = 10), high-calcium solution (Ca +2 , 65.2 mM, 10 μl) given centrally (i.c.v.) elicited a marked decrease in mean blood pressure (MBP; 170 ± 4 to 138 ± 5 mm Hg, p < 0.01) with a decrease in heart rate (HR; 390 ± 18 to 344 ± 17 beats/min, p < 0.05) lasting for 40 min. In 2-K, 1C (n = 10), high-Ca 2+ i.c.v. showed a lesser decrease in MBP (178 ± 4 to 171 ± 5 mm Hg) and HR (419 ± 10 to 395 ± 12 beats/min) with shorter duration (for 20 min) than in DOCA. This significant depressor and bradycardic response to Ca 2+ i.c.v. observed in DOCA was dose dependent at Ca 2+ concentrations between 65.2 and 130.4 mM. In DOCA, high Ca 2+ i.c.v. reduced the plasma noradrenaline (Nad) concentration significantly (479 ± 81 to 319 ± 62 pg/ml, p < 0.05). These results suggest that central Ca 2+ plays a more important role in regulating sympathetic nerve activity and BP in salt-dependent than in renin-dependent experimental hypertension.