Contribution of the central interaction between calcium and sodium to hemodynamic regulation in spontaneously hypertensive rats

The contribution of the central interaction between calcium and sodium to hemodynamic regulation was assessed in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats. The effect of a high calcium solution (Ca2+, 130 mg/dl, 10 μl) infused into the cerebral ventricle (i.c.v.) on hemodynamic responses induced by a high sodium solution (Na+, 1,000 mEq/l, 10 μl) i.c.v. and the mechanism by which high Ca2+ affects the hemodynamic responses induced by high Na+ i.c.v. were studied. High Na+ i.c.v. induced a pressor response with tachycardia in the SHRs, but induced a pressor response with reflex bradycardia in the WKYs. Prior treatment with high Ca2+ i.c.v. attenuated the pressor response induced by high Na+ i.c.v. (+55.6 ± 4.4 to 33.1 ± 3.2 mmHg, P < 0.01) and restored reflex bradycardia (+86.4 ± 7.7 to −26.7 ± 7.6 bpm, P < 0.01) in SHRs. Whereas prior treatment with high Ca2+ i.c.v. attenuated the pressor response (+35.7 ±2.0 to +22.2 ± 4.0 mmHg, P < 0.05), it did not alter the degree of reflex bradycardia (−81.7 ± 7.1 to −69.2 ± 120 bpm, n.s.) in WKYs. Ganglionic blockade attenuated the pressor response (56.9 ± 3.5 to 42.9 ± 2.3 mmHg, P < 0.05) and restored reflex bradycardia (+82.1 ± 10.3 to −65.9 ± 11.0 bpm, P < 0.01) in SHRs, whereas, inhibition of arginine vasopressin attenuated the pressor response without modification of the tachycardic response. These results suggest (i) that central Ca2+ antagonizes the pressor response to central Na+ by inhibiting sympathetic nervous system activity and (ii) that central Ca2+ functions in the regulation of baroreflex control of the heart rate in SHRs. Central Ca2+ may have importance in cardiovascular regulation of hypertension.